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class="vector-toc-list"> </ul> </li> <li id="toc-Management" class="vector-toc-list-item vector-toc-level-1"> <a class="vector-toc-link" href="#Management"> <div class="vector-toc-text"> 4 Management </div> </a> <button aria-controls="toc-Management-sublist" class="cdx-button cdx-button--weight-quiet cdx-button--icon-only vector-toc-toggle"> Toggle Management subsection </button> <ul id="toc-Management-sublist" class="vector-toc-list"> <li id="toc-Lifestyle" class="vector-toc-list-item vector-toc-level-2"> <a class="vector-toc-link" href="#Lifestyle"> <div class="vector-toc-text"> 4.1 Lifestyle </div> </a> <ul id="toc-Lifestyle-sublist" class="vector-toc-list"> </ul> </li> <li id="toc-Transplant" class="vector-toc-list-item vector-toc-level-2"> <a class="vector-toc-link" href="#Transplant"> <div class="vector-toc-text"> 4.2 Transplant </div> </a> <ul id="toc-Transplant-sublist" class="vector-toc-list"> </ul> </li> </ul> </li> <li id="toc-Pathogenesis" class="vector-toc-list-item vector-toc-level-1"> <a class="vector-toc-link" href="#Pathogenesis"> <div class="vector-toc-text"> 5 Pathogenesis </div> </a> <button aria-controls="toc-Pathogenesis-sublist" class="cdx-button cdx-button--weight-quiet cdx-button--icon-only vector-toc-toggle"> Toggle Pathogenesis subsection </button> <ul id="toc-Pathogenesis-sublist" class="vector-toc-list"> <li id="toc-Alpha_cell_dysfunction" class="vector-toc-list-item vector-toc-level-2"> <a class="vector-toc-link" href="#Alpha_cell_dysfunction"> <div class="vector-toc-text"> 5.1 Alpha cell dysfunction </div> </a> <ul id="toc-Alpha_cell_dysfunction-sublist" class="vector-toc-list"> <li id="toc-Hyperglucagonemia" class="vector-toc-list-item vector-toc-level-3"> <a class="vector-toc-link" href="#Hyperglucagonemia"> <div class="vector-toc-text"> 5.1.1 Hyperglucagonemia </div> </a> <ul id="toc-Hyperglucagonemia-sublist" class="vector-toc-list"> </ul> </li> <li id="toc-Hypoglycemic_glucagon_impairment" class="vector-toc-list-item vector-toc-level-3"> <a class="vector-toc-link" href="#Hypoglycemic_glucagon_impairment"> <div class="vector-toc-text"> 5.1.2 Hypoglycemic glucagon impairment </div> </a> <ul id="toc-Hypoglycemic_glucagon_impairment-sublist" class="vector-toc-list"> </ul> </li> </ul> </li> </ul> </li> <li id="toc-Complications" class="vector-toc-list-item vector-toc-level-1"> <a class="vector-toc-link" href="#Complications"> <div class="vector-toc-text"> 6 Complications </div> </a> <button aria-controls="toc-Complications-sublist" class="cdx-button cdx-button--weight-quiet cdx-button--icon-only vector-toc-toggle"> Toggle Complications subsection </button> <ul id="toc-Complications-sublist" class="vector-toc-list"> <li id="toc-Long-term_complications" class="vector-toc-list-item vector-toc-level-2"> <a class="vector-toc-link" href="#Long-term_complications"> <div class="vector-toc-text"> 6.1 Long-term complications </div> </a> <ul id="toc-Long-term_complications-sublist" class="vector-toc-list"> </ul> </li> <li id="toc-Urinary_tract_infection" class="vector-toc-list-item vector-toc-level-2"> <a class="vector-toc-link" href="#Urinary_tract_infection"> <div class="vector-toc-text"> 6.2 Urinary tract infection </div> </a> <ul id="toc-Urinary_tract_infection-sublist" class="vector-toc-list"> </ul> </li> <li id="toc-Sexual_dysfunction" class="vector-toc-list-item vector-toc-level-2"> <a class="vector-toc-link" href="#Sexual_dysfunction"> <div class="vector-toc-text"> 6.3 Sexual dysfunction </div> </a> <ul id="toc-Sexual_dysfunction-sublist" class="vector-toc-list"> </ul> </li> <li id="toc-Autoimmune_disorders" class="vector-toc-list-item vector-toc-level-2"> <a class="vector-toc-link" href="#Autoimmune_disorders"> <div class="vector-toc-text"> 6.4 Autoimmune disorders </div> </a> <ul id="toc-Autoimmune_disorders-sublist" class="vector-toc-list"> </ul> </li> </ul> </li> <li id="toc-Prevention" class="vector-toc-list-item vector-toc-level-1"> <a class="vector-toc-link" href="#Prevention"> <div class="vector-toc-text"> 7 Prevention </div> </a> <ul id="toc-Prevention-sublist" class="vector-toc-list"> </ul> </li> <li id="toc-Epidemiology" class="vector-toc-list-item vector-toc-level-1"> <a class="vector-toc-link" href="#Epidemiology"> <div class="vector-toc-text"> 8 Epidemiology </div> </a> <ul id="toc-Epidemiology-sublist" class="vector-toc-list"> </ul> </li> <li id="toc-Type_1_Diabetes_in_Youth" class="vector-toc-list-item vector-toc-level-1"> <a class="vector-toc-link" href="#Type_1_Diabetes_in_Youth"> <div class="vector-toc-text"> 9 Type 1 Diabetes in Youth </div> </a> <button aria-controls="toc-Type_1_Diabetes_in_Youth-sublist" class="cdx-button cdx-button--weight-quiet cdx-button--icon-only vector-toc-toggle"> Toggle Type 1 Diabetes in Youth subsection </button> <ul id="toc-Type_1_Diabetes_in_Youth-sublist" class="vector-toc-list"> <li id="toc-Management-_Exercise" class="vector-toc-list-item vector-toc-level-2"> <a class="vector-toc-link" href="#Management-_Exercise"> <div class="vector-toc-text"> 9.1 Management- Exercise </div> </a> <ul id="toc-Management-_Exercise-sublist" class="vector-toc-list"> </ul> </li> </ul> </li> <li id="toc-History" class="vector-toc-list-item vector-toc-level-1"> <a class="vector-toc-link" href="#History"> <div class="vector-toc-text"> 10 History </div> </a> <ul id="toc-History-sublist" class="vector-toc-list"> </ul> </li> <li id="toc-Society_and_culture" class="vector-toc-list-item vector-toc-level-1"> <a class="vector-toc-link" href="#Society_and_culture"> <div class="vector-toc-text"> 11 Society and culture </div> </a> <ul id="toc-Society_and_culture-sublist" class="vector-toc-list"> </ul> </li> <li id="toc-Research" class="vector-toc-list-item vector-toc-level-1"> <a class="vector-toc-link" href="#Research"> <div class="vector-toc-text"> 12 Research </div> </a> <button aria-controls="toc-Research-sublist" class="cdx-button cdx-button--weight-quiet cdx-button--icon-only vector-toc-toggle"> Toggle Research subsection </button> <ul id="toc-Research-sublist" class="vector-toc-list"> <li id="toc-Artificial_pancreas" class="vector-toc-list-item vector-toc-level-2"> <a class="vector-toc-link" href="#Artificial_pancreas"> <div class="vector-toc-text"> 12.1 Artificial pancreas </div> </a> <ul id="toc-Artificial_pancreas-sublist" class="vector-toc-list"> </ul> </li> <li id="toc-Disease_models" class="vector-toc-list-item vector-toc-level-2"> <a class="vector-toc-link" href="#Disease_models"> <div class="vector-toc-text"> 12.2 Disease models </div> </a> <ul id="toc-Disease_models-sublist" class="vector-toc-list"> <li id="toc-Chemically_induced" class="vector-toc-list-item vector-toc-level-3"> <a class="vector-toc-link" href="#Chemically_induced"> <div class="vector-toc-text"> 12.2.1 Chemically induced </div> </a> <ul id="toc-Chemically_induced-sublist" class="vector-toc-list"> </ul> </li> <li id="toc-Genetically_induced" class="vector-toc-list-item vector-toc-level-3"> <a class="vector-toc-link" href="#Genetically_induced"> <div class="vector-toc-text"> 12.2.2 Genetically induced </div> </a> <ul id="toc-Genetically_induced-sublist" class="vector-toc-list"> </ul> </li> <li id="toc-Virally_induced" class="vector-toc-list-item vector-toc-level-3"> <a class="vector-toc-link" href="#Virally_induced"> <div class="vector-toc-text"> 12.2.3 Virally induced </div> </a> <ul id="toc-Virally_induced-sublist" class="vector-toc-list"> </ul> </li> </ul> </li> </ul> </li> <li id="toc-References" class="vector-toc-list-item vector-toc-level-1"> <a class="vector-toc-link" href="#References"> <div class="vector-toc-text"> 13 References </div> </a> <ul id="toc-References-sublist" class="vector-toc-list"> </ul> </li> <li id="toc-Works_cited" class="vector-toc-list-item vector-toc-level-1"> <a class="vector-toc-link" href="#Works_cited"> <div class="vector-toc-text"> 14 Works cited </div> </a> <ul id="toc-Works_cited-sublist" class="vector-toc-list"> </ul> </li> <li id="toc-External_links" class="vector-toc-list-item vector-toc-level-1"> <a class="vector-toc-link" href="#External_links"> <div class="vector-toc-text"> 15 External links </div> </a> <ul id="toc-External_links-sublist" class="vector-toc-list"> </ul> </li> </ul> </div> </div> </nav> </div> </div> <div class="mw-content-container"> <main id="content" class="mw-body"> <header class="mw-body-header vector-page-titlebar"> <nav aria-label="Contents" class="vector-toc-landmark"> <div id="vector-page-titlebar-toc" class="vector-dropdown vector-page-titlebar-toc vector-button-flush-left" > <input type="checkbox" id="vector-page-titlebar-toc-checkbox" role="button" aria-haspopup="true" data-event-name="ui.dropdown-vector-page-titlebar-toc" class="vector-dropdown-checkbox " aria-label="Toggle the table of contents" > <label id="vector-page-titlebar-toc-label" for="vector-page-titlebar-toc-checkbox" class="vector-dropdown-label cdx-button cdx-button--fake-button cdx-button--fake-button--enabled cdx-button--weight-quiet cdx-button--icon-only " aria-hidden="true" > Toggle the table of contents </label> <div class="vector-dropdown-content"> <div id="vector-page-titlebar-toc-unpinned-container" class="vector-unpinned-container"> </div> </div> </div> </nav> <h1 id="firstHeading" class="firstHeading mw-first-heading">Type 1 diabetes</h1> <div id="p-lang-btn" class="vector-dropdown mw-portlet mw-portlet-lang" > <input type="checkbox" id="p-lang-btn-checkbox" role="button" aria-haspopup="true" data-event-name="ui.dropdown-p-lang-btn" class="vector-dropdown-checkbox mw-interlanguage-selector" aria-label="Go to an article in another language. Available in 42 languages" > <label id="p-lang-btn-label" for="p-lang-btn-checkbox" class="vector-dropdown-label cdx-button cdx-button--fake-button cdx-button--fake-button--enabled cdx-button--weight-quiet cdx-button--action-progressive mw-portlet-lang-heading-42" aria-hidden="true" > 42 languages </label> <div class="vector-dropdown-content"> <div class="vector-menu-content"> <ul class="vector-menu-content-list"> <li class="interlanguage-link interwiki-ar mw-list-item"><a href="https://ar.wikipedia.org/wiki/%D8%B3%D9%83%D8%B1%D9%8A_%D8%A7%D9%84%D9%86%D9%88%D8%B9_%D8%A7%D9%84%D8%A3%D9%88%D9%84" title="سكري النوع الأول – Arabic" lang="ar" hreflang="ar" data-title="سكري النوع الأول" data-language-autonym="العربية" data-language-local-name="Arabic" class="interlanguage-link-target">العربية</a></li><li class="interlanguage-link interwiki-bn mw-list-item"><a href="https://bn.wikipedia.org/wiki/%E0%A6%9F%E0%A6%BE%E0%A6%87%E0%A6%AA_%E0%A7%A7_%E0%A6%A1%E0%A6%BE%E0%A6%AF%E0%A6%BC%E0%A6%BE%E0%A6%AC%E0%A7%87%E0%A6%9F%E0%A6%BF%E0%A6%B8" title="টাইপ ১ ডায়াবেটিস – Bangla" lang="bn" hreflang="bn" data-title="টাইপ ১ ডায়াবেটিস" data-language-autonym="বাংলা" data-language-local-name="Bangla" class="interlanguage-link-target">বাংলা</a></li><li class="interlanguage-link interwiki-bs mw-list-item"><a href="https://bs.wikipedia.org/wiki/Dijabetes_melitus_tip_1" title="Dijabetes melitus tip 1 – Bosnian" lang="bs" hreflang="bs" data-title="Dijabetes melitus tip 1" data-language-autonym="Bosanski" data-language-local-name="Bosnian" class="interlanguage-link-target">Bosanski</a></li><li class="interlanguage-link interwiki-ca mw-list-item"><a href="https://ca.wikipedia.org/wiki/Diabetis_mellitus_de_tipus_1" title="Diabetis mellitus de tipus 1 – Catalan" lang="ca" hreflang="ca" data-title="Diabetis mellitus de tipus 1" data-language-autonym="Català" data-language-local-name="Catalan" class="interlanguage-link-target">Català</a></li><li class="interlanguage-link interwiki-de mw-list-item"><a href="https://de.wikipedia.org/wiki/Diabetes_mellitus#Diabetes_Typ_1" title="Diabetes mellitus – German" lang="de" hreflang="de" data-title="Diabetes mellitus" data-language-autonym="Deutsch" data-language-local-name="German" class="interlanguage-link-target">Deutsch</a></li><li class="interlanguage-link interwiki-dv mw-list-item"><a href="https://dv.wikipedia.org/wiki/%DE%80%DE%A6%DE%86%DE%AA%DE%83%DE%AA_%DE%84%DE%A6%DE%8D%DE%A9%DE%8E%DE%AC_%DE%8A%DE%AA%DE%83%DE%A6%DE%8C%DE%A6%DE%89%DE%A6_%DE%88%DE%A6%DE%87%DE%B0%DE%8C%DE%A6%DE%83%DE%AA" title="ހަކުރު ބަލީގެ ފުރަތަމަ ވައްތަރު – Divehi" lang="dv" hreflang="dv" data-title="ހަކުރު ބަލީގެ ފުރަތަމަ ވައްތަރު" data-language-autonym="ދިވެހިބަސް" data-language-local-name="Divehi" class="interlanguage-link-target">ދިވެހިބަސް</a></li><li class="interlanguage-link interwiki-et mw-list-item"><a href="https://et.wikipedia.org/wiki/I_t%C3%BC%C3%BCpi_diabeet" title="I tüüpi diabeet – Estonian" lang="et" hreflang="et" data-title="I tüüpi diabeet" data-language-autonym="Eesti" data-language-local-name="Estonian" class="interlanguage-link-target">Eesti</a></li><li class="interlanguage-link interwiki-el mw-list-item"><a href="https://el.wikipedia.org/wiki/%CE%A3%CE%B1%CE%BA%CF%87%CE%B1%CF%81%CF%8E%CE%B4%CE%B7%CF%82_%CE%B4%CE%B9%CE%B1%CE%B2%CE%AE%CF%84%CE%B7%CF%82_%CF%84%CF%8D%CF%80%CE%BF%CF%85_1" title="Σακχαρώδης διαβήτης τύπου 1 – Greek" lang="el" hreflang="el" data-title="Σακχαρώδης διαβήτης τύπου 1" data-language-autonym="Ελληνικά" data-language-local-name="Greek" class="interlanguage-link-target">Ελληνικά</a></li><li class="interlanguage-link interwiki-es mw-list-item"><a href="https://es.wikipedia.org/wiki/Diabetes_mellitus_tipo_1" title="Diabetes mellitus tipo 1 – Spanish" lang="es" hreflang="es" data-title="Diabetes mellitus tipo 1" data-language-autonym="Español" data-language-local-name="Spanish" class="interlanguage-link-target">Español</a></li><li class="interlanguage-link interwiki-eu mw-list-item"><a href="https://eu.wikipedia.org/wiki/1._motako_diabetes_mellitus" title="1. motako diabetes mellitus – Basque" lang="eu" hreflang="eu" data-title="1. motako diabetes mellitus" data-language-autonym="Euskara" data-language-local-name="Basque" class="interlanguage-link-target">Euskara</a></li><li class="interlanguage-link interwiki-fa mw-list-item"><a href="https://fa.wikipedia.org/wiki/%D8%AF%DB%8C%D8%A7%D8%A8%D8%AA_%D9%86%D9%88%D8%B9_%DB%B1" title="دیابت نوع ۱ – Persian" lang="fa" hreflang="fa" data-title="دیابت نوع ۱" data-language-autonym="فارسی" data-language-local-name="Persian" class="interlanguage-link-target">فارسی</a></li><li class="interlanguage-link interwiki-fr mw-list-item"><a href="https://fr.wikipedia.org/wiki/Diab%C3%A8te_de_type_1" title="Diabète de type 1 – French" lang="fr" hreflang="fr" data-title="Diabète de type 1" data-language-autonym="Français" data-language-local-name="French" class="interlanguage-link-target">Français</a></li><li class="interlanguage-link interwiki-gu mw-list-item"><a href="https://gu.wikipedia.org/wiki/%E0%AA%9F%E0%AA%BE%E0%AA%87%E0%AA%AA_%E0%AB%A7_%E0%AA%A1%E0%AA%BE%E0%AA%AF%E0%AA%BE%E0%AA%AC%E0%AA%BF%E0%AA%9F%E0%AB%80%E0%AA%B8" title="ટાઇપ ૧ ડાયાબિટીસ – Gujarati" lang="gu" hreflang="gu" data-title="ટાઇપ ૧ ડાયાબિટીસ" data-language-autonym="ગુજરાતી" data-language-local-name="Gujarati" class="interlanguage-link-target">ગુજરાતી</a></li><li class="interlanguage-link interwiki-ko mw-list-item"><a href="https://ko.wikipedia.org/wiki/%EC%A0%9C1%ED%98%95_%EB%8B%B9%EB%87%A8%EB%B3%91" title="제1형 당뇨병 – Korean" lang="ko" hreflang="ko" data-title="제1형 당뇨병" data-language-autonym="한국어" data-language-local-name="Korean" class="interlanguage-link-target">한국어</a></li><li class="interlanguage-link interwiki-hy mw-list-item"><a href="https://hy.wikipedia.org/wiki/%D5%8F%D5%AB%D5%BA_1_%D5%B7%D5%A1%D6%84%D5%A1%D6%80%D5%A1%D5%B5%D5%AB%D5%B6_%D5%A4%D5%AB%D5%A1%D5%A2%D5%A5%D5%BF" title="Տիպ 1 շաքարային դիաբետ – Armenian" lang="hy" hreflang="hy" data-title="Տիպ 1 շաքարային դիաբետ" data-language-autonym="Հայերեն" data-language-local-name="Armenian" class="interlanguage-link-target">Հայերեն</a></li><li class="interlanguage-link interwiki-hi mw-list-item"><a href="https://hi.wikipedia.org/wiki/%E0%A4%9F%E0%A4%BE%E0%A4%87%E0%A4%AA_1_%E0%A4%A1%E0%A4%BE%E0%A4%AF%E0%A4%AC%E0%A4%BF%E0%A4%9F%E0%A5%80%E0%A4%9C_%E0%A4%AE%E0%A5%87%E0%A4%B2%E0%A5%87%E0%A4%9F%E0%A4%B8" title="टाइप 1 डायबिटीज मेलेटस – Hindi" lang="hi" hreflang="hi" data-title="टाइप 1 डायबिटीज मेलेटस" data-language-autonym="हिन्दी" data-language-local-name="Hindi" class="interlanguage-link-target">हिन्दी</a></li><li class="interlanguage-link interwiki-id mw-list-item"><a href="https://id.wikipedia.org/wiki/Diabetes_melitus_tipe_1" title="Diabetes melitus tipe 1 – Indonesian" lang="id" hreflang="id" data-title="Diabetes melitus tipe 1" data-language-autonym="Bahasa Indonesia" data-language-local-name="Indonesian" class="interlanguage-link-target">Bahasa Indonesia</a></li><li class="interlanguage-link interwiki-it mw-list-item"><a href="https://it.wikipedia.org/wiki/Diabete_mellito_di_tipo_1" title="Diabete mellito di tipo 1 – Italian" lang="it" hreflang="it" data-title="Diabete mellito di tipo 1" data-language-autonym="Italiano" data-language-local-name="Italian" class="interlanguage-link-target">Italiano</a></li><li class="interlanguage-link interwiki-he mw-list-item"><a href="https://he.wikipedia.org/wiki/%D7%A1%D7%95%D7%9B%D7%A8%D7%AA_%D7%9E%D7%A1%D7%95%D7%92_1" title="סוכרת מסוג 1 – Hebrew" lang="he" hreflang="he" data-title="סוכרת מסוג 1" data-language-autonym="עברית" data-language-local-name="Hebrew" class="interlanguage-link-target">עברית</a></li><li class="interlanguage-link interwiki-pam mw-list-item"><a href="https://pam.wikipedia.org/wiki/Diabetes_mellitus_type_1" title="Diabetes mellitus type 1 – Pampanga" lang="pam" hreflang="pam" data-title="Diabetes mellitus type 1" data-language-autonym="Kapampangan" data-language-local-name="Pampanga" class="interlanguage-link-target">Kapampangan</a></li><li class="interlanguage-link interwiki-lfn mw-list-item"><a href="https://lfn.wikipedia.org/wiki/Diabete_(tipo_1)" title="Diabete (tipo 1) – Lingua Franca Nova" lang="lfn" hreflang="lfn" data-title="Diabete (tipo 1)" data-language-autonym="Lingua Franca Nova" data-language-local-name="Lingua Franca Nova" class="interlanguage-link-target">Lingua Franca Nova</a></li><li class="interlanguage-link interwiki-mk mw-list-item"><a href="https://mk.wikipedia.org/wiki/%D0%94%D0%B8%D1%98%D0%B0%D0%B1%D0%B5%D1%82%D0%B5%D1%81_%D0%BC%D0%B5%D0%BB%D0%B8%D1%82%D1%83%D1%81_%D1%82%D0%B8%D0%BF_1" title="Дијабетес мелитус тип 1 – Macedonian" lang="mk" hreflang="mk" data-title="Дијабетес мелитус тип 1" data-language-autonym="Македонски" data-language-local-name="Macedonian" class="interlanguage-link-target">Македонски</a></li><li class="interlanguage-link interwiki-ms mw-list-item"><a href="https://ms.wikipedia.org/wiki/Diabetis_melitus_jenis_1" title="Diabetis melitus jenis 1 – Malay" lang="ms" hreflang="ms" data-title="Diabetis melitus jenis 1" data-language-autonym="Bahasa Melayu" data-language-local-name="Malay" class="interlanguage-link-target">Bahasa Melayu</a></li><li class="interlanguage-link interwiki-my mw-list-item"><a href="https://my.wikipedia.org/wiki/%E1%80%86%E1%80%AE%E1%80%B8%E1%80%81%E1%80%BB%E1%80%AD%E1%80%AF%E1%80%A1%E1%80%99%E1%80%BB%E1%80%AD%E1%80%AF%E1%80%B8%E1%80%A1%E1%80%85%E1%80%AC%E1%80%B8-%E1%81%81" title="ဆီးချိုအမျိုးအစား-၁ – Burmese" lang="my" hreflang="my" data-title="ဆီးချိုအမျိုးအစား-၁" data-language-autonym="မြန်မာဘာသာ" data-language-local-name="Burmese" class="interlanguage-link-target">မြန်မာဘာသာ</a></li><li class="interlanguage-link interwiki-ja mw-list-item"><a href="https://ja.wikipedia.org/wiki/1%E5%9E%8B%E7%B3%96%E5%B0%BF%E7%97%85" title="1型糖尿病 – Japanese" lang="ja" hreflang="ja" data-title="1型糖尿病" data-language-autonym="日本語" data-language-local-name="Japanese" class="interlanguage-link-target">日本語</a></li><li class="interlanguage-link interwiki-no badge-Q17437796 badge-featuredarticle mw-list-item" title="featured article badge"><a href="https://no.wikipedia.org/wiki/Diabetes_type_1" title="Diabetes type 1 – Norwegian Bokmål" lang="nb" hreflang="nb" data-title="Diabetes type 1" data-language-autonym="Norsk bokmål" data-language-local-name="Norwegian Bokmål" class="interlanguage-link-target">Norsk bokmål</a></li><li class="interlanguage-link interwiki-or mw-list-item"><a href="https://or.wikipedia.org/wiki/%E0%AC%AE%E0%AC%A7%E0%AD%81%E0%AC%AE%E0%AD%87%E0%AC%B9_%E0%AC%9F%E0%AC%BE%E0%AC%87%E0%AC%AA_%E0%AD%A7" title="ମଧୁମେହ ଟାଇପ ୧ – Odia" lang="or" hreflang="or" data-title="ମଧୁମେହ ଟାଇପ ୧" data-language-autonym="ଓଡ଼ିଆ" data-language-local-name="Odia" class="interlanguage-link-target">ଓଡ଼ିଆ</a></li><li class="interlanguage-link interwiki-pl mw-list-item"><a href="https://pl.wikipedia.org/wiki/Cukrzyca_typu_1" title="Cukrzyca typu 1 – Polish" lang="pl" hreflang="pl" data-title="Cukrzyca typu 1" data-language-autonym="Polski" data-language-local-name="Polish" class="interlanguage-link-target">Polski</a></li><li class="interlanguage-link interwiki-pt mw-list-item"><a href="https://pt.wikipedia.org/wiki/Diabetes_mellitus_tipo_1" title="Diabetes mellitus tipo 1 – Portuguese" lang="pt" hreflang="pt" data-title="Diabetes mellitus tipo 1" data-language-autonym="Português" data-language-local-name="Portuguese" class="interlanguage-link-target">Português</a></li><li class="interlanguage-link interwiki-ru mw-list-item"><a href="https://ru.wikipedia.org/wiki/%D0%A1%D0%B0%D1%85%D0%B0%D1%80%D0%BD%D1%8B%D0%B9_%D0%B4%D0%B8%D0%B0%D0%B1%D0%B5%D1%82_1-%D0%B3%D0%BE_%D1%82%D0%B8%D0%BF%D0%B0" title="Сахарный диабет 1-го типа – Russian" lang="ru" hreflang="ru" data-title="Сахарный диабет 1-го типа" data-language-autonym="Русский" data-language-local-name="Russian" class="interlanguage-link-target">Русский</a></li><li class="interlanguage-link interwiki-sq mw-list-item"><a href="https://sq.wikipedia.org/wiki/Diabeti_i_tipit_1" title="Diabeti i tipit 1 – Albanian" lang="sq" hreflang="sq" data-title="Diabeti i tipit 1" data-language-autonym="Shqip" data-language-local-name="Albanian" class="interlanguage-link-target">Shqip</a></li><li class="interlanguage-link interwiki-simple mw-list-item"><a href="https://simple.wikipedia.org/wiki/Type_1_diabetes" title="Type 1 diabetes – Simple English" lang="en-simple" hreflang="en-simple" data-title="Type 1 diabetes" data-language-autonym="Simple English" data-language-local-name="Simple English" class="interlanguage-link-target">Simple English</a></li><li class="interlanguage-link interwiki-sl mw-list-item"><a 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class="interlanguage-link-target">Suomi</a></li><li class="interlanguage-link interwiki-sv mw-list-item"><a href="https://sv.wikipedia.org/wiki/Typ_1-diabetes" title="Typ 1-diabetes – Swedish" lang="sv" hreflang="sv" data-title="Typ 1-diabetes" data-language-autonym="Svenska" data-language-local-name="Swedish" class="interlanguage-link-target">Svenska</a></li><li class="interlanguage-link interwiki-th mw-list-item"><a href="https://th.wikipedia.org/wiki/%E0%B9%80%E0%B8%9A%E0%B8%B2%E0%B8%AB%E0%B8%A7%E0%B8%B2%E0%B8%99%E0%B8%8A%E0%B8%99%E0%B8%B4%E0%B8%94%E0%B8%97%E0%B8%B5%E0%B9%88_1" title="เบาหวานชนิดที่ 1 – Thai" lang="th" hreflang="th" data-title="เบาหวานชนิดที่ 1" data-language-autonym="ไทย" data-language-local-name="Thai" class="interlanguage-link-target">ไทย</a></li><li class="interlanguage-link interwiki-tr mw-list-item"><a href="https://tr.wikipedia.org/wiki/Tip_1_diyabet" title="Tip 1 diyabet – Turkish" lang="tr" hreflang="tr" data-title="Tip 1 diyabet" 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.infobox-subbox{padding:0;border:none;margin:-3px;width:auto;min-width:100%;font-size:100%;clear:none;float:none;background-color:transparent}.mw-parser-output .infobox-3cols-child{margin:auto}.mw-parser-output .infobox .navbar{font-size:100%}@media screen{html.skin-theme-clientpref-night .mw-parser-output .infobox-full-data:not(.notheme)>div:not(.notheme)[style]{background:#1f1f23!important;color:#f8f9fa}}@media screen and (prefers-color-scheme:dark){html.skin-theme-clientpref-os .mw-parser-output .infobox-full-data:not(.notheme) div:not(.notheme){background:#1f1f23!important;color:#f8f9fa}}@media(min-width:640px){body.skin--responsive .mw-parser-output .infobox-table{display:table!important}body.skin--responsive .mw-parser-output .infobox-table>caption{display:table-caption!important}body.skin--responsive .mw-parser-output .infobox-table>tbody{display:table-row-group}body.skin--responsive .mw-parser-output .infobox-table tr{display:table-row!important}body.skin--responsive .mw-parser-output .infobox-table th,body.skin--responsive .mw-parser-output .infobox-table td{padding-left:inherit;padding-right:inherit}}</style><table class="infobox ib-medical-condition"><tbody><tr><th colspan="2" class="infobox-above" style="background:#ccc">Type 1 diabetes</th></tr><tr><th scope="row" class="infobox-label">Other names</th><td class="infobox-data">Diabetes mellitus type 1, insulin-dependent diabetes, juvenile diabetes</td></tr><tr style="background-color: #f8f9fa;"><td colspan="2" class="infobox-full-data"><a href="/wiki/File:Blue_circle_for_diabetes.svg" class="mw-file-description"><img src="//upload.wikimedia.org/wikipedia/commons/thumb/4/43/Blue_circle_for_diabetes.svg/200px-Blue_circle_for_diabetes.svg.png" decoding="async" width="200" height="200" class="mw-file-element" srcset="//upload.wikimedia.org/wikipedia/commons/thumb/4/43/Blue_circle_for_diabetes.svg/300px-Blue_circle_for_diabetes.svg.png 1.5x, //upload.wikimedia.org/wikipedia/commons/thumb/4/43/Blue_circle_for_diabetes.svg/400px-Blue_circle_for_diabetes.svg.png 2x" data-file-width="240" data-file-height="240" /></a></td></tr><tr><td colspan="2" class="infobox-full-data">A blue circle, the symbol for diabetes</td></tr><tr><th scope="row" class="infobox-label">Pronunciation</th><td class="infobox-data"><style data-mw-deduplicate="TemplateStyles:r1126788409">.mw-parser-output .plainlist ol,.mw-parser-output .plainlist ul{line-height:inherit;list-style:none;margin:0;padding:0}.mw-parser-output .plainlist ol li,.mw-parser-output .plainlist ul li{margin-bottom:0}</style><div class="plainlist"><ul><li><a href="/wiki/Help:IPA/English" title="Help:IPA/English">/daɪəˈbiːtiːz/</a> </li></ul></div></td></tr><tr><th scope="row" class="infobox-label"><a href="/wiki/Medical_specialty" title="Medical specialty">Specialty</a></th><td class="infobox-data"><a href="/wiki/Endocrinology" title="Endocrinology">Endocrinology</a></td></tr><tr><th scope="row" class="infobox-label"><a href="/wiki/Signs_and_symptoms" title="Signs and symptoms">Symptoms</a></th><td class="infobox-data"><a href="/wiki/Polyuria" title="Polyuria">Frequent urination</a>, <a href="/wiki/Polydipsia" title="Polydipsia">increased thirst</a>, <a href="/wiki/Weight_loss" title="Weight loss">weight loss</a></td></tr><tr><th scope="row" class="infobox-label"><a href="/wiki/Complication_(medicine)" title="Complication (medicine)">Complications</a></th><td class="infobox-data"><a href="/wiki/Diabetic_ketoacidosis" title="Diabetic ketoacidosis">Diabetic ketoacidosis</a>, severe <a href="/wiki/Hypoglycemia" title="Hypoglycemia">hypoglycemia</a>, <a href="/wiki/Cardiovascular_disease" title="Cardiovascular disease">cardiovascular disease</a>, and damage to the eyes, kidneys, and nerves</td></tr><tr><th scope="row" class="infobox-label">Usual onset</th><td class="infobox-data">At any age; over days to weeks</td></tr><tr><th scope="row" class="infobox-label">Duration</th><td class="infobox-data">Lifelong</td></tr><tr><th scope="row" class="infobox-label">Causes</th><td class="infobox-data">Body does not produce enough <a href="/wiki/Insulin" title="Insulin">insulin</a></td></tr><tr><th scope="row" class="infobox-label"><a href="/wiki/Risk_factor" title="Risk factor">Risk factors</a></th><td class="infobox-data">Family history, <a href="/wiki/Celiac_disease" class="mw-redirect" title="Celiac disease">celiac disease</a>, autoimmune diseases</td></tr><tr><th scope="row" class="infobox-label"><a href="/wiki/Medical_diagnosis" title="Medical diagnosis">Diagnostic method</a></th><td class="infobox-data">High blood sugar levels, <a href="/wiki/Autoantibody" title="Autoantibody">autoantibodies</a> targeting insulin-producing cells</td></tr><tr><th scope="row" class="infobox-label">Prevention</th><td class="infobox-data"><a href="/wiki/Teplizumab" title="Teplizumab">Teplizumab</a></td></tr><tr><th scope="row" class="infobox-label">Treatment</th><td class="infobox-data">Monitoring blood sugar, injected <a href="/wiki/Insulin_(medication)" title="Insulin (medication)">insulin</a>, managing diet</td></tr><tr><th scope="row" class="infobox-label"><a href="/wiki/Prognosis" title="Prognosis">Prognosis</a></th><td class="infobox-data">10-12 years shorter <a href="/wiki/Life_expectancy" title="Life expectancy">life expectancy</a><a href="#cite_note-1">[1]</a><a href="#cite_note-2">[2]</a><a href="#cite_note-3">[3]</a></td></tr><tr><th scope="row" class="infobox-label">Frequency</th><td class="infobox-data">11–22 million cases globally<a href="#cite_note-WHO11-4">[4]</a></td></tr></tbody></table> Type 1 diabetes (T1D), formerly known as juvenile diabetes, is an <a href="/wiki/Autoimmune_disease" title="Autoimmune disease">autoimmune disease</a> that occurs when pancreatic cells (beta cells) are destroyed by the body's <a href="/wiki/Immune_system" title="Immune system">immune system</a>.<a href="#cite_note-WHO2016-5">[5]</a> In healthy persons, beta cells produce insulin. Insulin is a hormone required by the body to store and convert <a href="/wiki/Blood_sugar" class="mw-redirect" title="Blood sugar">blood sugar</a> into energy.<a href="#cite_note-NIH2014Type-6">[6]</a> T1D results in <a href="/wiki/Hyperglycemia" title="Hyperglycemia">high blood sugar</a> levels in the body prior to treatment.<a href="#cite_note-NIH2014Cau-7">[7]</a> Common symptoms include <a href="/wiki/Polyuria" title="Polyuria">frequent urination</a>, <a href="/wiki/Polydipsia" title="Polydipsia">increased thirst</a>, <a href="/wiki/Polyphagia" title="Polyphagia">increased hunger</a>, weight loss, and other complications.<a href="#cite_note-WHO2016-5">[5]</a><a href="#cite_note-8">[8]</a> Additional symptoms may include <a href="/wiki/Blurry_vision" class="mw-redirect" title="Blurry vision">blurry vision</a>, <a href="/wiki/Fatigue_(medical)" class="mw-redirect" title="Fatigue (medical)">tiredness</a>, and slow wound healing (owing to impaired blood flow).<a href="#cite_note-NIH2014Type-6">[6]</a> While some cases take longer, symptoms usually appear within weeks or a few months.<a href="#cite_note-9">[9]</a><a href="#cite_note-NIH2014Cau-7">[7]</a> The cause of type 1 diabetes is not completely understood, though there have been recent studies that suggest linkage with HLA-DR3/DR4-DQ8.<a href="#cite_note-10">[10]</a><a href="#cite_note-WHO2016-5">[5]</a> Further, it is believed to involve a combination of genetic and environmental factors.<a href="#cite_note-11">[11]</a><a href="#cite_note-NIH2014Cau-7">[7]</a> The underlying mechanism involves an <a href="/wiki/Autoimmune" class="mw-redirect" title="Autoimmune">autoimmune</a> destruction of the insulin-producing <a href="/wiki/Beta_cells" class="mw-redirect" title="Beta cells">beta cells</a> in the <a href="/wiki/Pancreas" title="Pancreas">pancreas</a>.<a href="#cite_note-NIH2014Type-6">[6]</a> <a href="/wiki/Diabetes" title="Diabetes">Diabetes</a> is diagnosed by testing the level of sugar or <a href="/wiki/Glycated_hemoglobin" title="Glycated hemoglobin">glycated hemoglobin</a> (HbA1C) in the blood.<a href="#cite_note-Change2014-12">[12]</a><a href="#cite_note-NIH2015Diag-13">[13]</a> Type 1 diabetes can typically be distinguished from <a href="/wiki/Type_2_Diabetes" class="mw-redirect" title="Type 2 Diabetes">type 2</a> by testing for the presence of <a href="/wiki/Autoantibody" title="Autoantibody">autoantibodies</a><a href="#cite_note-Change2014-12">[12]</a> and/or declining levels/absence of <a href="/wiki/C-peptide" title="C-peptide">C-peptide</a>. There is no known way to prevent type 1 diabetes.<a href="#cite_note-WHO2016-5">[5]</a> Treatment with <a href="/wiki/Insulin" title="Insulin">insulin</a> is required for survival.<a href="#cite_note-NIH2014Cau-7">[7]</a> <a href="/wiki/Insulin_therapy" class="mw-redirect" title="Insulin therapy">Insulin therapy</a> is usually given by injection just under the skin but can also be delivered by an <a href="/wiki/Insulin_pump" title="Insulin pump">insulin pump</a>.<a href="#cite_note-14">[14]</a> A <a href="/wiki/Diabetic_diet" class="mw-redirect" title="Diabetic diet">diabetic diet</a>, exercise, and lifestyle modifications are considered cornerstones of management.<a href="#cite_note-NIH2014Type-6">[6]</a> If left untreated, diabetes can cause many complications.<a href="#cite_note-WHO2016-5">[5]</a> Complications of relatively rapid onset include <a href="/wiki/Diabetic_ketoacidosis" title="Diabetic ketoacidosis">diabetic ketoacidosis</a> and <a href="/wiki/Nonketotic_hyperosmolar_coma" class="mw-redirect" title="Nonketotic hyperosmolar coma">nonketotic hyperosmolar coma</a>.<a href="#cite_note-Change2014-12">[12]</a> Long-term complications include <a href="/wiki/Cardiovascular_disease" title="Cardiovascular disease">heart disease</a>, stroke, <a href="/wiki/Chronic_renal_failure" class="mw-redirect" title="Chronic renal failure">kidney failure</a>, <a href="/wiki/Diabetic_foot_ulcer" title="Diabetic foot ulcer">foot ulcers</a>, and <a href="/wiki/Diabetic_retinopathy" title="Diabetic retinopathy">damage to the eyes</a>.<a href="#cite_note-WHO2016-5">[5]</a> Furthermore, since insulin lowers blood sugar levels, complications may arise from <a href="/wiki/Hypoglycemia" title="Hypoglycemia">low blood sugar</a> if more insulin is taken than necessary.<a href="#cite_note-Change2014-12">[12]</a> Type 1 diabetes makes up an estimated 5–10% of all diabetes cases.<a href="#cite_note-Lancet06-15">[15]</a> The number of people affected globally is unknown, although it is estimated that about 80,000 children develop the disease each year.<a href="#cite_note-Change2014-12">[12]</a> Within the United States the number of people affected is estimated to be one to three million.<a href="#cite_note-Change2014-12">[12]</a><a href="#cite_note-16">[16]</a> Rates of disease vary widely, with approximately one new case per 100,000 per year in East Asia and Latin America and around 30 new cases per 100,000 per year in <a href="/wiki/Scandinavia" title="Scandinavia">Scandinavia</a> and <a href="/wiki/Kuwait" title="Kuwait">Kuwait</a>.<a href="#cite_note-17">[17]</a><a href="#cite_note-18">[18]</a> It typically begins in children and young adults but can begin at any age.<a href="#cite_note-NIH2014Cau-7">[7]</a><a href="#cite_note-:5-19">[19]</a> <style data-mw-deduplicate="TemplateStyles:r886046785">.mw-parser-output .toclimit-2 .toclevel-1 ul,.mw-parser-output .toclimit-3 .toclevel-2 ul,.mw-parser-output .toclimit-4 .toclevel-3 ul,.mw-parser-output .toclimit-5 .toclevel-4 ul,.mw-parser-output .toclimit-6 .toclevel-5 ul,.mw-parser-output .toclimit-7 .toclevel-6 ul{display:none}</style><div class="toclimit-3"><meta property="mw:PageProp/toc" /></div> <div class="mw-heading mw-heading2"><h2 id="Signs_and_symptoms">Signs and symptoms</h2>[<a href="/w/index.php?title=Type_1_diabetes&action=edit&section=1" title="Edit section: Signs and symptoms">edit</a>]</div> <figure class="mw-default-size" typeof="mw:File/Thumb"><a href="/wiki/File:Main_symptoms_of_diabetes.png" class="mw-file-description"><img src="//upload.wikimedia.org/wikipedia/commons/thumb/2/28/Main_symptoms_of_diabetes.png/310px-Main_symptoms_of_diabetes.png" decoding="async" width="310" height="317" class="mw-file-element" srcset="//upload.wikimedia.org/wikipedia/commons/thumb/2/28/Main_symptoms_of_diabetes.png/465px-Main_symptoms_of_diabetes.png 1.5x, //upload.wikimedia.org/wikipedia/commons/thumb/2/28/Main_symptoms_of_diabetes.png/620px-Main_symptoms_of_diabetes.png 2x" data-file-width="2286" data-file-height="2338" /></a><figcaption>Overview of the most significant symptoms of diabetes</figcaption></figure> Type 1 diabetes can develop at any age, with a peak in onsets during childhood and adolescence. Adult onsets on the other hand are often initially misdiagnosed as <a href="/wiki/Type_2_Diabetes" class="mw-redirect" title="Type 2 Diabetes">type 2</a>.<a href="#cite_note-:5-19">[19]</a><a href="#cite_note-20">[20]</a><a href="#cite_note-FOOTNOTEAtkinsonMcgillDassauLaffel2020Table_36.1-21">[21]</a><a href="#cite_note-:4-22">[22]</a> The major sign of type 1 diabetes is very high blood sugar, which typically manifests in children as a few days to weeks of <a href="/wiki/Polyuria" title="Polyuria">polyuria</a> (increased urination), <a href="/wiki/Polydipsia" title="Polydipsia">polydipsia</a> (increased thirst), and weight loss after being exposed to a triggering factor including infections, strenuous exercise, dehydration.<a href="#cite_note-23">[23]</a><a href="#cite_note-24">[24]</a><a href="#cite_note-25">[25]</a><a href="#cite_note-FOOTNOTEWolsdorfGarvey2016"Type_1_Diabetes"-26">[26]</a><a href="#cite_note-FOOTNOTEAtkinsonMcgillDassauLaffel2020"Clinical_presentation"-27">[27]</a> Children may also experience <a href="/wiki/Polyphagia" title="Polyphagia">increased appetite</a>, blurred vision, <a href="/wiki/Nocturnal_enuresis" title="Nocturnal enuresis">bedwetting</a>, recurrent skin infections, <a href="/wiki/Candidiasis" title="Candidiasis">candidiasis</a> of the <a href="/wiki/Perineum" title="Perineum">perineum</a>, irritability, and reduced scholastic performance.<a href="#cite_note-FOOTNOTEWolsdorfGarvey2016"Type_1_Diabetes"-26">[26]</a><a href="#cite_note-FOOTNOTEAtkinsonMcgillDassauLaffel2020"Clinical_presentation"-27">[27]</a> Adults with type 1 diabetes tend to have more varied symptoms, which come on over months, rather than days or weeks.<a href="#cite_note-FOOTNOTEDiMeglioEvans-MolinaOram20182449-28">[28]</a><a href="#cite_note-FOOTNOTEAtkinsonMcgillDassauLaffel2020"Clinical_presentation"-27">[27]</a> Prolonged lack of insulin can cause <a href="/wiki/Diabetic_ketoacidosis" title="Diabetic ketoacidosis">diabetic ketoacidosis</a>, characterized by fruity breath odor, mental confusion, persistent fatigue, dry or flushed skin, abdominal pain, nausea or vomiting, and labored breathing.<a href="#cite_note-FOOTNOTEDiMeglioEvans-MolinaOram20182449-28">[28]</a><a href="#cite_note-ADA-Keto-29">[29]</a> Blood and urine tests reveal unusually high glucose and <a href="/wiki/Ketone" title="Ketone">ketones</a> in the blood and urine.<a href="#cite_note-FOOTNOTEDelliLernmark2016"Signs_and_symptoms"-30">[30]</a> Untreated ketoacidosis can rapidly progress to loss of consciousness, coma, and death.<a href="#cite_note-FOOTNOTEDelliLernmark2016"Signs_and_symptoms"-30">[30]</a> The percentage of children whose type 1 diabetes begins with an episode of diabetic ketoacidosis varies widely by geography, as low as 15% in parts of Europe and North America, and as high as 80% in the developing world.<a href="#cite_note-FOOTNOTEDelliLernmark2016"Signs_and_symptoms"-30">[30]</a> <div class="mw-heading mw-heading2"><h2 id="Causes">Causes</h2>[<a href="/w/index.php?title=Type_1_diabetes&action=edit&section=2" title="Edit section: Causes">edit</a>]</div> Type 1 diabetes is caused by the destruction of <a href="/wiki/Beta_cell" title="Beta cell">β-cells</a>—the only cells in the body that produce insulin—and the consequent progressive insulin deficiency. Without insulin, the body cannot respond effectively to increases in blood sugar. Due to this, people with diabetes have persistent hyperglycemia.<a href="#cite_note-FOOTNOTEKatsarouGudbjörnsdottirRawshaniDabelea20171-31">[31]</a> In 70–90% of cases, β-cells are destroyed by one's own immune system, for reasons that are not entirely clear.<a href="#cite_note-FOOTNOTEKatsarouGudbjörnsdottirRawshaniDabelea20171-31">[31]</a> The best-studied components of this autoimmune response are β-cell-targeted antibodies that begin to develop in the months or years before symptoms arise.<a href="#cite_note-FOOTNOTEKatsarouGudbjörnsdottirRawshaniDabelea20171-31">[31]</a> Typically, someone will first develop antibodies against <a href="/wiki/Insulin" title="Insulin">insulin</a> or the protein <a href="/wiki/GAD65" class="mw-redirect" title="GAD65">GAD65</a>, followed eventually by antibodies against the proteins <a href="/wiki/PTPRN" title="PTPRN">IA-2</a>, <a href="/wiki/PTPRN2" title="PTPRN2">IA-2β</a>, and/or <a href="/wiki/ZNT8" class="mw-redirect" title="ZNT8">ZNT8</a>. People with a higher level of these antibodies, especially those who develop them earlier in life, are at higher risk for developing symptomatic type 1 diabetes.<a href="#cite_note-FOOTNOTEKatsarouGudbjörnsdottirRawshaniDabelea2017"Epidemiology"-32">[32]</a> The trigger for the development of these antibodies remains unclear.<a href="#cite_note-FOOTNOTEKatsarouGudbjörnsdottirRawshaniDabelea2017"Introduction"-33">[33]</a> A number of explanatory theories have been put forward, and the cause may involve genetic susceptibility, a diabetogenic trigger, and/or exposure to an <a href="/wiki/Antigen" title="Antigen">antigen</a>.<a href="#cite_note-knip2005-34">[34]</a> The remaining 10–30% of type 1 diabetics have <a href="/wiki/Beta_cell" title="Beta cell">β-cell</a> destruction but no sign of autoimmunity; this is called <a href="/wiki/Idiopathic_disease" title="Idiopathic disease">idiopathic</a> type 1 diabetes and its cause is unknown.<a href="#cite_note-FOOTNOTEKatsarouGudbjörnsdottirRawshaniDabelea20171-31">[31]</a> <div class="mw-heading mw-heading3"><h3 id="Environmental">Environmental</h3>[<a href="/w/index.php?title=Type_1_diabetes&action=edit&section=3" title="Edit section: Environmental">edit</a>]</div> Various <a href="/wiki/Environmental_health" title="Environmental health">environmental risks</a> have been studied in an attempt to understand what triggers β-cell destroying <a href="/wiki/Autoimmunity" title="Autoimmunity">autoimmunity</a>. Many aspects of environment and life history are associated with slight increases in type 1 diabetes risk, however the connection between each risk and diabetes often remains unclear. Type 1 diabetes risk is slightly higher for children whose mothers are obese or older than 35, or for children born by <a href="/wiki/Caesarean_section" title="Caesarean section">caesarean section</a>.<a href="#cite_note-FOOTNOTENorrisJohnsonStene2020"Environmental_factors"-35">[35]</a> Similarly, a child's weight gain in the first year of life, total weight, and <a href="/wiki/Body_mass_index" title="Body mass index">BMI</a> are associated with slightly increased type 1 diabetes risk.<a href="#cite_note-FOOTNOTENorrisJohnsonStene2020"Environmental_factors"-35">[35]</a> Some dietary habits have also been associated with type 1 diabetes risk, namely consumption of cow's milk and dietary sugar intake.<a href="#cite_note-FOOTNOTENorrisJohnsonStene2020"Environmental_factors"-35">[35]</a> Animal studies and some large human studies have found small associations between type 1 diabetes risk and intake of <a href="/wiki/Gluten" title="Gluten">gluten</a> or <a href="/wiki/Dietary_fiber" title="Dietary fiber">dietary fiber</a>; however, other large human studies have found no such association.<a href="#cite_note-FOOTNOTENorrisJohnsonStene2020"Environmental_factors"-35">[35]</a> Many potential environmental triggers have been investigated in large human studies and found to be unassociated with type 1 diabetes risk including duration of breastfeeding, time of introduction of cow milk into the diet, vitamin D consumption, blood levels of active vitamin D, and maternal intake of <a href="/wiki/Omega-3_fatty_acid" title="Omega-3 fatty acid">omega-3 fatty acids</a>.<a href="#cite_note-FOOTNOTENorrisJohnsonStene2020"Environmental_factors"-35">[35]</a><a href="#cite_note-FOOTNOTENorrisJohnsonStene2020"Trends_in_epidemiology"-36">[36]</a> A longstanding hypothesis for an environmental trigger is that some viral infection early in life contributes to type 1 diabetes development. Much of this work has focused on <a href="/wiki/Enterovirus" title="Enterovirus">enteroviruses</a>, with some studies finding slight associations with type 1 diabetes, and others finding none.<a href="#cite_note-FOOTNOTENorrisJohnsonStene2020"Infections"-37">[37]</a> Large human studies have searched for, but not yet found an association between type 1 diabetes and various other viral infections, including infections of the mother during pregnancy.<a href="#cite_note-FOOTNOTENorrisJohnsonStene2020"Infections"-37">[37]</a> Conversely, some have postulated that reduced exposure to pathogens in the developed world increases the risk of autoimmune diseases, often called the <a href="/wiki/Hygiene_hypothesis" title="Hygiene hypothesis">hygiene hypothesis</a>. Various studies of hygiene-related factors—including household crowding, daycare attendance, population density, childhood vaccinations, antihelminth medication, and antibiotic usage during early life or pregnancy—show no association with type 1 diabetes.<a href="#cite_note-FOOTNOTENorrisJohnsonStene2020"The_hygiene_hypothesis_and_proxies_of_microbial_exposures"-38">[38]</a> <div class="mw-heading mw-heading3"><h3 id="Genetics">Genetics</h3>[<a href="/w/index.php?title=Type_1_diabetes&action=edit&section=4" title="Edit section: Genetics">edit</a>]</div> Type 1 diabetes is partially caused by genetics, and family members of type 1 diabetics have a higher risk of developing the disease themselves. In the general population, the risk of developing type 1 diabetes is around 1 in 250. For someone whose parent has type 1 diabetes, the risk rises to 1–9%. If a sibling has type 1 diabetes, the risk is 6–7%. If someone's identical twin has type 1 diabetes, they have a 30–70% risk of developing it themselves.<a href="#cite_note-FOOTNOTEDiMeglioEvans-MolinaOram20182450-39">[39]</a> About half of the disease's heritability is due to variations in three <a href="/wiki/MHC_class_II" title="MHC class II">HLA class II</a> genes involved in <a href="/wiki/Antigen_presentation" title="Antigen presentation">antigen presentation</a>: <a href="/wiki/HLA-DRB1" title="HLA-DRB1">HLA-DRB1</a>, <a href="/wiki/HLA-DQA1" class="mw-redirect" title="HLA-DQA1">HLA-DQA1</a>, and <a href="/wiki/HLA-DQB1" title="HLA-DQB1">HLA-DQB1</a>.<a href="#cite_note-FOOTNOTEDiMeglioEvans-MolinaOram20182450-39">[39]</a> The <a href="/wiki/Haplotype" title="Haplotype">variation patterns</a> associated with increased risk of type 1 diabetes are called <a href="/wiki/HLA-DR3" title="HLA-DR3">HLA-DR3</a> and <a href="/wiki/HLA-DR4" title="HLA-DR4">HLA-DR4</a>-<a href="/wiki/HLA-DQ8" title="HLA-DQ8">HLA-DQ8</a>, and are common in people of European descent. A pattern associated with reduced risk of type 1 diabetes is called <a href="/wiki/HLA-DR15" title="HLA-DR15">HLA-DR15</a>-<a href="/wiki/HLA-DQ6" title="HLA-DQ6">HLA-DQ6</a>.<a href="#cite_note-FOOTNOTEDiMeglioEvans-MolinaOram20182450-39">[39]</a> Large <a href="/wiki/Genome-wide_association_studies" class="mw-redirect" title="Genome-wide association studies">genome-wide association studies</a> have identified dozens of other genes associated with type 1 diabetes risk, mostly genes involved in the <a href="/wiki/Immune_system" title="Immune system">immune system</a>.<a href="#cite_note-FOOTNOTEDiMeglioEvans-MolinaOram20182450-39">[39]</a> <div class="mw-heading mw-heading3"><h3 id="Chemicals_and_drugs">Chemicals and drugs</h3>[<a href="/w/index.php?title=Type_1_diabetes&action=edit&section=5" title="Edit section: Chemicals and drugs">edit</a>]</div> Some medicines can reduce insulin production or damage β cells, resulting in disease that resembles type 1 diabetes. The <a href="/wiki/Antiviral_drug" title="Antiviral drug">antiviral drug</a> <a href="/wiki/Didanosine" title="Didanosine">didanosine</a> triggers pancreas inflammation in 5 to 10% of those who take it, sometimes causing lasting β-cell damage.<a href="#cite_note-FOOTNOTERepaske2016"Additional_medications_that_decrease_insulin_release"-40">[40]</a> Similarly, up to 5% of those who take the anti-<a href="/wiki/Protozoa" title="Protozoa">protozoal</a> drug <a href="/wiki/Pentamidine" title="Pentamidine">pentamidine</a> experience β-cell destruction and diabetes.<a href="#cite_note-FOOTNOTERepaske2016"Additional_medications_that_decrease_insulin_release"-40">[40]</a> Several other drugs cause diabetes by reversibly reducing insulin secretion, namely <a href="/wiki/Statin" title="Statin">statins</a> (which may also damage β cells), the post-transplant <a href="/wiki/Immunosuppressant" class="mw-redirect" title="Immunosuppressant">immunosuppressants</a> <a href="/wiki/Cyclosporin_A" class="mw-redirect" title="Cyclosporin A">cyclosporin A</a> and <a href="/wiki/Tacrolimus" title="Tacrolimus">tacrolimus</a>, the <a href="/wiki/Leukemia" title="Leukemia">leukemia</a> drug <a href="/wiki/L-asparaginase" class="mw-redirect" title="L-asparaginase">L-asparaginase</a>, and the <a href="/wiki/Antibiotic" title="Antibiotic">antibiotic</a> <a href="/w/index.php?title=Gatifloxicin&action=edit&redlink=1" class="new" title="Gatifloxicin (page does not exist)">gatifloxicin</a>.<a href="#cite_note-FOOTNOTERepaske2016"Additional_medications_that_decrease_insulin_release"-40">[40]</a><a href="#cite_note-FOOTNOTERepaske2016"A_common_medication_that_decreases_insulin_release"-41">[41]</a> <div class="mw-heading mw-heading2"><h2 id="Diagnosis">Diagnosis</h2>[<a href="/w/index.php?title=Type_1_diabetes&action=edit&section=6" title="Edit section: Diagnosis">edit</a>]</div> Diabetes is typically diagnosed by a blood test showing unusually high blood sugar. The <a href="/wiki/World_Health_Organization" title="World Health Organization">World Health Organization</a> defines diabetes as blood sugar levels at or above 7.0 mmol/L (126 mg/dL) after fasting for at least eight hours, or a glucose level at or above 11.1 mmol/L (200 mg/dL) two hours after an <a href="/wiki/Oral_glucose_tolerance_test" class="mw-redirect" title="Oral glucose tolerance test">oral glucose tolerance test</a>.<a href="#cite_note-WHO2006-42">[42]</a> The <a href="/wiki/American_Diabetes_Association" title="American Diabetes Association">American Diabetes Association</a> additionally recommends a diagnosis of diabetes for anyone with symptoms of hyperglycemia and blood sugar at any time at or above 11.1 mmol/L, or <a href="/wiki/Glycated_hemoglobin" title="Glycated hemoglobin">glycated hemoglobin</a> (hemoglobin A1C) levels at or above 48 mmol/mol.<a href="#cite_note-ADA2021-43">[43]</a> Once a diagnosis of diabetes is established, type 1 diabetes is distinguished from other types by a blood test for the presence of <a href="/wiki/Autoantibodies" class="mw-redirect" title="Autoantibodies">autoantibodies</a> that target various components of the beta cell.<a href="#cite_note-FOOTNOTEButlerMisselbrook2020"What_is_the_next_investigation?"-44">[44]</a> The most commonly available tests detect antibodies against <a href="/wiki/Glutamic_acid_decarboxylase" class="mw-redirect" title="Glutamic acid decarboxylase">glutamic acid decarboxylase</a>, the beta cell cytoplasm, or insulin, each of which are targeted by antibodies in around 80% of type 1 diabetics.<a href="#cite_note-FOOTNOTEButlerMisselbrook2020"What_is_the_next_investigation?"-44">[44]</a> Some healthcare providers also have access to tests for antibodies targeting the beta cell proteins <a href="/wiki/Insulinoma_associated-2" class="mw-redirect" title="Insulinoma associated-2">IA-2</a> and <a href="/wiki/Zinc_transporter_8" title="Zinc transporter 8">ZnT8</a>; these antibodies are present in around 58% and 80% of type 1 diabetics respectively.<a href="#cite_note-FOOTNOTEButlerMisselbrook2020"What_is_the_next_investigation?"-44">[44]</a> Some also test for <a href="/wiki/C-peptide" title="C-peptide">C-peptide</a>, a byproduct of insulin synthesis. Very low C-peptide levels are suggestive of type 1 diabetes.<a href="#cite_note-FOOTNOTEButlerMisselbrook2020"What_is_the_next_investigation?"-44">[44]</a> <div class="mw-heading mw-heading2"><h2 id="Management">Management</h2>[<a href="/w/index.php?title=Type_1_diabetes&action=edit&section=7" title="Edit section: Management">edit</a>]</div> <style data-mw-deduplicate="TemplateStyles:r1236090951">.mw-parser-output .hatnote{font-style:italic}.mw-parser-output div.hatnote{padding-left:1.6em;margin-bottom:0.5em}.mw-parser-output .hatnote i{font-style:normal}.mw-parser-output .hatnote+link+.hatnote{margin-top:-0.5em}@media print{body.ns-0 .mw-parser-output .hatnote{display:none!important}}</style><div role="note" class="hatnote navigation-not-searchable">Further information: <a href="/wiki/Diabetes_management" title="Diabetes management">Diabetes management</a></div> The mainstay of type 1 diabetes treatment is the regular injection of insulin to manage hyperglycemia.<a href="#cite_note-FOOTNOTEDiMeglioEvans-MolinaOram20182453-45">[45]</a> Injections of insulin via <a href="/wiki/Subcutaneous_injection" class="mw-redirect" title="Subcutaneous injection">subcutaneous injection</a> using either a <a href="/wiki/Syringe" title="Syringe">syringe</a> or an <a href="/wiki/Insulin_pump" title="Insulin pump">insulin pump</a> are necessary multiple times per day, adjusting dosages to account for food intake, blood glucose levels, and physical activity.<a href="#cite_note-FOOTNOTEDiMeglioEvans-MolinaOram20182453-45">[45]</a> The goal of treatment is to maintain blood sugar in a normal range—80–130 mg/dL before a meal; <180 mg/dL after—as often as possible.<a href="#cite_note-FOOTNOTEKatsarouGudbjörnsdottirRawshaniDabelea201711-46">[46]</a> To achieve this, people with diabetes often monitor their blood glucose levels at home. Around 83% of type 1 diabetics monitor their blood glucose by <a href="/wiki/Blood_glucose_monitoring" title="Blood glucose monitoring">capillary blood testing</a>: pricking the finger to draw a drop of blood, and determining blood glucose with a <a href="/wiki/Glucose_meter" title="Glucose meter">glucose meter</a>.<a href="#cite_note-FOOTNOTESmithHarris2018"Self_monitoring"-47">[47]</a> The American Diabetes Association recommends testing blood glucose around 6–10 times per day: before each meal, before exercise, at bedtime, occasionally after a meal, and any time someone feels the symptoms of <a href="/wiki/Hypoglycemia" title="Hypoglycemia">hypoglycemia</a>.<a href="#cite_note-FOOTNOTESmithHarris2018"Self_monitoring"-47">[47]</a> Around 17% of people with type 1 diabetes use a <a href="/wiki/Continuous_glucose_monitor" title="Continuous glucose monitor">continuous glucose monitor</a>, a device with a sensor under the skin that constantly measures glucose levels and communicates those levels to an external device.<a href="#cite_note-FOOTNOTESmithHarris2018"Self_monitoring"-47">[47]</a> Continuous glucose monitoring is associated with better blood sugar control than capillary blood testing alone; however, continuous glucose monitoring tends to be substantially more expensive.<a href="#cite_note-FOOTNOTESmithHarris2018"Self_monitoring"-47">[47]</a> Healthcare providers can also monitor someone's hemoglobin A1C levels which reflect the average blood sugar over the last three months.<a href="#cite_note-FOOTNOTEAmerican_Diabetes_Association_(6)2021"Glycemic_assessment"-48">[48]</a> The American Diabetes Association recommends a goal of keeping hemoglobin A1C levels under 7% for most adults and 7.5% for children.<a href="#cite_note-FOOTNOTEAmerican_Diabetes_Association_(6)2021"Glycemic_assessment"-48">[48]</a><a href="#cite_note-FOOTNOTEDiMeglioEvans-MolinaOram2018"Management_of_clinical_disease"-49">[49]</a> The goal of insulin therapy is to mimic normal pancreatic insulin secretion: low levels of insulin constantly present to support basic metabolism, plus the two-phase secretion of additional insulin in response to high blood sugar, then an extended phase of continued insulin secretion.<a href="#cite_note-FOOTNOTEAtkinsonMcgillDassauLaffel2020"Insulin_Therapy"-50">[50]</a> This is accomplished by combining different insulin preparations that act with differing speeds and durations. The <a href="/wiki/Standard_treatment" title="Standard treatment">standard of care</a> for type 1 diabetes is a <a href="/wiki/Bolus_(medicine)" title="Bolus (medicine)">bolus</a> of <a href="/wiki/Insulin_(medication)#Types" title="Insulin (medication)">rapid-acting insulin</a> 10–15 minutes before each meal or snack, and as-needed to correct hyperglycemia.<a href="#cite_note-FOOTNOTEAtkinsonMcgillDassauLaffel2020"Insulin_Therapy"-50">[50]</a> In addition, constant low levels of insulin are achieved with one or two daily doses of <a href="/wiki/Insulin_(medication)#Types" title="Insulin (medication)">long-acting insulin</a>, or by steady infusion by an insulin pump.<a href="#cite_note-FOOTNOTEAtkinsonMcgillDassauLaffel2020"Insulin_Therapy"-50">[50]</a> The exact dose of insulin appropriate for each injection depends on the content of the meal/snack, and the individual person's sensitivity to insulin, and is therefore typically calculated by the individual with diabetes or a family member by hand or assistive device (calculator, chart, <a href="/wiki/Mobile_app" title="Mobile app">mobile app</a>, etc.).<a href="#cite_note-FOOTNOTEAtkinsonMcgillDassauLaffel2020"Insulin_Therapy"-50">[50]</a> People unable to manage these intensive insulin regimens are sometimes prescribed alternate plans relying on mixtures of rapid- or <a href="/wiki/Insulin_(medication)#Types" title="Insulin (medication)">short-acting</a> and <a href="/wiki/Insulin_(medication)#Types" title="Insulin (medication)">intermediate-acting</a> insulin, which are administered at fixed times along with meals of pre-planned times and carbohydrate composition.<a href="#cite_note-FOOTNOTEAtkinsonMcgillDassauLaffel2020"Insulin_Therapy"-50">[50]</a> The <a href="/wiki/National_Institute_for_Health_and_Care_Excellence" title="National Institute for Health and Care Excellence">National Institute for Health and Care Excellence</a> now recommends closed-loop insulin systems as an option for all women with type 1 diabetes who are pregnant or planning pregnancy.<a href="#cite_note-51">[51]</a><a href="#cite_note-52">[52]</a><a href="#cite_note-53">[53]</a> A non-insulin medication approved by the U.S. <a href="/wiki/Food_and_Drug_Administration" title="Food and Drug Administration">Food and Drug Administration</a> for treating type 1 diabetes is the <a href="/wiki/Amylin" title="Amylin">amylin</a> analog <a href="/wiki/Pramlintide" title="Pramlintide">pramlintide</a>, which replaces the beta-cell hormone amylin. Addition of pramlintide to mealtime insulin injections reduces the boost in blood sugar after a meal, improving blood sugar control.<a href="#cite_note-FOOTNOTEAtkinsonMcgillDassauLaffel2020"Use_of_Adjunctive_Drugs_in_T1DM"-54">[54]</a> Occasionally, <a href="/wiki/Metformin" title="Metformin">metformin</a>, <a href="/wiki/Glucagon-like_peptide-1_receptor_agonist" class="mw-redirect" title="Glucagon-like peptide-1 receptor agonist">GLP-1 receptor agonists</a>, <a href="/wiki/Dipeptidyl_peptidase-4_inhibitor" title="Dipeptidyl peptidase-4 inhibitor">dipeptidyl peptidase-4 inhibitors</a>, or <a href="/wiki/SGLT2_inhibitor" title="SGLT2 inhibitor">SGLT2 inhibitor</a> are prescribed <a href="/wiki/Off-label_use" title="Off-label use">off-label</a> to people with type 1 diabetes, although fewer than 5% of type 1 diabetics use these drugs.<a href="#cite_note-FOOTNOTEDiMeglioEvans-MolinaOram20182453-45">[45]</a> <div class="mw-heading mw-heading3"><h3 id="Lifestyle">Lifestyle</h3>[<a href="/w/index.php?title=Type_1_diabetes&action=edit&section=8" title="Edit section: Lifestyle">edit</a>]</div> Besides insulin, the major way type 1 diabetics control their blood sugar is by learning how various foods impact their blood sugar levels. This is primarily done by tracking their intake of <a href="/wiki/Carbohydrate" title="Carbohydrate">carbohydrates</a>, the type of food with the greatest impact on blood sugar.<a href="#cite_note-FOOTNOTEAtkinsonMcgillDassauLaffel2020"Nutrition_Therapy"-55">[55]</a> In general, people with type 1 diabetes are advised to follow an individualized eating plan rather than a pre-decided one.<a href="#cite_note-ups-56">[56]</a> There are camps for children to teach them how and when to use or monitor their insulin without parental help.<a href="#cite_note-57">[57]</a> As psychological stress may have a negative effect on diabetes, a number of measures have been recommended including: exercising, taking up a new hobby, or joining a charity, among others.<a href="#cite_note-58">[58]</a> Regular exercise is important for maintaining general health, though the effect of exercise on blood sugar can be challenging to predict.<a href="#cite_note-FOOTNOTEAtkinsonMcgillDassauLaffel2020"Physical_Activity_and_Exercise"-59">[59]</a> Exogenous insulin can drive down blood sugar, leaving those with diabetes at risk of hypoglycemia during and immediately after exercise, then again seven to eleven hours after exercise (called the "lag effect").<a href="#cite_note-FOOTNOTEAtkinsonMcgillDassauLaffel2020"Physical_Activity_and_Exercise"-59">[59]</a> Conversely, high-intensity exercise can result in a shortage of insulin, and consequent hyperglycemia.<a href="#cite_note-FOOTNOTEAtkinsonMcgillDassauLaffel2020"Physical_Activity_and_Exercise"-59">[59]</a> The risk of hypoglycemia can be managed by beginning exercise when blood sugar is relatively high (above 100 mg/dL), ingesting carbohydrates during or shortly after exercise, and reducing the amount of injected insulin within two hours of the planned exercise.<a href="#cite_note-FOOTNOTEAtkinsonMcgillDassauLaffel2020"Physical_Activity_and_Exercise"-59">[59]</a> Similarly, the risk of exercise-induced hyperglycemia can be managed by avoiding exercise when insulin levels are very low, when blood sugar is extremely high (above 350 mg/dL), or when one feels unwell.<a href="#cite_note-FOOTNOTEAtkinsonMcgillDassauLaffel2020"Physical_Activity_and_Exercise"-59">[59]</a> While there is a lot of research on diabetes in youth, it is important to keep progressing, expanding and building our knowledge of Type 1 Diabetes and Type 2 Diabetes.  T1DM is an autoimmune disease that prevents the pancreas from producing insulin, which helps the body regulate blood sugar levels.  T2DM is a chronic disease that occurs when your body produces insulin but doesn’t use it properly or doesn’t produce enough, resulting in high blood sugar levels or hyperglycemia.  There is not a definitive answer on what type of exercise is the best for either of these metabolic diseases, but the physical activity guidelines state that children should get at least 60 minutes of moderate to vigorous intensity activity each day, which is the same for children without T1DM or T2DM. Addressing challenges is vital for enhancing care and health outcomes for pediatric diabetes patients.  Prior to engaging in physical activity, it is important to know your diagnosis and be able to manage it properly. When focusing on the type of exercise, the first two studies explicitly focus on the role of exercise in managing diabetes, with the first study exploring the benefits of HIIT for psychological and physical health in T1DM and the second focusing on the effectiveness of exercise in T2DM.<a href="#cite_note-:6-60">[60]</a><a href="#cite_note-:7-61">[61]</a> The third study, however, discusses the implications of diabetes misdiagnosis, which indirectly relates to exercise by stressing the importance of managing diabetes properly before engaging in physical activity.<a href="#cite_note-:8-62">[62]</a>  For the impacts that exercise has, the first and second studies highlight exercise as a beneficial tool for managing diabetes, but they present different outcomes.<a href="#cite_note-:6-60">[60]</a><a href="#cite_note-:7-61">[61]</a> In T2DM, exercise is shown to be a powerful tool for improving glycemic control and reducing cardiovascular risk. In T1DM, while exercise can improve lipid profiles and other aspects of health, it doesn't necessarily lead to better blood sugar control, and there are additional barriers such as fear of hypoglycemia.<a href="#cite_note-:7-61">[61]</a> The first study, however, finds that HIIT can still be effective in improving psychological well-being and exercise adherence for T1DM, showing that exercise has a broader benefit beyond just metabolic control.<a href="#cite_note-:6-60">[60]</a>  All three studies provide insight into the barriers to exercise in diabetes. The first study mentions fear of hypoglycemia and low motivation as challenges for T1DM, while the second reinforces the issue of blood sugar fluctuations and the unpredictability of exercise for those with T1DM.<a href="#cite_note-:6-60">[60]</a><a href="#cite_note-:7-61">[61]</a> The third study is more focused on the broader implications of misdiagnosis, but it implies that exercise could be counterproductive or harmful if a child's diabetes is misdiagnosed.<a href="#cite_note-:8-62">[62]</a> When looking at other factors such as psychological and motivational, the first study places a strong emphasis on psychological factors like exercise enjoyment and intrinsic motivation, suggesting that overcoming psychological barriers is key to exercise adherence in T1DM.<a href="#cite_note-:6-60">[60]</a> In contrast, the second study is more focused on the physical and metabolic effects of exercise, with less emphasis on motivation or enjoyment, although it does briefly mention that many individuals with T1DM are still motivated to exercise by the health benefits or inspiration from others.<a href="#cite_note-:7-61">[61]</a>  Clinical implications show the first two studies focus on the effectiveness of exercise for specific diabetes types, while the third study highlights the importance of correct diagnosis for appropriate care.<a href="#cite_note-:6-60">[60]</a><a href="#cite_note-:8-62">[62]</a><a href="#cite_note-:7-61">[61]</a> This suggests that exercise programs must be tailored not only to the type of diabetes but also to the individual’s health status and management plan. The third study emphasizes that without proper diagnosis and management, exercise recommendations could be inappropriate or unsafe.<a href="#cite_note-:8-62">[62]</a> In summary, while the first two studies explore the benefits and challenges of exercise in different diabetes types, the third study stresses the importance of accurate diagnosis and management before engaging in physical activity. Together, these studies highlight the complex interactions between exercise, diabetes type, treatment, and individual challenges. <div class="mw-heading mw-heading3"><h3 id="Transplant">Transplant</h3>[<a href="/w/index.php?title=Type_1_diabetes&action=edit&section=9" title="Edit section: Transplant">edit</a>]</div> In some cases, people can receive <a href="/wiki/Organ_transplantation" title="Organ transplantation">transplants</a> of the pancreas or isolated islet cells to restore insulin production and alleviate diabetic symptoms. <a href="/wiki/Pancreas_transplant" class="mw-redirect" title="Pancreas transplant">Transplantation of the whole pancreas</a> is rare, due in part to the few available donor organs, and to the need for lifelong <a href="/wiki/Immunosuppressive_therapy" class="mw-redirect" title="Immunosuppressive therapy">immunosuppressive therapy</a> to prevent <a href="/wiki/Transplant_rejection" title="Transplant rejection">transplant rejection</a>.<a href="#cite_note-FOOTNOTEAtkinsonMcgillDassauLaffel2020"Pancreas_and_Islet_Cell_Transplantation"-63">[63]</a><a href="#cite_note-ADA-Transplant-64">[64]</a> The American Diabetes Association recommends pancreas transplant only in people who also require a <a href="/wiki/Kidney_transplant" class="mw-redirect" title="Kidney transplant">kidney transplant</a>, or who struggle to perform regular insulin therapy and experience repeated severe side effects of poor blood sugar control.<a href="#cite_note-ADA-Transplant-64">[64]</a> Most pancreas transplants are done simultaneously with a kidney transplant, with both organs from the same <a href="/wiki/Organ_donor" class="mw-redirect" title="Organ donor">donor</a>.<a href="#cite_note-FOOTNOTEDeanKuklaStegallKudva2017"Simultaneous_pancreas-kidney_transplant"-65">[65]</a> The transplanted pancreas continues to function for at least five years in around three quarters of recipients, allowing them to stop taking insulin.<a href="#cite_note-FOOTNOTEDeanKuklaStegallKudva2017"Outcomes_of_pancreas_transplantation"-66">[66]</a> <a href="/wiki/Islet_cell_transplantation" title="Islet cell transplantation">Transplantations of islets alone</a> have become increasingly common.<a href="#cite_note-FOOTNOTEShapiroPokrywczynskaRicordi2017"Main"-67">[67]</a> Pancreatic islets are isolated from a donor pancreas, then injected into the recipient's <a href="/wiki/Portal_vein" title="Portal vein">portal vein</a> from which they implant onto the recipient's liver.<a href="#cite_note-FOOTNOTERickelsRobertson2019"Islet_allotransplantation_for_the_treatment_of_type_1_diabetes"-68">[68]</a> In nearly half of recipients, the islet transplant continues to work well enough that they still do not need exogenous insulin five years after transplantation.<a href="#cite_note-FOOTNOTERickelsRobertson2019"Long-term_outcomes_and_comparison_with_pancreas_transplantation"-69">[69]</a> If a transplant fails, recipients can receive subsequent injections of islets from additional donors into the portal vein.<a href="#cite_note-FOOTNOTERickelsRobertson2019"Islet_allotransplantation_for_the_treatment_of_type_1_diabetes"-68">[68]</a> Like with whole pancreas transplantation, islet transplantation requires lifelong immunosuppression and depends on the limited supply of donor organs; it is therefore similarly limited to people with severe poorly controlled diabetes and those who have had or are scheduled for a kidney transplant.<a href="#cite_note-FOOTNOTEShapiroPokrywczynskaRicordi2017"Main"-67">[67]</a><a href="#cite_note-FOOTNOTEShapiroPokrywczynskaRicordi2017"Indications_for_islet_transplantation"-70">[70]</a> <a href="/wiki/Donislecel" title="Donislecel">Donislecel</a> (Lantidra) allogeneic (donor) pancreatic islet cellular therapy was approved for medical use in the United States in June 2023.<a href="#cite_note-FDA_PR_20230628-71">[71]</a> <div class="mw-heading mw-heading2"><h2 id="Pathogenesis">Pathogenesis</h2>[<a href="/w/index.php?title=Type_1_diabetes&action=edit&section=10" title="Edit section: Pathogenesis">edit</a>]</div> Type 1 diabetes is a result of the destruction of pancreatic beta cells, although what triggers that destruction remains unclear.<a href="#cite_note-FOOTNOTEDiMeglioEvans-MolinaOram2018"The_immune_phenotype_of_type_1_diabetes"-72">[72]</a> People with type 1 diabetes tend to have more <a href="/wiki/CD8%2B_T-cell" class="mw-redirect" title="CD8+ T-cell">CD8+ T-cells</a> and <a href="/wiki/B-cell" class="mw-redirect" title="B-cell">B-cells</a> that specifically target islet antigens than those without type 1 diabetes, suggesting a role for the <a href="/wiki/Adaptive_immune_system" title="Adaptive immune system">adaptive immune system</a> in beta cell destruction.<a href="#cite_note-FOOTNOTEDiMeglioEvans-MolinaOram2018"The_immune_phenotype_of_type_1_diabetes"-72">[72]</a><a href="#cite_note-FOOTNOTEDiMeglioEvans-MolinaOram2018"Diagnosis"-73">[73]</a> Type 1 diabetics also tend to have reduced <a href="/wiki/Regulatory_T_cell" title="Regulatory T cell">regulatory T cell</a> function, which may exacerbate autoimmunity.<a href="#cite_note-FOOTNOTEDiMeglioEvans-MolinaOram2018"The_immune_phenotype_of_type_1_diabetes"-72">[72]</a> Destruction of beta cells results in inflammation of the islet of Langerhans, called <a href="/wiki/Insulitis" title="Insulitis">insulitis</a>. These inflamed islets tend to contain CD8+ T-cells and – to a lesser extent – <a href="/wiki/CD4%2B_T_cell" class="mw-redirect" title="CD4+ T cell">CD4+ T cells</a>.<a href="#cite_note-FOOTNOTEDiMeglioEvans-MolinaOram2018"The_immune_phenotype_of_type_1_diabetes"-72">[72]</a> Abnormalities in the pancreas or the beta cells themselves may also contribute to beta-cell destruction. The pancreases of people with type 1 diabetes tend to be smaller, lighter, and have abnormal blood vessels, <a href="/wiki/Nerve" title="Nerve">nerve</a> innervations, and <a href="/wiki/Extracellular_matrix" title="Extracellular matrix">extracellular matrix</a> organization.<a href="#cite_note-FOOTNOTEDiMeglioEvans-MolinaOram2018"The_β-cell_phenotype_of_type_1_diabetes"-74">[74]</a> In addition, beta cells from people with type 1 diabetes sometimes <a href="/wiki/Gene_expression" title="Gene expression">overexpress</a> <a href="/wiki/MHC_class_I" title="MHC class I">HLA class I</a> molecules (responsible for signaling to the immune system) and have increased <a href="/wiki/Endoplasmic_reticulum_stress" class="mw-redirect" title="Endoplasmic reticulum stress">endoplasmic reticulum stress</a> and issues with <a href="/wiki/Translation_(biology)" title="Translation (biology)">synthesizing</a> and <a href="/wiki/Protein_folding" title="Protein folding">folding</a> new proteins, any of which could contribute to their demise.<a href="#cite_note-FOOTNOTEDiMeglioEvans-MolinaOram2018"The_β-cell_phenotype_of_type_1_diabetes"-74">[74]</a> The mechanism by which the beta cells actually die likely involves both <a href="/wiki/Necroptosis" title="Necroptosis">necroptosis</a> and <a href="/wiki/Apoptosis" title="Apoptosis">apoptosis</a>, induced or exacerbated by CD8+ T-cells and <a href="/wiki/Macrophage" title="Macrophage">macrophages</a>.<a href="#cite_note-FOOTNOTEAtkinsonMcgillDassauLaffel2020"Mechanisms_of_Beta-Cell_Death_in_T1DM"-75">[75]</a> Necroptosis can be triggered by activated T cells – which secrete toxic <a href="/wiki/Granzyme" title="Granzyme">granzymes</a> and <a href="/wiki/Perforin" class="mw-redirect" title="Perforin">perforin</a> – or indirectly as a result of <a href="/wiki/Ischemia" title="Ischemia">reduced blood flow</a> or the generation of <a href="/wiki/Reactive_oxygen_species" title="Reactive oxygen species">reactive oxygen species</a>.<a href="#cite_note-FOOTNOTEAtkinsonMcgillDassauLaffel2020"Mechanisms_of_Beta-Cell_Death_in_T1DM"-75">[75]</a> As some beta cells die, they may release cellular components that amplify the immune response, exacerbating inflammation and cell death.<a href="#cite_note-FOOTNOTEAtkinsonMcgillDassauLaffel2020"Mechanisms_of_Beta-Cell_Death_in_T1DM"-75">[75]</a> Pancreases from people with type 1 diabetes also have signs of beta cell apoptosis, linked to activation of the <a href="/wiki/Janus_kinase" title="Janus kinase">janus kinase</a> and <a href="/wiki/TYK2" class="mw-redirect" title="TYK2">TYK2</a> pathways.<a href="#cite_note-FOOTNOTEAtkinsonMcgillDassauLaffel2020"Mechanisms_of_Beta-Cell_Death_in_T1DM"-75">[75]</a> Partial ablation of beta-cell function is enough to cause diabetes; at diagnosis, people with type 1 diabetes often still have detectable beta-cell function. Once insulin therapy is started, many people experience a resurgence in beta-cell function, and can go some time with little-to-no insulin treatment – called the "honeymoon phase".<a href="#cite_note-FOOTNOTEDiMeglioEvans-MolinaOram2018"The_β-cell_phenotype_of_type_1_diabetes"-74">[74]</a> This eventually fades as beta-cells continue to be destroyed, and insulin treatment is required again.<a href="#cite_note-FOOTNOTEDiMeglioEvans-MolinaOram2018"The_β-cell_phenotype_of_type_1_diabetes"-74">[74]</a> Beta-cell destruction is not always complete, as 30–80% of type 1 diabetics produce small amounts of insulin years or decades after diagnosis.<a href="#cite_note-FOOTNOTEDiMeglioEvans-MolinaOram2018"The_β-cell_phenotype_of_type_1_diabetes"-74">[74]</a> <div class="mw-heading mw-heading3"><h3 id="Alpha_cell_dysfunction">Alpha cell dysfunction</h3>[<a href="/w/index.php?title=Type_1_diabetes&action=edit&section=11" title="Edit section: Alpha cell dysfunction">edit</a>]</div> Onset of autoimmune diabetes is accompanied by impaired ability to regulate the hormone <a href="/wiki/Glucagon" title="Glucagon">glucagon</a>,<a href="#cite_note-Farhy_2015-76">[76]</a> which acts in antagonism with insulin to regulate blood sugar and metabolism. Progressive beta cell destruction leads to dysfunction in the neighboring <a href="/wiki/Alpha_cell" title="Alpha cell">alpha cells</a> which secrete glucagon, exacerbating excursions away from euglycemia in both directions; overproduction of glucagon after meals causes sharper hyperglycemia, and failure to stimulate glucagon upon hypoglycemia prevents a glucagon-mediated rescue of glucose levels.<a href="#cite_note-Yosten_2018-77">[77]</a> <div class="mw-heading mw-heading4"><h4 id="Hyperglucagonemia">Hyperglucagonemia</h4>[<a href="/w/index.php?title=Type_1_diabetes&action=edit&section=12" title="Edit section: Hyperglucagonemia">edit</a>]</div> Onset of type 1 diabetes is followed by an increase in glucagon secretion after meals. Increases have been measured up to 37% during the first year of diagnosis, while C-peptide levels (indicative of islet-derived insulin), decline by up to 45%.<a href="#cite_note-78">[78]</a> Insulin production will continue to fall as the immune system destroys beta cells, and islet-derived insulin will continue to be replaced by therapeutic exogenous insulin. Simultaneously, there is measurable alpha cell hypertrophy and hyperplasia in the early stage of the disease, leading to expanded alpha cell mass. This, together with failing beta cell insulin secretion, begins to account for rising glucagon levels that contribute to hyperglycemia.<a href="#cite_note-Yosten_2018-77">[77]</a> Some researchers believe glucagon dysregulation to be the primary cause of early stage hyperglycemia.<a href="#cite_note-79">[79]</a> Leading hypotheses for the cause of postprandial hyperglucagonemia suggest that exogenous insulin therapy is inadequate to replace the lost intraislet signalling to alpha cells previously mediated by beta cell-derived pulsatile insulin secretion.<a href="#cite_note-80">[80]</a><a href="#cite_note-81">[81]</a> Under this working hypothesis intensive insulin therapy has attempted to mimic natural insulin secretion profiles in exogenous insulin infusion therapies.<a href="#cite_note-82">[82]</a> In young people with type 1 diabetes, unexplained deaths could be due to nighttime hypoglycemia triggering abnormal heart rhythms or cardiac autonomic neuropathy, damage to nerves that control the function of the heart. <div class="mw-heading mw-heading4"><h4 id="Hypoglycemic_glucagon_impairment">Hypoglycemic glucagon impairment</h4>[<a href="/w/index.php?title=Type_1_diabetes&action=edit&section=13" title="Edit section: Hypoglycemic glucagon impairment">edit</a>]</div> Glucagon secretion is normally increased upon falling glucose levels, but normal glucagon response to hypoglycemia is blunted in type 1 diabetics.<a href="#cite_note-Banarer_2002-83">[83]</a><a href="#cite_note-84">[84]</a> Beta cell glucose sensing and subsequent suppression of administered insulin secretion is absent, leading to islet hyperinsulinemia which inhibits glucagon release.<a href="#cite_note-Banarer_2002-83">[83]</a><a href="#cite_note-Tesfaye_2010-85">[85]</a> Autonomic inputs to alpha cells are much more important for glucagon stimulation in the moderate to severe ranges of hypoglycemia, yet the autonomic response is blunted in a number of ways. Recurrent hypoglycemia leads to metabolic adjustments in the glucose sensing areas of the brain, shifting the threshold for counter regulatory activation of the <a href="/wiki/Sympathetic_nervous_system" title="Sympathetic nervous system">sympathetic nervous system</a> to lower glucose concentration.<a href="#cite_note-Tesfaye_2010-85">[85]</a> This is known as hypoglycemic unawareness. Subsequent hypoglycemia is met with impairment in sending of counter regulatory signals to the islets and <a href="/wiki/Adrenal_cortex" title="Adrenal cortex">adrenal cortex</a>. This accounts for the lack of glucagon stimulation and epinephrine release that would normally stimulate and enhance glucose release and production from the liver, rescuing the diabetic from severe hypoglycemia, coma, and death. Numerous hypotheses have been produced in the search for a cellular mechanism of hypoglycemic unawareness, and a consensus has yet to be reached.<a href="#cite_note-Reno_2013-86">[86]</a> The major hypotheses are summarized in the following table:<a href="#cite_note-87">[87]</a><a href="#cite_note-Tesfaye_2010-85">[85]</a><a href="#cite_note-Reno_2013-86">[86]</a> <table class="wikitable"> <tbody><tr> <td colspan="2">Mechanisms of hypoglycemic unawareness </td></tr> <tr> <td>Glycogen supercompensation </td> <td>Increased <a href="/wiki/Glycogen" title="Glycogen">glycogen</a> stores in <a href="/wiki/Astrocyte" title="Astrocyte">astrocytes</a> might contribute supplementary <a href="/wiki/Glycosyl" title="Glycosyl">glycosyl</a> units for metabolism, counteracting the central nervous system perception of hypoglycemia. </td></tr> <tr> <td>Enhanced glucose metabolism </td> <td>Altered glucose transport and enhanced metabolic efficiency upon recurring hypoglycemia relieves oxidative stress that would activate sympathetic response. </td></tr> <tr> <td>Alternative fuel hypothesis </td> <td>Decreased reliance on glucose, supplementation of lactate from astrocytes, or ketones meet metabolic demands and reduce stress to brain. </td></tr> <tr> <td>Brain neuronal communication </td> <td><a href="/wiki/Hypothalamus" title="Hypothalamus">Hypothalamic</a> inhibitory <a href="/wiki/Gamma-Aminobutyric_acid" class="mw-redirect" title="Gamma-Aminobutyric acid">GABA</a> normally decreases during hypoglycemia, disinhibiting signals for sympathetic tone. Recurrent episodes of hypoglycemia result in increased basal GABA which fails to decrease normally during subsequent hypoglycemia. Inhibitory tone remains and sympathetic tone is not increased. </td></tr></tbody></table> In addition, autoimmune diabetes is characterized by a loss of islet specific sympathetic innervation.<a href="#cite_note-Mundinger_2016-88">[88]</a> This loss constitutes an 80–90% reduction of islet sympathetic nerve endings, happens early in the progression of the disease, and is persistent through the life of the patient.<a href="#cite_note-89">[89]</a> It is linked to the autoimmune aspect of type 1 diabetics and fails to occur in type 2 diabetics. Early in the autoimmune event, the axon pruning is activated in islet sympathetic nerves. Increased <a href="/wiki/Brain-derived_neurotrophic_factor" title="Brain-derived neurotrophic factor">BDNF</a> and <a href="/wiki/Reactive_oxygen_species" title="Reactive oxygen species">ROS</a> that result from <a href="/wiki/Insulitis" title="Insulitis">insulitis</a> and beta cell death stimulate the <a href="/wiki/Low-affinity_nerve_growth_factor_receptor" title="Low-affinity nerve growth factor receptor">p75 neurotrophin receptor</a> (p75NTR), which acts to prune off axons. Axons are normally protected from pruning by activation of tropomyosin receptor kinase A (Trk A) receptors by <a href="/wiki/Nerve_growth_factor" title="Nerve growth factor">NGF</a>, which in islets is primarily produced by beta cells. Progressive autoimmune beta cell destruction, therefore, causes both the activation of pruning factors and the loss of protective factors to the islet sympathetic nerves. This unique form of neuropathy is a hallmark of type 1 diabetes, and plays a part in the loss of glucagon rescue of severe hypoglycemia.<a href="#cite_note-Mundinger_2016-88">[88]</a> <div class="mw-heading mw-heading2"><h2 id="Complications">Complications</h2>[<a href="/w/index.php?title=Type_1_diabetes&action=edit&section=14" title="Edit section: Complications">edit</a>]</div> <link rel="mw-deduplicated-inline-style" href="mw-data:TemplateStyles:r1236090951"><div role="note" class="hatnote navigation-not-searchable">Further information: <a href="/wiki/Complications_of_diabetes" title="Complications of diabetes">Complications of diabetes</a></div> The most pressing complication of type 1 diabetes are the always present risks of poor blood sugar control: severe hypoglycemia and diabetic ketoacidosis. Hypoglycemia – typically blood sugar below 70 mg/dL – triggers the release of <a href="/wiki/Epinephrine" class="mw-redirect" title="Epinephrine">epinephrine</a>, and can cause people to feel shaky, anxious, or irritable.<a href="#cite_note-ADAHypo-90">[90]</a> People with hypoglycemia may also experience hunger, nausea, sweats, chills, headaches, dizziness, and a <a href="/wiki/Tachycardia" title="Tachycardia">fast heartbeat</a>.<a href="#cite_note-ADAHypo-90">[90]</a> Some feel lightheaded, sleepy, or weak.<a href="#cite_note-ADAHypo-90">[90]</a> Severe hypoglycemia can develop rapidly, causing confusion, coordination problems, loss of consciousness, and seizure.<a href="#cite_note-ADAHypo-90">[90]</a><a href="#cite_note-FOOTNOTEDiMeglioEvans-MolinaOram20182455-91">[91]</a> On average, people with type 1 diabetes experience a hypoglycemia event that requires assistance of another 16–20 times in 100 person-years, and an event leading to unconsciousness or seizure 2–8 times per 100 person-years.<a href="#cite_note-FOOTNOTEDiMeglioEvans-MolinaOram20182455-91">[91]</a> The American Diabetes Association recommends treating hypoglycemia by the "15–15 rule": eat 15 grams of carbohydrates, then wait 15 minutes before checking blood sugar; repeat until blood sugar is at least 70 mg/dL.<a href="#cite_note-ADAHypo-90">[90]</a> Severe hypoglycemia that impairs someone's ability to eat is typically treated with <a href="/wiki/Glucagon_(medication)" title="Glucagon (medication)">injectable glucagon</a>, which triggers glucose release from the <a href="/wiki/Liver" title="Liver">liver</a> into the bloodstream.<a href="#cite_note-ADAHypo-90">[90]</a> People with repeated bouts of hypoglycemia can develop <a href="/w/index.php?title=Hypoglycemia_unawareness&action=edit&redlink=1" class="new" title="Hypoglycemia unawareness (page does not exist)">hypoglycemia unawareness</a>, where the blood sugar threshold at which they experience symptoms of hypoglycemia decreases, increasing their risk of severe hypoglycemic events.<a href="#cite_note-FOOTNOTEDiMeglioEvans-MolinaOram2018"Complications_of_type_1_diabetes"-92">[92]</a> Rates of severe hypoglycemia have generally declined due to the advent of rapid-acting and long-acting insulin products in the 1990s and early 2000s;<a href="#cite_note-FOOTNOTEAtkinsonMcgillDassauLaffel2020"Insulin_Therapy"-50">[50]</a> however, acute hypoglycemia still causes 4–10% of type 1 diabetes-related deaths.<a href="#cite_note-FOOTNOTEDiMeglioEvans-MolinaOram20182455-91">[91]</a> The other persistent risk is diabetic ketoacidosis – a state where lack of insulin results in cells burning fat rather than sugar, producing toxic ketones as a byproduct.<a href="#cite_note-ADA-Keto-29">[29]</a> Ketoacidosis symptoms can develop rapidly, with frequent urination, excessive thirst, nausea, vomiting, and severe abdominal pain all common.<a href="#cite_note-FOOTNOTECashenPetersen2019"Diagnosis,_screening_and_prevention"-93">[93]</a> More severe ketoacidosis can result in <a href="/wiki/Kussmaul_breathing" title="Kussmaul breathing">labored breathing</a>, and loss of consciousness due to <a href="/wiki/Cerebral_edema" title="Cerebral edema">cerebral edema</a>.<a href="#cite_note-FOOTNOTECashenPetersen2019"Diagnosis,_screening_and_prevention"-93">[93]</a> People with type 1 diabetes experience diabetic ketoacidosis 1–5 times per 100 person-years, the majority of which result in hospitalization.<a href="#cite_note-FOOTNOTECashenPetersen2019"Epidemiology"-94">[94]</a> 13–19% of type 1 diabetes-related deaths are caused by ketoacidosis,<a href="#cite_note-FOOTNOTEDiMeglioEvans-MolinaOram20182455-91">[91]</a> making ketoacidosis the leading cause of death in people with type 1 diabetes less than 58 years old.<a href="#cite_note-FOOTNOTECashenPetersen2019"Epidemiology"-94">[94]</a> <div class="mw-heading mw-heading3"><h3 id="Long-term_complications">Long-term complications</h3>[<a href="/w/index.php?title=Type_1_diabetes&action=edit&section=15" title="Edit section: Long-term complications">edit</a>]</div> In addition to the acute complications of diabetes, long-term hyperglycemia results in <a href="/wiki/Microangiopathy" title="Microangiopathy">damage to the small blood vessels</a> throughout the body. This damage tends to manifest particularly in the eyes, nerves, and kidneys causing <a href="/wiki/Diabetic_retinopathy" title="Diabetic retinopathy">diabetic retinopathy</a>, <a href="/wiki/Diabetic_neuropathy" title="Diabetic neuropathy">diabetic neuropathy</a>, and <a href="/wiki/Diabetic_nephropathy" title="Diabetic nephropathy">diabetic nephropathy</a> respectively.<a href="#cite_note-FOOTNOTEDiMeglioEvans-MolinaOram2018"Complications_of_type_1_diabetes"-92">[92]</a> In the eyes, prolonged high blood sugar causes the blood vessels in the <a href="/wiki/Retina" title="Retina">retina</a> to become fragile.<a href="#cite_note-FOOTNOTEBrownleeAielloSunCooper2020"Pathophysiology_of_diabetic_retinopathy"-95">[95]</a> People with type 1 diabetes also have increased risk of <a href="/wiki/Cardiovascular_disease" title="Cardiovascular disease">cardiovascular disease</a>, which is estimated to shorten the life of the average type 1 diabetic by 8–13 years.<a href="#cite_note-FOOTNOTEDiMeglioEvans-MolinaOram20182456-96">[96]</a> Cardiovascular disease<a href="#cite_note-pmid16505242-97">[97]</a> as well as neuropathy<a href="#cite_note-pmid16043739-98">[98]</a> may have an autoimmune basis, as well. Women with type 1 DM have a 40% higher risk of death as compared to men with type 1 DM.<a href="#cite_note-99">[99]</a> About 12 percent of people with type 1 diabetes have clinical depression.<a href="#cite_note-Roy,_T._2012-100">[100]</a> About 6 percent of people with type 1 diabetes also have <a href="/wiki/Celiac_disease" class="mw-redirect" title="Celiac disease">celiac disease</a>, but in most cases there are no digestive symptoms<a href="#cite_note-ElfstromSundstrom2014-101">[101]</a><a href="#cite_note-SeeKaukinen2015-102">[102]</a> or are mistakenly attributed to poor control of diabetes, gastroparesis, or diabetic neuropathy.<a href="#cite_note-SeeKaukinen2015-102">[102]</a> In most cases, celiac disease is diagnosed after onset of type 1 diabetes. The association of celiac disease with type 1 diabetes increases the risk of complications, such as <a href="/wiki/Retinopathy" title="Retinopathy">retinopathy</a> and mortality. This association can be explained by shared genetic factors, and inflammation or nutritional deficiencies caused by untreated celiac disease, even if type 1 diabetes is diagnosed first.<a href="#cite_note-ElfstromSundstrom2014-101">[101]</a> <div class="mw-heading mw-heading3"><h3 id="Urinary_tract_infection">Urinary tract infection</h3>[<a href="/w/index.php?title=Type_1_diabetes&action=edit&section=16" title="Edit section: Urinary tract infection">edit</a>]</div> People with diabetes show an increased rate of <a href="/wiki/Urinary_tract_infection" title="Urinary tract infection">urinary tract infection</a>.<a href="#cite_note-103">[103]</a> The reason is bladder dysfunction is more common in people with diabetes than people without diabetes due to diabetes nephropathy. When present, nephropathy can cause a decrease in bladder sensation, which in turn, can cause increased residual urine, a risk factor for urinary tract infections.<a href="#cite_note-104">[104]</a> <div class="mw-heading mw-heading3"><h3 id="Sexual_dysfunction">Sexual dysfunction</h3>[<a href="/w/index.php?title=Type_1_diabetes&action=edit&section=17" title="Edit section: Sexual dysfunction">edit</a>]</div> <a href="/wiki/Sexual_dysfunction" title="Sexual dysfunction">Sexual dysfunction</a> in people with diabetes is often a result of physical factors such as nerve damage and poor circulation, and psychological factors such as stress and/or depression caused by the demands of the disease.<a href="#cite_note-Sexual_Dysfunction_in_Women-105">[105]</a> The most common sexual issues in males with diabetes are problems with erections and ejaculation: "With diabetes, blood vessels supplying the penis's erectile tissue can get hard and narrow, preventing the adequate blood supply needed for a firm erection. The nerve damage caused by poor blood glucose control can also cause ejaculate to go into the bladder instead of through the penis during ejaculation, called retrograde ejaculation. When this happens, semen leaves the body in the urine." Another cause of erectile dysfunction is reactive oxygen species created as a result of the disease. Antioxidants can be used to help combat this.<a href="#cite_note-106">[106]</a> Sexual problems are common in women who have diabetes,<a href="#cite_note-Sexual_Dysfunction_in_Women-105">[105]</a> including reduced sensation in the genitals, dryness, difficulty/inability to orgasm, pain during sex, and decreased libido. Diabetes sometimes decreases estrogen levels in females, which can affect vaginal lubrication. Less is known about the correlation between diabetes and sexual dysfunction in females than in males.<a href="#cite_note-Sexual_Dysfunction_in_Women-105">[105]</a> <a href="/wiki/Oral_contraceptive_pill" title="Oral contraceptive pill">Oral contraceptive pills</a> can cause blood sugar imbalances in women who have diabetes. Dosage changes can help address that, at the risk of side effects and complications.<a href="#cite_note-Sexual_Dysfunction_in_Women-105">[105]</a> Women with type 1 diabetes show a higher than normal rate of <a href="/wiki/Polycystic_ovarian_syndrome" class="mw-redirect" title="Polycystic ovarian syndrome">polycystic ovarian syndrome</a> (PCOS).<a href="#cite_note-107">[107]</a> The reason may be that the ovaries are exposed to high insulin concentrations since women with type 1 diabetes can have frequent hyperglycemia.<a href="#cite_note-108">[108]</a> <div class="mw-heading mw-heading3"><h3 id="Autoimmune_disorders">Autoimmune disorders</h3>[<a href="/w/index.php?title=Type_1_diabetes&action=edit&section=18" title="Edit section: Autoimmune disorders">edit</a>]</div> People with type 1 diabetes are at an increased risk for developing several <a href="/wiki/Autoimmune_disorder" class="mw-redirect" title="Autoimmune disorder">autoimmune disorders</a>, particularly thyroid problems – around 20% of people with type 1 diabetes have <a href="/wiki/Hypothyroidism" title="Hypothyroidism">hypothyroidism</a> or <a href="/wiki/Hyperthyroidism" title="Hyperthyroidism">hyperthyroidism</a>, typically caused by <a href="/wiki/Hashimoto_thyroiditis" class="mw-redirect" title="Hashimoto thyroiditis">Hashimoto thyroiditis</a> or <a href="/wiki/Graves%27_disease" title="Graves' disease">Graves' disease</a> respectively.<a href="#cite_note-FOOTNOTEAtkinsonMcgillDassauLaffel2020"Other_Complications"-109">[109]</a><a href="#cite_note-FOOTNOTEDiMeglioEvans-MolinaOram20182455-91">[91]</a> <a href="/wiki/Celiac_disease" class="mw-redirect" title="Celiac disease">Celiac disease</a> affects 2–8% of people with type 1 diabetes, and is more common in those who were younger at diabetes diagnosis, and in <a href="/wiki/White_people" title="White people">white people</a>.<a href="#cite_note-FOOTNOTEAtkinsonMcgillDassauLaffel2020"Other_Complications"-109">[109]</a> Type 1 diabetics are also at increased risk of <a href="/wiki/Rheumatoid_arthritis" title="Rheumatoid arthritis">rheumatoid arthritis</a>, <a href="/wiki/Lupus" title="Lupus">lupus</a>, <a href="/wiki/Autoimmune_gastritis" class="mw-redirect" title="Autoimmune gastritis">autoimmune gastritis</a>, <a href="/wiki/Pernicious_anemia" title="Pernicious anemia">pernicious anemia</a>, <a href="/wiki/Vitiligo" title="Vitiligo">vitiligo</a>, and <a href="/wiki/Addison%27s_disease" title="Addison's disease">Addison's disease</a>.<a href="#cite_note-FOOTNOTEDiMeglioEvans-MolinaOram20182455-91">[91]</a> Conversely, complex autoimmune syndromes caused by mutations in the immunity-related genes <a href="/wiki/AIRE" class="mw-redirect" title="AIRE">AIRE</a> (causing <a href="/wiki/Autoimmune_polyglandular_syndrome" class="mw-redirect" title="Autoimmune polyglandular syndrome">autoimmune polyglandular syndrome</a>), <a href="/wiki/FoxP3" class="mw-redirect" title="FoxP3">FoxP3</a> (causing <a href="/wiki/IPEX_syndrome" title="IPEX syndrome">IPEX syndrome</a>), or <a href="/wiki/STAT3" title="STAT3">STAT3</a> include type 1 diabetes in their effects.<a href="#cite_note-FOOTNOTERedondoSteckPugliese2018"Evidence_for_the_contribution_of_genetics_to_type_I_diabetes"-110">[110]</a> <div class="mw-heading mw-heading2"><h2 id="Prevention">Prevention</h2>[<a href="/w/index.php?title=Type_1_diabetes&action=edit&section=19" title="Edit section: Prevention">edit</a>]</div> There is no way to prevent type 1 diabetes;<a href="#cite_note-111">[111]</a> however, the development of diabetes symptoms can be delayed in some people who are at high risk of developing the disease. In 2022 the FDA approved an <a href="/wiki/Intravenous" class="mw-redirect" title="Intravenous">intravenous</a> injection of <a href="/wiki/Teplizumab" title="Teplizumab">teplizumab</a> to delay the progression of type 1 diabetes in those older than eight who have already developed diabetes-related autoantibodies and problems with blood sugar control. In that population, the <a href="/wiki/Anti-CD3_monoclonal_antibody" title="Anti-CD3 monoclonal antibody">anti-CD3 monoclonal antibody</a> teplizumab can delay the development of type 1 diabetes symptoms by around two years.<a href="#cite_note-112">[112]</a> In addition to anti-CD3 antibodies, several other <a href="/wiki/Immunosuppressive_agent" class="mw-redirect" title="Immunosuppressive agent">immunosuppressive agents</a> have been trialled with the aim of preventing beta cell destruction. Large trials of <a href="/wiki/Cyclosporine" class="mw-redirect" title="Cyclosporine">cyclosporine</a> treatment suggested that cyclosporine could improve insulin secretion in those recently diagnosed with type 1 diabetes; however, people who stopped taking cyclosporine rapidly stopped making insulin, and cyclosporine's <a href="/wiki/Nephrotoxicity" title="Nephrotoxicity">kidney toxicity</a> and increased risk of cancer prevented people from using it long-term.<a href="#cite_note-FOOTNOTEAtkinsonMcgillDassauLaffel2020"Immunosuppresion"-113">[113]</a> Several other immunosuppressive agents – <a href="/wiki/Prednisone" title="Prednisone">prednisone</a>, <a href="/wiki/Azathioprine" title="Azathioprine">azathioprine</a>, <a href="/wiki/Anti-thymocyte_globulin" title="Anti-thymocyte globulin">anti-thymocyte globulin</a>, <a href="/wiki/Mycophenolate" class="mw-redirect" title="Mycophenolate">mycophenolate</a>, and antibodies against <a href="/wiki/CD20" title="CD20">CD20</a> and <a href="/wiki/IL2RA" title="IL2RA">IL2 receptor α</a> – have been the subject of research, but none have provided lasting protection from development of type 1 diabetes.<a href="#cite_note-FOOTNOTEAtkinsonMcgillDassauLaffel2020"Immunosuppresion"-113">[113]</a> There have also been clinical trials attempting to induce <a href="/wiki/Immune_tolerance" title="Immune tolerance">immune tolerance</a> by vaccination with insulin, GAD65, and various short peptides targeted by immune cells during type 1 diabetes; none have yet delayed or prevented development of disease.<a href="#cite_note-FOOTNOTEvon_ScholtenKreinerGoughvon_Herrath2021"Antigen_vaccination"-114">[114]</a> Several trials have attempted dietary interventions with the hope of reducing the autoimmunity that leads to type 1 diabetes. Trials that withheld cow's milk or gave infants formula free of bovine insulin decreased the development of β-cell-targeted antibodies, but did not prevent the development of type 1 diabetes.<a href="#cite_note-FOOTNOTEDayanKorahTatovicBundy2019"Previous_prevention_trials"-115">[115]</a> Similarly, trials that gave high-risk individuals injected insulin, oral insulin, or <a href="/wiki/Nicotinamide" title="Nicotinamide">nicotinamide</a> did not prevent diabetes development.<a href="#cite_note-FOOTNOTEDayanKorahTatovicBundy2019"Previous_prevention_trials"-115">[115]</a> Other strategies under investigation for the prevention of type 1 diabetes include gene therapy, stem cell therapy, and modulation of the gut microbiome. Gene therapy approaches, while still in early stages, aim to alter genetic factors that contribute to beta-cell destruction by editing immune responses.<a href="#cite_note-116">[116]</a> Stem cell therapies are also being researched, with the hope that they can either regenerate insulin-producing beta cells or protect them from immune attack.<a href="#cite_note-117">[117]</a> Trials using stem cells to restore beta cell function or regulate immune responses are ongoing. Modifying the gut microbiota through the use of probiotics, prebiotics, or specific diets has also gained attention. Some evidence suggests that the gut microbiome plays a role in immune regulation, and researchers are investigating whether altering the microbiome could reduce the risk of autoimmunity and, subsequently, type 1 diabetes.<a href="#cite_note-118">[118]</a> Tolerogenic therapies, which seek to induce immune tolerance to beta-cell antigens, are another area of interest. Techniques such as using dendritic cells or regulatory T cells engineered to promote tolerance to beta cells are being studied in clinical trials, though these approaches remain experimental.<a href="#cite_note-119">[119]</a> There is also a hypothesis that certain viral infections, particularly enteroviruses, may trigger type 1 diabetes in genetically predisposed individuals. Researchers are investigating whether vaccines targeting these viruses could reduce the risk of developing the disease.<a href="#cite_note-120">[120]</a> Combination immunotherapies are being explored as well, with the aim of achieving more durable immune protection by using multiple agents together. For example, anti-CD3 antibodies may be combined with other immunomodulatory agents such as IL-1 blockers or checkpoint inhibitors.<a href="#cite_note-121">[121]</a> Finally, researchers are studying how environmental factors such as infections, diet, and stress may affect immune regulation through epigenetic modifications. The hope is that targeting these epigenetic changes could delay or prevent the onset of type 1 diabetes in high-risk individuals.<a href="#cite_note-122">[122]</a> <div class="mw-heading mw-heading2"><h2 id="Epidemiology">Epidemiology</h2>[<a href="/w/index.php?title=Type_1_diabetes&action=edit&section=20" title="Edit section: Epidemiology">edit</a>]</div> Type 1 diabetes makes up an estimated 10–15% of all diabetes cases<a href="#cite_note-FOOTNOTEKatsarouGudbjörnsdottirRawshaniDabelea2017"Epidemiology"-32">[32]</a> or 11–22 million cases worldwide.<a href="#cite_note-WHO11-4">[4]</a> Symptoms can begin at any age, but onset is most common in children, with diagnoses slightly more common in 5 to 7 year olds, and much more common around the age of puberty.<a href="#cite_note-FOOTNOTEAtkinsonMcgillDassauLaffel2020"Diagnosis"-123">[123]</a><a href="#cite_note-FOOTNOTEAtkinsonMcgillDassauLaffel2020Table_36.1-21">[21]</a> In contrast to most autoimmune diseases, type 1 diabetes is slightly more common in males than in females.<a href="#cite_note-FOOTNOTEAtkinsonMcgillDassauLaffel2020"Diagnosis"-123">[123]</a> In 2006, type 1 diabetes affected 440,000 children under 14 years of age and was the primary cause of diabetes in those less than 15 years of age.<a href="#cite_note-Epi07-124">[124]</a><a href="#cite_note-FOOTNOTEKatsarouGudbjörnsdottirRawshaniDabelea2017"Epidemiology"-32">[32]</a> Rates vary widely by country and region. Incidence is highest in Scandinavia, at 30–60 new cases per 100,000 children per year, intermediate in the U.S. and Southern Europe at 10–20 cases per 100,000 per year, and lowest in China, much of Asia, and South America at 1–3 cases per 100,000 per year.<a href="#cite_note-FOOTNOTENorrisJohnsonStene2020"Trends_in_epidemiology"-36">[36]</a> In the United States, type 1 and 2 diabetes affected about 208,000 youths under the age of 20 in 2015. Over 18,000 youths are diagnosed with Type 1 diabetes every year. Every year about 234,051 Americans die due to diabetes (type I or II) or diabetes-related complications, with 69,071 having it as the primary cause of death.<a href="#cite_note-:0-125">[125]</a> In Australia, about one million people have been diagnosed with diabetes and of this figure 130,000 people have been diagnosed with type 1 diabetes. Australia ranks 6th-highest in the world with children under 14 years of age. Between 2000 and 2013, 31,895 new cases were established, with 2,323 in 2013, a rate of 10–13 cases per 100,00 people each year. Aboriginals and Torres Strait Islander people are less affected.<a href="#cite_note-126">[126]</a><a href="#cite_note-127">[127]</a> Since the 1950s, the incidence of type 1 diabetes has been gradually increasing across the world by an average 3–4% per year.<a href="#cite_note-FOOTNOTENorrisJohnsonStene2020"Trends_in_epidemiology"-36">[36]</a> The increase is more pronounced in countries that began with a lower incidence of type 1 diabetes.<a href="#cite_note-FOOTNOTENorrisJohnsonStene2020"Trends_in_epidemiology"-36">[36]</a> A single 2023 study suggested a relationship between <a href="/wiki/Coronavirus_disease_2019" class="mw-redirect" title="Coronavirus disease 2019">COVID-19 infection</a> and the incidence of type 1 diabetes in children;<a href="#cite_note-128">[128]</a> confirmatory studies have not appeared to date. <div class="mw-heading mw-heading2"><h2 id="Type_1_Diabetes_in_Youth">Type 1 Diabetes in Youth</h2>[<a href="/w/index.php?title=Type_1_diabetes&action=edit&section=21" title="Edit section: Type 1 Diabetes in Youth">edit</a>]</div> Type 1 diabetes, also known as "Juvenile-onset" Diabetes is increasing in children and adolescents under the age of 15.<a href="#cite_note-:9-129">[129]</a> Type 1 diabetes is an autoimmune disease where the body attacks the beta-cells produced by the pancreas; therefore, causing the body to have insulin deficiency.<a href="#cite_note-:10-130">[130]</a> Type 1 diabetes is mainly diagnosed in children, and the number of diagnoses is increasing all around the world.<a href="#cite_note-:10-130">[130]</a> <div class="mw-heading mw-heading3"><h3 id="Management-_Exercise">Management- Exercise</h3>[<a href="/w/index.php?title=Type_1_diabetes&action=edit&section=22" title="Edit section: Management- Exercise">edit</a>]</div> Children with type 1 diabetes typically manage their blood sugar levels with regular insulin injections; however, exercise can also play a vital role in the management of type 1 diabetes.<a href="#cite_note-:9-129">[129]</a> For youth with type 1 diabetes, exercise is correlated with greater blood sugar control.<a href="#cite_note-:10-130">[130]</a> HbA1c levels are reduced significantly when children with type 1 diabetes participate in structured exercise interventions.<a href="#cite_note-:10-130">[130]</a> In one study, Garcia-Hermoso and colleagues found that high-intensity exercise, concurrent training, exercise intervention lasting 24 weeks or more, and exercise sessions lasting 60 minutes or more caused greater HbA1c reduction in children with type 1 diabetes.<a href="#cite_note-:10-130">[130]</a> Garcia-Hermoso and colleagues also observed that exercise sessions lasting 60 minutes or more, high-intensity exercise, and concurrent training interventions led to a decrease in insulin dosage per day.<a href="#cite_note-:10-130">[130]</a> Additionally, Petschnig and colleagues looked at the effect of strength training on blood sugar levels and they found that children with type 1 diabetes who performed strength training exercises for 17 weeks did not experience any change in HbA1c levels, but after 32 weeks of training experienced a significant decrease in HbA1c levels.<a href="#cite_note-:9-129">[129]</a> Petschnig and colleagues also observed blood sugar levels decrease significantly following strength training sessions.<a href="#cite_note-:9-129">[129]</a> Finally, the Diabetes Research in Children Network Study Group found that children who participated in prolonged aerobic exercise after school experienced a decrease in plasma glucose levels 40% below their baseline values.<a href="#cite_note-:11-131">[131]</a> The Diabetes Research in Children Network Study Group observed blood sugar levels decrease rapidly in the first 15 minutes of exercise and continue to drop during the 75-minute session.<a href="#cite_note-:11-131">[131]</a> The Diabetes Research Group also found that after participating in prolonged aerobic exercise, 83% of participants had at least a 25% decrease in blood sugar levels.<a href="#cite_note-:11-131">[131]</a> High-intensity and concurrent training interventions,<a href="#cite_note-:10-130">[130]</a> strength training,<a href="#cite_note-:9-129">[129]</a> and prolonged aerobic exercise<a href="#cite_note-:11-131">[131]</a> all have been shown to help reduce HbA1c and blood glucose levels in children with type 1 diabetes; therefore, demonstrating that exercise plays a vital role in the management of type 1 diabetes.<a href="#cite_note-:9-129">[129]</a> <div class="mw-heading mw-heading2"><h2 id="History">History</h2>[<a href="/w/index.php?title=Type_1_diabetes&action=edit&section=23" title="Edit section: History">edit</a>]</div> <link rel="mw-deduplicated-inline-style" href="mw-data:TemplateStyles:r1236090951"><div role="note" class="hatnote navigation-not-searchable">Main article: <a href="/wiki/History_of_diabetes" title="History of diabetes">History of diabetes</a></div> The connection between diabetes and pancreatic damage was first described by the German pathologist <a href="/wiki/Martin_Benno_Schmidt" title="Martin Benno Schmidt">Martin Schmidt</a>, who in a 1902 paper noted inflammation around the pancreatic islet of a child who had died of diabetes.<a href="#cite_note-FOOTNOTEAtkinsonMcgillDassauLaffel2020"Introduction"-132">[132]</a> The connection between this inflammation and diabetes onset was further developed through the 1920s by <a href="/wiki/Shields_Warren" title="Shields Warren">Shields Warren</a>, and the term "insulitis" was coined by <a href="/wiki/Hanns_von_Meyenburg" title="Hanns von Meyenburg">Hanns von Meyenburg</a> in 1940 to describe the phenomenon.<a href="#cite_note-FOOTNOTEAtkinsonMcgillDassauLaffel2020"Introduction"-132">[132]</a> Type 1 diabetes was described as an autoimmune disease in the 1970s, based on observations that autoantibodies against islets were discovered in diabetics with other autoimmune deficiencies.<a href="#cite_note-133">[133]</a> It was also shown in the 1980s that immunosuppressive therapies could slow disease progression, further supporting the idea that type 1 diabetes is an autoimmune disorder.<a href="#cite_note-134">[134]</a> The name juvenile diabetes was used earlier as it often first is diagnosed in childhood. <div class="mw-heading mw-heading2"><h2 id="Society_and_culture">Society and culture</h2>[<a href="/w/index.php?title=Type_1_diabetes&action=edit&section=24" title="Edit section: Society and culture">edit</a>]</div> <link rel="mw-deduplicated-inline-style" href="mw-data:TemplateStyles:r1236090951"><div role="note" class="hatnote navigation-not-searchable">See also: <a href="/wiki/List_of_people_with_type_1_diabetes" title="List of people with type 1 diabetes">List of people with type 1 diabetes</a></div> Type 1 and 2 diabetes was estimated to cause $10.5 billion in annual medical costs ($875 per month per diabetic) and an additional $4.4 billion in indirect costs ($366 per month per person with diabetes) in the U.S.<a href="#cite_note-135">[135]</a> In the United States $245 billion every year is attributed to diabetes. Individuals diagnosed with diabetes have 2.3 times the health care costs as individuals who do not have diabetes. One in ten health care dollars are spent on individuals with type 1 and 2 diabetes.<a href="#cite_note-:0-125">[125]</a> <div class="mw-heading mw-heading2"><h2 id="Research">Research</h2>[<a href="/w/index.php?title=Type_1_diabetes&action=edit&section=25" title="Edit section: Research">edit</a>]</div> <link rel="mw-deduplicated-inline-style" href="mw-data:TemplateStyles:r1236090951"><div role="note" class="hatnote navigation-not-searchable">Further information: <a href="/wiki/Diabetes_management#Research" title="Diabetes management">Diabetes management § Research</a></div> Funding for research into type 1 diabetes originates from government, industry (e.g., pharmaceutical companies), and charitable organizations. Government funding in the United States is distributed via the <a href="/wiki/National_Institutes_of_Health" title="National Institutes of Health">National Institutes of Health</a>, and in the UK via the <a href="/wiki/National_Institute_for_Health_and_Care_Research" title="National Institute for Health and Care Research">National Institute for Health and Care Research</a> or the <a href="/wiki/Medical_Research_Council_(United_Kingdom)" title="Medical Research Council (United Kingdom)">Medical Research Council</a>. The <a href="/wiki/Juvenile_Diabetes_Research_Foundation" class="mw-redirect" title="Juvenile Diabetes Research Foundation">Juvenile Diabetes Research Foundation</a> (JDRF), founded by parents of children with type 1 diabetes, is the world's largest provider of charity-based funding for type 1 diabetes research.<a href="#cite_note-136">[136]</a> Other charities include the <a href="/wiki/American_Diabetes_Association" title="American Diabetes Association">American Diabetes Association</a>, <a href="/wiki/Diabetes_UK" title="Diabetes UK">Diabetes UK</a>, Diabetes Research and Wellness Foundation,<a href="#cite_note-137">[137]</a> <a href="/wiki/Diabetes_Australia" title="Diabetes Australia">Diabetes Australia</a>, and the <a href="/wiki/Canadian_Diabetes_Association" class="mw-redirect" title="Canadian Diabetes Association">Canadian Diabetes Association</a>. <div class="mw-heading mw-heading3"><h3 id="Artificial_pancreas">Artificial pancreas</h3>[<a href="/w/index.php?title=Type_1_diabetes&action=edit&section=26" title="Edit section: Artificial pancreas">edit</a>]</div> There has also been substantial effort to develop a fully <a href="/wiki/Automated_insulin_delivery_system" title="Automated insulin delivery system">automated insulin delivery system</a> or "artificial pancreas" that could sense glucose levels and inject appropriate insulin without conscious input from the user.<a href="#cite_note-FOOTNOTEBoughtonHovorka2020"Introduction"-138">[138]</a> Current "hybrid closed-loop systems" use a continuous glucose monitor to sense blood sugar levels, and a subcutaneous insulin pump to deliver insulin; however, due to the delay between insulin injection and its action, current systems require the user to initiate insulin before taking meals.<a href="#cite_note-FOOTNOTEBoughtonHovorka2020"Regulatory_Approval_of_Closed-Loop_Systems"-139">[139]</a> Several improvements to these systems are currently undergoing clinical trials in humans, including a dual-hormone system that injects <a href="/wiki/Glucagon" title="Glucagon">glucagon</a> in addition to insulin, and an implantable device that injects insulin <a href="/wiki/Intraperitoneal_injection" title="Intraperitoneal injection">intraperitoneally</a> where it can be absorbed more quickly.<a href="#cite_note-140">[140]</a> <div class="mw-heading mw-heading3"><h3 id="Disease_models">Disease models</h3>[<a href="/w/index.php?title=Type_1_diabetes&action=edit&section=27" title="Edit section: Disease models">edit</a>]</div> Various <a href="/wiki/Animal_model" class="mw-redirect" title="Animal model">animal models</a> of disease are used to understand the pathogenesis and etiology of type 1 diabetes. Currently available models of T1D can be divided into spontaneously autoimmune, chemically induced, virus induced and genetically induced.<a href="#cite_note-:1-141">[141]</a> The <a href="/wiki/NOD_mice" title="NOD mice">nonobese diabetic</a> (NOD) mouse is the most widely studied model of type 1 diabetes.<a href="#cite_note-:1-141">[141]</a> It is an <a href="/wiki/Inbred_strain" title="Inbred strain">inbred strain</a> that spontaneously develops type 1 diabetes in 30–100% of female mice depending on housing conditions.<a href="#cite_note-FOOTNOTEAtkinsonMcgillDassauLaffel2020"Animal_models"-142">[142]</a> Diabetes in NOD mice is caused by several genes, primarily <a href="/wiki/Major_histocompatibility_complex" title="Major histocompatibility complex">MHC</a> genes involved in <a href="/wiki/Antigen_presentation" title="Antigen presentation">antigen presentation</a>.<a href="#cite_note-FOOTNOTEAtkinsonMcgillDassauLaffel2020"Animal_models"-142">[142]</a> Like diabetic humans, NOD mice develop islet autoantibodies and inflammation in the islet, followed by reduced insulin production and hyperglycemia.<a href="#cite_note-FOOTNOTEAtkinsonMcgillDassauLaffel2020"Animal_models"-142">[142]</a><a href="#cite_note-143">[143]</a> Some features of human diabetes are exaggerated in NOD mice, namely the mice have more severe islet inflammation than humans, and have a much more pronounced sex bias, with females developing diabetes far more frequently than males.<a href="#cite_note-FOOTNOTEAtkinsonMcgillDassauLaffel2020"Animal_models"-142">[142]</a> In NOD mice the onset of insulitis occurs at 3–4 weeks of age. The islets of Langerhans are infiltrated by CD4+, CD8+ T lymphocytes, NK cells, B lymphocytes, dendritic cells, macrophages, and neutrophils, similar to the disease process in humans.<a href="#cite_note-:2-144">[144]</a> In addition to sex, breeding conditions, gut microbiome composition or diet also influence the onset of T1D.<a href="#cite_note-145">[145]</a> The BioBreeding Diabetes-Prone (BB) rat is another widely used spontaneous experimental model for T1D. The onset of diabetes occurs, in up to 90% of individuals (regardless of sex) at 8–16 weeks of age.<a href="#cite_note-:2-144">[144]</a> During insulitis, the pancreatic islets are infiltrated by T lymphocytes, B lymphocytes, macrophages, and NK cells, with the difference from the human course of insulitis being that CD4 + T lymphocytes are markedly reduced and CD8 + T lymphocytes are almost absent. The aforementioned lymphopenia is the major drawback of this model. The disease is characterized by hyperglycemia, hypoinsulinemia, weight loss, ketonuria, and the need for insulin therapy for survival.<a href="#cite_note-:2-144">[144]</a> BB Rats are used to study the genetic aspects of T1D and are also used for interventional studies and diabetic nephropathy studies.<a href="#cite_note-146">[146]</a> LEW-1AR1 / -iddm rats are derived from congenital Lewis rats and represent a rarer spontaneous model for T1D. These rats develop diabetes at about 8–9 weeks of age with no sex differences unlike NOD mice.<a href="#cite_note-147">[147]</a> In LEW mice, diabetes presents with hyperglycemia, glycosuria, ketonuria, and polyuria.<a href="#cite_note-148">[148]</a><a href="#cite_note-:2-144">[144]</a> The advantage of the model is the progression of the prediabetic phase, which is very similar to human disease, with infiltration of islet by immune cells about a week before hyperglycemia is observed. This model is suitable for intervention studies or for the search for predictive biomarkers. It is also possible to observe individual phases of pancreatic infiltration by immune cells. The advantage of congenic LEW mice is also the good viability after the manifestation of T1D (compared to NOD mice and BB rats).<a href="#cite_note-:3-149">[149]</a> <div class="mw-heading mw-heading4"><h4 id="Chemically_induced">Chemically induced</h4>[<a href="/w/index.php?title=Type_1_diabetes&action=edit&section=28" title="Edit section: Chemically induced">edit</a>]</div> The chemical compounds aloxan and <a href="/wiki/Streptozotocin" title="Streptozotocin">streptozotocin</a> (STZ) are commonly used to induce diabetes and destroy β-cells in mouse/rat animal models.<a href="#cite_note-:2-144">[144]</a> In both cases, it is a cytotoxic analog of glucose that passes GLUT2 transport and accumulates in β-cells, causing their destruction. The chemically induced destruction of β-cells leads to decreased insulin production, hyperglycemia, and weight loss in the experimental animal.<a href="#cite_note-150">[150]</a> The animal models prepared in this way are suitable for research into blood sugar-lowering drugs and therapies (e.g. for testing new insulin preparations). They are also the most commonly used genetically induced T1D model is the so-called AKITA mouse (originally C57BL/6NSIc mouse). The development of diabetes in AKITA mice is caused by a spontaneous point mutation in the Ins2 gene, which is responsible for the correct composition of insulin in the endoplasmic reticulum. Decreased insulin production is then associated with hyperglycemia, polydipsia, and polyuria. If severe diabetes develops within 3–4 weeks, AKITA mice survive no longer than 12 weeks without treatment intervention. The description of the etiology of the disease shows that, unlike spontaneous models, the early stages of the disease are not accompanied by insulitis.<a href="#cite_note-151">[151]</a> AKITA mice are used to test drugs targeting endoplasmic reticulum stress reduction, to test islet transplants, and to study diabetes-related complications such as nephropathy, sympathetic autonomic neuropathy, and vascular disease.<a href="#cite_note-:2-144">[144]</a><a href="#cite_note-152">[152]</a> for testing transplantation therapies. Their advantage is mainly the low cost, the disadvantage is the cytotoxicity of the chemical compounds.<a href="#cite_note-153">[153]</a> <div class="mw-heading mw-heading4"><h4 id="Genetically_induced">Genetically induced</h4>[<a href="/w/index.php?title=Type_1_diabetes&action=edit&section=29" title="Edit section: Genetically induced">edit</a>]</div> Type 1 diabetes (T1D) is a multifactorial autoimmune disease with a strong genetic component. Although environmental factors also play a significant role, the genetic susceptibility to T1D is well established, with several genes and loci implicated in disease development. The most significant genetic contribution to T1D comes from the human leukocyte antigen (HLA) region on chromosome 6p21.<a href="#cite_note-154">[154]</a> The HLA class II genes, particularly HLA-DR and HLA-DQ, are the strongest genetic determinants of T1D risk. Specific combinations of alleles such as HLA-DR3-DQ2 and HLA-DR4-DQ8 have been associated with a higher risk of developing T1D.<a href="#cite_note-Todd_457–467-155">[155]</a> Individuals carrying both of these haplotypes (heterozygous DR3/DR4) are at an even greater risk. These HLA variants are thought to influence the immune system’s ability to differentiate between self and non-self antigens, leading to the autoimmune destruction of pancreatic beta cells.<a href="#cite_note-156">[156]</a> Conversely, some HLA haplotypes, such as HLA-DR15-DQ6, are associated with protection against T1D, suggesting that variations in these immune-related genes can either predispose or protect against the disease.<a href="#cite_note-157">[157]</a> In addition to HLA, multiple non-HLA genes have been implicated in T1D susceptibility. Genome-wide association studies (GWAS) have identified over 50 loci associated with an increased risk of T1D.<a href="#cite_note-158">[158]</a> Some of the most notable genes include: <ul><li>INS: The insulin gene (INS) on chromosome 11p15 is one of the earliest identified non-HLA genes linked to T1D. A variable number tandem repeat (VNTR) polymorphism in the promoter region of the insulin gene affects its thymic expression, with certain alleles reducing the ability to develop immune tolerance to insulin, a key autoantigen in T1D.<a href="#cite_note-159">[159]</a></li> <li>PTPN22: This gene encodes a protein tyrosine phosphatase involved in T-cell receptor signaling. A common single nucleotide polymorphism (SNP), R620W, in the PTPN22 gene is associated with an increased risk of T1D and other autoimmune diseases, suggesting its role in modulating immune responses.<a href="#cite_note-160">[160]</a></li> <li>IL2RA: The interleukin-2 receptor alpha (IL2RA) gene, located on chromosome 10p15, plays a crucial role in regulating immune tolerance and T-cell activation. Variants in IL2RA affect the susceptibility to T1D by altering the function of regulatory T-cells, which help maintain immune homeostasis.<a href="#cite_note-161">[161]</a></li> <li>CTLA4: The cytotoxic T-lymphocyte-associated protein 4 (CTLA4) gene is another immune-related gene associated with T1D. CTLA4 acts as a negative regulator of T-cell activation, and certain variants are linked to impaired immune regulation and a higher risk of autoimmunity.</li></ul> T1D is considered a polygenic disease, meaning that multiple genes contribute to its development. While individual genes confer varying degrees of risk, it is the combination of several genetic factors, along with environmental triggers, that ultimately leads to disease onset.<a href="#cite_note-162">[162]</a> Family studies show that T1D has a relatively high heritability, with siblings of affected individuals having about a 6–10% risk of developing the disease, compared to a 0.3% risk in the general population.<a href="#cite_note-163">[163]</a> The risk of T1D is also influenced by the presence of affected first-degree relatives. For instance, children of fathers with T1D have a higher risk of developing the disease compared to children of mothers with T1D. Monozygotic (identical) twins have a concordance rate of about 30–50%, highlighting the importance of both genetic and environmental factors in disease onset.<a href="#cite_note-Todd_457–467-155">[155]</a> Recent research has also focused on the role of epigenetics and gene-environment interactions in T1D development.<a href="#cite_note-164">[164]</a> Environmental factors such as viral infections, early childhood diet, and gut microbiome composition are thought to trigger the autoimmune process in genetically susceptible individuals.<a href="#cite_note-165">[165]</a> Epigenetic modifications, such as DNA methylation and histone modifications, may influence gene expression in response to these environmental triggers, further modulating the risk of developing T1D. While much progress has been made in understanding the genetic basis of T1D, ongoing research aims to unravel the complex interplay between genetic susceptibility, immune regulation, and environmental influences that contribute to disease pathogenesis.<a href="#cite_note-166">[166]</a> <div class="mw-heading mw-heading4"><h4 id="Virally_induced">Virally induced</h4>[<a href="/w/index.php?title=Type_1_diabetes&action=edit&section=30" title="Edit section: Virally induced">edit</a>]</div> Viral infections play a role in the development of a number of autoimmune diseases, including human type 1 diabetes. However, the mechanisms by which viruses are involved in the induction of type 1 DM are not fully understood. Virus-induced models are used to study the etiology and pathogenesis of the disease, in particular the mechanisms by which environmental factors contribute to or protect against the occurrence of type 1 DM.<a href="#cite_note-167">[167]</a> Among the most commonly used are <a href="/wiki/Coxsackievirus" title="Coxsackievirus">coxsackievirus</a>, <a href="/wiki/Lymphocytic_choriomeningitis_virus" class="mw-redirect" title="Lymphocytic choriomeningitis virus">lymphocytic choriomeningitis virus</a>, <a href="/wiki/Encephalomyocarditis_virus" class="mw-redirect" title="Encephalomyocarditis virus">encephalomyocarditis virus</a>, and <a href="/wiki/Kilham_rat_virus" class="mw-redirect" title="Kilham rat virus">Kilham rat virus</a>. Examples of virus-induced animals include NOD mice infected with coxsackie B4 that developed type 1 DM within two weeks.<a href="#cite_note-168">[168]</a> <div class="mw-heading mw-heading2"><h2 id="References">References</h2>[<a href="/w/index.php?title=Type_1_diabetes&action=edit&section=31" title="Edit section: References">edit</a>]</div> <style data-mw-deduplicate="TemplateStyles:r1239543626">.mw-parser-output .reflist{margin-bottom:0.5em;list-style-type:decimal}@media screen{.mw-parser-output .reflist{font-size:90%}}.mw-parser-output .reflist .references{font-size:100%;margin-bottom:0;list-style-type:inherit}.mw-parser-output .reflist-columns-2{column-width:30em}.mw-parser-output .reflist-columns-3{column-width:25em}.mw-parser-output .reflist-columns{margin-top:0.3em}.mw-parser-output .reflist-columns ol{margin-top:0}.mw-parser-output .reflist-columns li{page-break-inside:avoid;break-inside:avoid-column}.mw-parser-output .reflist-upper-alpha{list-style-type:upper-alpha}.mw-parser-output .reflist-upper-roman{list-style-type:upper-roman}.mw-parser-output .reflist-lower-alpha{list-style-type:lower-alpha}.mw-parser-output .reflist-lower-greek{list-style-type:lower-greek}.mw-parser-output .reflist-lower-roman{list-style-type:lower-roman}</style><div class="reflist"> <div class="mw-references-wrap mw-references-columns"><ol class="references"> <li id="cite_note-1"><a href="#cite_ref-1">^</a> <style data-mw-deduplicate="TemplateStyles:r1238218222">.mw-parser-output cite.citation{font-style:inherit;word-wrap:break-word}.mw-parser-output .citation q{quotes:"\"""\"""'""'"}.mw-parser-output .citation:target{background-color:rgba(0,127,255,0.133)}.mw-parser-output .id-lock-free.id-lock-free a{background:url("//upload.wikimedia.org/wikipedia/commons/6/65/Lock-green.svg")right 0.1em center/9px no-repeat}.mw-parser-output .id-lock-limited.id-lock-limited a,.mw-parser-output .id-lock-registration.id-lock-registration a{background:url("//upload.wikimedia.org/wikipedia/commons/d/d6/Lock-gray-alt-2.svg")right 0.1em center/9px no-repeat}.mw-parser-output .id-lock-subscription.id-lock-subscription a{background:url("//upload.wikimedia.org/wikipedia/commons/a/aa/Lock-red-alt-2.svg")right 0.1em center/9px no-repeat}.mw-parser-output .cs1-ws-icon a{background:url("//upload.wikimedia.org/wikipedia/commons/4/4c/Wikisource-logo.svg")right 0.1em center/12px no-repeat}body:not(.skin-timeless):not(.skin-minerva) .mw-parser-output .id-lock-free a,body:not(.skin-timeless):not(.skin-minerva) .mw-parser-output .id-lock-limited a,body:not(.skin-timeless):not(.skin-minerva) .mw-parser-output .id-lock-registration a,body:not(.skin-timeless):not(.skin-minerva) .mw-parser-output .id-lock-subscription a,body:not(.skin-timeless):not(.skin-minerva) .mw-parser-output .cs1-ws-icon a{background-size:contain;padding:0 1em 0 0}.mw-parser-output .cs1-code{color:inherit;background:inherit;border:none;padding:inherit}.mw-parser-output .cs1-hidden-error{display:none;color:var(--color-error,#d33)}.mw-parser-output .cs1-visible-error{color:var(--color-error,#d33)}.mw-parser-output .cs1-maint{display:none;color:#085;margin-left:0.3em}.mw-parser-output .cs1-kern-left{padding-left:0.2em}.mw-parser-output .cs1-kern-right{padding-right:0.2em}.mw-parser-output .citation .mw-selflink{font-weight:inherit}@media screen{.mw-parser-output .cs1-format{font-size:95%}html.skin-theme-clientpref-night .mw-parser-output .cs1-maint{color:#18911f}}@media screen and (prefers-color-scheme:dark){html.skin-theme-clientpref-os .mw-parser-output .cs1-maint{color:#18911f}}</style><cite id="CITEREFZhengPermanyerCanudas-RomoAburto2023" class="citation journal cs1">Zheng Y, Permanyer I, Canudas-Romo V, Aburto JM, Nigri A, Plana-Ripoll O (2023). <a rel="nofollow" class="external text" href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10473533">"Lifespan variation among people with a given disease or condition"</a>. 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Endocr Rev. 40 (2): 631–668. <a href="/wiki/Doi_(identifier)" class="mw-redirect" title="Doi (identifier)">doi</a>:<a rel="nofollow" class="external text" href="https://doi.org/10.1210%2Fer.2018-00154">10.1210/er.2018-00154</a>. <a href="/wiki/PMC_(identifier)" class="mw-redirect" title="PMC (identifier)">PMC</a> <a rel="nofollow" class="external text" href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6424003">6424003</a>. <a href="/wiki/PMID_(identifier)" class="mw-redirect" title="PMID (identifier)">PMID</a> <a rel="nofollow" class="external text" href="https://pubmed.ncbi.nlm.nih.gov/30541144">30541144</a>.</cite><span title="ctx_ver=Z39.88-2004&rft_val_fmt=info%3Aofi%2Ffmt%3Akev%3Amtx%3Ajournal&rft.genre=article&rft.jtitle=Endocr+Rev&rft.atitle=Pancreatic+Islet+Transplantation+in+Humans%3A+Recent+Progress+and+Future+Directions&rft.volume=40&rft.issue=2&rft.pages=631-668&rft.date=2019-04&rft_id=https%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fpmc%2Farticles%2FPMC6424003%23id-name%3DPMC&rft_id=info%3Apmid%2F30541144&rft_id=info%3Adoi%2F10.1210%2Fer.2018-00154&rft.aulast=Rickels&rft.aufirst=MR&rft.au=Robertson%2C+RP&rft_id=https%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fpmc%2Farticles%2FPMC6424003&rfr_id=info%3Asid%2Fen.wikipedia.org%3AType+1+diabetes" class="Z3988"></li> <li><link rel="mw-deduplicated-inline-style" href="mw-data:TemplateStyles:r1238218222"><cite id="CITEREFShapiroPokrywczynskaRicordi2017" class="citation journal cs1">Shapiro AM, Pokrywczynska M, Ricordi C (May 2017). "Clinical pancreatic islet transplantation". Nat Rev Endocrinol. 13 (5): 268–277. <a href="/wiki/Doi_(identifier)" class="mw-redirect" title="Doi (identifier)">doi</a>:<a rel="nofollow" class="external text" href="https://doi.org/10.1038%2Fnrendo.2016.178">10.1038/nrendo.2016.178</a>. <a href="/wiki/PMID_(identifier)" class="mw-redirect" title="PMID (identifier)">PMID</a> <a rel="nofollow" class="external text" href="https://pubmed.ncbi.nlm.nih.gov/27834384">27834384</a>. <a href="/wiki/S2CID_(identifier)" class="mw-redirect" title="S2CID (identifier)">S2CID</a> <a rel="nofollow" class="external text" href="https://api.semanticscholar.org/CorpusID:28784928">28784928</a>.</cite><span title="ctx_ver=Z39.88-2004&rft_val_fmt=info%3Aofi%2Ffmt%3Akev%3Amtx%3Ajournal&rft.genre=article&rft.jtitle=Nat+Rev+Endocrinol&rft.atitle=Clinical+pancreatic+islet+transplantation&rft.volume=13&rft.issue=5&rft.pages=268-277&rft.date=2017-05&rft_id=https%3A%2F%2Fapi.semanticscholar.org%2FCorpusID%3A28784928%23id-name%3DS2CID&rft_id=info%3Apmid%2F27834384&rft_id=info%3Adoi%2F10.1038%2Fnrendo.2016.178&rft.aulast=Shapiro&rft.aufirst=AM&rft.au=Pokrywczynska%2C+M&rft.au=Ricordi%2C+C&rfr_id=info%3Asid%2Fen.wikipedia.org%3AType+1+diabetes" class="Z3988"></li> <li><link rel="mw-deduplicated-inline-style" href="mw-data:TemplateStyles:r1238218222"><cite id="CITEREFSmithHarris2018" class="citation journal cs1">Smith A, Harris C (August 2018). <a rel="nofollow" class="external text" href="https://www.aafp.org/afp/2018/0801/p154.html">"Type 1 diabetes: Management strategies"</a>. American Family Physician. 98 (3): 154–156. <a href="/wiki/PMID_(identifier)" class="mw-redirect" title="PMID (identifier)">PMID</a> <a rel="nofollow" class="external text" href="https://pubmed.ncbi.nlm.nih.gov/30215903">30215903</a>. Retrieved 12 January 2022.</cite><span title="ctx_ver=Z39.88-2004&rft_val_fmt=info%3Aofi%2Ffmt%3Akev%3Amtx%3Ajournal&rft.genre=article&rft.jtitle=American+Family+Physician&rft.atitle=Type+1+diabetes%3A+Management+strategies&rft.volume=98&rft.issue=3&rft.pages=154-156&rft.date=2018-08&rft_id=info%3Apmid%2F30215903&rft.aulast=Smith&rft.aufirst=A&rft.au=Harris%2C+C&rft_id=https%3A%2F%2Fwww.aafp.org%2Fafp%2F2018%2F0801%2Fp154.html&rfr_id=info%3Asid%2Fen.wikipedia.org%3AType+1+diabetes" class="Z3988"></li> <li><link rel="mw-deduplicated-inline-style" href="mw-data:TemplateStyles:r1238218222"><cite id="CITEREFvon_ScholtenKreinerGoughvon_Herrath2021" class="citation journal cs1">von Scholten BJ, Kreiner FF, Gough SC, von Herrath M (May 2021). <a rel="nofollow" class="external text" href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8012324">"Current and future therapies for type 1 diabetes"</a>. Diabetologia. 64 (5): 1037–1048. <a href="/wiki/Doi_(identifier)" class="mw-redirect" title="Doi (identifier)">doi</a>:<a rel="nofollow" class="external text" href="https://doi.org/10.1007%2Fs00125-021-05398-3">10.1007/s00125-021-05398-3</a>. <a href="/wiki/PMC_(identifier)" class="mw-redirect" title="PMC (identifier)">PMC</a> <a rel="nofollow" class="external text" href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8012324">8012324</a>. <a href="/wiki/PMID_(identifier)" class="mw-redirect" title="PMID (identifier)">PMID</a> <a rel="nofollow" class="external text" href="https://pubmed.ncbi.nlm.nih.gov/33595677">33595677</a>.</cite><span title="ctx_ver=Z39.88-2004&rft_val_fmt=info%3Aofi%2Ffmt%3Akev%3Amtx%3Ajournal&rft.genre=article&rft.jtitle=Diabetologia&rft.atitle=Current+and+future+therapies+for+type+1+diabetes&rft.volume=64&rft.issue=5&rft.pages=1037-1048&rft.date=2021-05&rft_id=https%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fpmc%2Farticles%2FPMC8012324%23id-name%3DPMC&rft_id=info%3Apmid%2F33595677&rft_id=info%3Adoi%2F10.1007%2Fs00125-021-05398-3&rft.aulast=von+Scholten&rft.aufirst=BJ&rft.au=Kreiner%2C+FF&rft.au=Gough%2C+SC&rft.au=von+Herrath%2C+M&rft_id=https%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fpmc%2Farticles%2FPMC8012324&rfr_id=info%3Asid%2Fen.wikipedia.org%3AType+1+diabetes" class="Z3988"></li> <li><link rel="mw-deduplicated-inline-style" href="mw-data:TemplateStyles:r1238218222"><cite id="CITEREFWolsdorfGarvey2016" class="citation book cs1">Wolsdorf JI, Garvey KC (2016). 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class="mw-heading mw-heading2"><h2 id="External_links">External links</h2>[<a href="/w/index.php?title=Type_1_diabetes&action=edit&section=33" title="Edit section: External links">edit</a>]</div> <ul><li><a rel="nofollow" class="external text" href="https://www.niddk.nih.gov/about-niddk/strategic-plans-reports/diabetes-in-america-2nd-edition">Diabetes in America, 2nd Edition</a> (textbook) (PDFs) <a rel="nofollow" class="external text" href="https://web.archive.org/web/20110425052512/http://diabetes.niddk.nih.gov/dm/pubs/america/contents.htm">Archived</a> 25 April 2011 at the <a href="/wiki/Wayback_Machine" title="Wayback Machine">Wayback Machine</a> – National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK)</li> <li><a rel="nofollow" class="external text" href="https://diabetesatlas.org/">IDF Diabetes Atlas</a></li> <li><a rel="nofollow" class="external text" href="http://www.diabetes.org/type-1-diabetes.jsp">Type 1 Diabetes</a> <a rel="nofollow" class="external text" href="https://web.archive.org/web/20091030082136/https://www.diabetes.org/type-1-diabetes.jsp">Archived</a> 30 October 2009 at the <a href="/wiki/Wayback_Machine" title="Wayback Machine">Wayback Machine</a> at the <a href="/wiki/American_Diabetes_Association" title="American Diabetes Association">American Diabetes Association</a></li> <li><a rel="nofollow" class="external text" href="https://diabetesjournals.org/care/issue/42/Supplement_1">ADA's Standards of Medical Care in Diabetes 2019</a></li></ul> <div class="navbox-styles"><style data-mw-deduplicate="TemplateStyles:r1236075235">.mw-parser-output .navbox{box-sizing:border-box;border:1px solid #a2a9b1;width:100%;clear:both;font-size:88%;text-align:center;padding:1px;margin:1em auto 0}.mw-parser-output .navbox .navbox{margin-top:0}.mw-parser-output .navbox+.navbox,.mw-parser-output .navbox+.navbox-styles+.navbox{margin-top:-1px}.mw-parser-output .navbox-inner,.mw-parser-output .navbox-subgroup{width:100%}.mw-parser-output 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.navbox-even{background-color:#f7f7f7}.mw-parser-output .navbox-odd{background-color:transparent}.mw-parser-output .navbox .hlist td dl,.mw-parser-output .navbox .hlist td ol,.mw-parser-output .navbox .hlist td ul,.mw-parser-output .navbox td.hlist dl,.mw-parser-output .navbox td.hlist ol,.mw-parser-output .navbox td.hlist ul{padding:0.125em 0}.mw-parser-output .navbox .navbar{display:block;font-size:100%}.mw-parser-output .navbox-title .navbar{float:left;text-align:left;margin-right:0.5em}body.skin--responsive .mw-parser-output .navbox-image img{max-width:none!important}@media print{body.ns-0 .mw-parser-output .navbox{display:none!important}}</style><style data-mw-deduplicate="TemplateStyles:r1129693374">.mw-parser-output .hlist dl,.mw-parser-output .hlist ol,.mw-parser-output .hlist ul{margin:0;padding:0}.mw-parser-output .hlist dd,.mw-parser-output .hlist dt,.mw-parser-output .hlist li{margin:0;display:inline}.mw-parser-output .hlist.inline,.mw-parser-output .hlist.inline dl,.mw-parser-output .hlist.inline ol,.mw-parser-output .hlist.inline ul,.mw-parser-output .hlist dl dl,.mw-parser-output .hlist dl ol,.mw-parser-output .hlist dl ul,.mw-parser-output .hlist ol dl,.mw-parser-output .hlist ol ol,.mw-parser-output .hlist ol ul,.mw-parser-output .hlist ul dl,.mw-parser-output .hlist ul ol,.mw-parser-output .hlist ul ul{display:inline}.mw-parser-output .hlist .mw-empty-li{display:none}.mw-parser-output .hlist dt::after{content:": "}.mw-parser-output .hlist dd::after,.mw-parser-output .hlist li::after{content:" · ";font-weight:bold}.mw-parser-output .hlist dd:last-child::after,.mw-parser-output .hlist dt:last-child::after,.mw-parser-output .hlist li:last-child::after{content:none}.mw-parser-output .hlist dd dd:first-child::before,.mw-parser-output .hlist dd dt:first-child::before,.mw-parser-output .hlist dd li:first-child::before,.mw-parser-output .hlist dt dd:first-child::before,.mw-parser-output .hlist dt dt:first-child::before,.mw-parser-output .hlist dt li:first-child::before,.mw-parser-output .hlist li dd:first-child::before,.mw-parser-output .hlist li dt:first-child::before,.mw-parser-output .hlist li li:first-child::before{content:" (";font-weight:normal}.mw-parser-output .hlist dd dd:last-child::after,.mw-parser-output .hlist dd dt:last-child::after,.mw-parser-output .hlist dd li:last-child::after,.mw-parser-output .hlist dt dd:last-child::after,.mw-parser-output .hlist dt dt:last-child::after,.mw-parser-output .hlist dt li:last-child::after,.mw-parser-output .hlist li dd:last-child::after,.mw-parser-output .hlist li dt:last-child::after,.mw-parser-output .hlist li li:last-child::after{content:")";font-weight:normal}.mw-parser-output .hlist ol{counter-reset:listitem}.mw-parser-output .hlist ol>li{counter-increment:listitem}.mw-parser-output .hlist ol>li::before{content:" "counter(listitem)"\a0 "}.mw-parser-output .hlist dd ol>li:first-child::before,.mw-parser-output .hlist dt ol>li:first-child::before,.mw-parser-output .hlist li ol>li:first-child::before{content:" ("counter(listitem)"\a0 "}</style><link rel="mw-deduplicated-inline-style" href="mw-data:TemplateStyles:r1129693374"></div><div role="navigation" class="navbox" aria-label="Navbox" style="width:100%; margin:0.5em 0 0.5em 0;;padding:3px"><table class="nowraplinks navbox-inner" style="border-spacing:0;background:transparent;color:inherit"><tbody><tr><th scope="row" class="navbox-group" style="width:1%;background: #EAECF0;color:black;">Classification</th><td class="navbox-list-with-group navbox-list navbox-odd" style="width:100%;padding:0"><div style="padding:0 0.25em"><div style="position:relative; float:right; font-size:0.8em;"><a href="https://www.wikidata.org/wiki/Q124407" class="extiw" title="d:Q124407">D</a></div><div class="hlist" style="text-align:left;"><ul><li><a href="/wiki/International_Statistical_Classification_of_Diseases_and_Related_Health_Problems" class="mw-redirect" title="International Statistical Classification of Diseases and Related Health Problems">ICD</a>-<a href="/wiki/ICD-10" title="ICD-10">10</a>: <a rel="nofollow" class="external text" href="https://icd.who.int/browse10/2019/en#/E10">E10</a></li><li><a href="/wiki/International_Statistical_Classification_of_Diseases_and_Related_Health_Problems" class="mw-redirect" title="International Statistical Classification of Diseases and Related Health Problems">ICD</a>-<a href="/wiki/List_of_ICD-9_codes" title="List of ICD-9 codes">9-CM</a>: <a rel="nofollow" class="external text" href="http://www.icd9data.com/getICD9Code.ashx?icd9=250.01">250.01</a></li><li><a href="/wiki/Online_Mendelian_Inheritance_in_Man" title="Online Mendelian Inheritance in Man">OMIM</a>: <a rel="nofollow" class="external text" href="https://omim.org/entry/222100">222100</a></li><li><a href="/wiki/Medical_Subject_Headings" title="Medical Subject Headings">MeSH</a>: <a rel="nofollow" class="external text" href="https://meshb.nlm.nih.gov/record/ui?ui=D003922">D003922</a></li><li><a href="/wiki/Diseases_Database" title="Diseases Database">DiseasesDB</a>: <a rel="nofollow" class="external text" href="http://www.diseasesdatabase.com/ddb3649.htm">3649</a></li></ul></div></div></td></tr><tr><th scope="row" class="navbox-group" style="width:1%;background: #EAECF0;color:black;">External resources</th><td class="navbox-list-with-group navbox-list navbox-even" style="width:100%;padding:0"><div style="padding:0 0.25em"><div class="hlist" style="text-align:left;"><ul><li><a href="/wiki/MedlinePlus" title="MedlinePlus">MedlinePlus</a>: <a rel="nofollow" class="external text" href="https://www.nlm.nih.gov/medlineplus/ency/article/000305.htm">000305</a></li><li><a href="/wiki/EMedicine" title="EMedicine">eMedicine</a>: <a rel="nofollow" class="external text" href="https://emedicine.medscape.com/med/546-overview">med/546</a></li><li>Scholia: <a class="external text" href="https://tools.wmflabs.org/scholia/topic/Q124407">Q124407</a></li></ul></div></div></td></tr></tbody></table></div> <div class="navbox-styles"><link rel="mw-deduplicated-inline-style" href="mw-data:TemplateStyles:r1129693374"><link rel="mw-deduplicated-inline-style" href="mw-data:TemplateStyles:r1236075235"></div><div role="navigation" class="navbox" aria-labelledby="Diabetes" style="padding:3px"><table class="nowraplinks mw-collapsible autocollapse navbox-inner" style="border-spacing:0;background:transparent;color:inherit"><tbody><tr><th scope="col" class="navbox-title" colspan="2" style="background-color:turquoise"><link rel="mw-deduplicated-inline-style" href="mw-data:TemplateStyles:r1129693374"><style data-mw-deduplicate="TemplateStyles:r1239400231">.mw-parser-output .navbar{display:inline;font-size:88%;font-weight:normal}.mw-parser-output .navbar-collapse{float:left;text-align:left}.mw-parser-output .navbar-boxtext{word-spacing:0}.mw-parser-output .navbar ul{display:inline-block;white-space:nowrap;line-height:inherit}.mw-parser-output .navbar-brackets::before{margin-right:-0.125em;content:"[ "}.mw-parser-output .navbar-brackets::after{margin-left:-0.125em;content:" ]"}.mw-parser-output .navbar li{word-spacing:-0.125em}.mw-parser-output .navbar a>span,.mw-parser-output .navbar a>abbr{text-decoration:inherit}.mw-parser-output .navbar-mini abbr{font-variant:small-caps;border-bottom:none;text-decoration:none;cursor:inherit}.mw-parser-output .navbar-ct-full{font-size:114%;margin:0 7em}.mw-parser-output .navbar-ct-mini{font-size:114%;margin:0 4em}html.skin-theme-clientpref-night .mw-parser-output .navbar li a abbr{color:var(--color-base)!important}@media(prefers-color-scheme:dark){html.skin-theme-clientpref-os .mw-parser-output .navbar li a abbr{color:var(--color-base)!important}}@media print{.mw-parser-output .navbar{display:none!important}}</style><div class="navbar plainlinks hlist navbar-mini"><ul><li class="nv-view"><a href="/wiki/Template:Diabetes" title="Template:Diabetes"><abbr title="View this template">v</abbr></a></li><li class="nv-talk"><a href="/wiki/Template_talk:Diabetes" title="Template talk:Diabetes"><abbr title="Discuss this template">t</abbr></a></li><li class="nv-edit"><a href="/wiki/Special:EditPage/Template:Diabetes" title="Special:EditPage/Template:Diabetes"><abbr title="Edit this template">e</abbr></a></li></ul></div><div id="Diabetes" style="font-size:114%;margin:0 4em"><a href="/wiki/Diabetes" title="Diabetes">Diabetes</a></div></th></tr><tr><th scope="row" class="navbox-group" style="background-color:turquoise;width:1%">Types</th><td class="navbox-list-with-group navbox-list navbox-odd hlist" style="width:100%;padding:0"><div style="padding:0 0.25em"> <ul><li><a class="mw-selflink selflink">Type 1</a> (SAID cluster)</li> <li>Type 1 diabetes (<a href="/wiki/Latent_autoimmune_diabetes_in_adults" title="Latent autoimmune diabetes in adults">LADA</a> cluster)</li> <li><a href="/wiki/Type_2_diabetes" title="Type 2 diabetes">Type 2</a> (SIDD, SIRD, MOD and MARD clusters)</li> <li>Type 4 (<a href="/wiki/Gestational_diabetes" title="Gestational diabetes">Gestational diabetes</a>) <ul><li><a href="/wiki/Diabetes_and_pregnancy" title="Diabetes and pregnancy">Diabetes and pregnancy</a></li></ul></li> <li><a href="/wiki/Prediabetes" title="Prediabetes">Prediabetes</a> <ul><li><a href="/wiki/Impaired_fasting_glucose" title="Impaired fasting glucose">Impaired fasting glucose</a></li> <li><a href="/wiki/Impaired_glucose_tolerance" class="mw-redirect" title="Impaired glucose tolerance">Impaired glucose tolerance</a></li></ul></li> <li><a href="/wiki/Insulin_resistance" title="Insulin resistance">Insulin resistance</a></li> <li><a href="/wiki/Ketosis-prone_diabetes" title="Ketosis-prone diabetes">Ketosis-prone diabetes</a> (KPD)</li> <li>Type 3a (<a href="/wiki/Maturity-onset_diabetes_of_the_young" title="Maturity-onset diabetes of the young">MODY</a>) <ul><li><a href="/wiki/MODY_1" title="MODY 1">Type 1</a> <a href="/wiki/MODY_2" title="MODY 2">2</a> <a href="/wiki/MODY_3" title="MODY 3">3</a> <a href="/wiki/MODY_4" title="MODY 4">4</a> <a href="/wiki/MODY_5" class="mw-redirect" title="MODY 5">5</a> <a href="/wiki/MODY_6" title="MODY 6">6</a></li></ul></li> <li><a href="/wiki/Neonatal_diabetes" title="Neonatal diabetes">Neonatal</a> <ul><li><a href="/wiki/Transient_neonatal_diabetes" title="Transient neonatal diabetes">Transient</a></li> <li><a href="/wiki/Permanent_neonatal_diabetes" title="Permanent neonatal diabetes">Permanent</a></li></ul></li> <li><a href="/wiki/Type_3c_diabetes" title="Type 3c diabetes">Type 3c (pancreatogenic)</a></li> <li><a href="/wiki/Type_3_diabetes" title="Type 3 diabetes">Type 3</a></li> <li><a href="/wiki/Diabetes_and_deafness" title="Diabetes and deafness">MIDD</a></li></ul> </div></td></tr><tr><th scope="row" class="navbox-group" style="background-color:turquoise;width:1%"><a href="/wiki/Blood_test" title="Blood test">Blood tests</a></th><td class="navbox-list-with-group navbox-list navbox-even hlist" style="width:100%;padding:0"><div style="padding:0 0.25em"> <ul><li><a href="/wiki/Blood_sugar_level" title="Blood sugar level">Blood sugar level</a></li> <li><a href="/wiki/Biomarkers_of_diabetes" title="Biomarkers of diabetes">Biomarkers</a></li> <li><a href="/wiki/Glycated_hemoglobin" title="Glycated hemoglobin">Glycated hemoglobin</a></li> <li><a href="/wiki/Glucose_tolerance_test" title="Glucose tolerance test">Glucose tolerance test</a></li> <li><a href="/wiki/Postprandial_glucose_test" title="Postprandial glucose test">Postprandial glucose test</a></li> <li><a href="/wiki/Fructosamine" title="Fructosamine">Fructosamine</a></li> <li><a href="/wiki/Glucose_test" title="Glucose test">Glucose test</a></li> <li><a href="/wiki/C-peptide" title="C-peptide">C-peptide</a></li> <li><a href="/wiki/Noninvasive_glucose_monitor" title="Noninvasive glucose monitor">Noninvasive glucose monitor</a></li> <li><a href="/wiki/Insulin_tolerance_test" title="Insulin tolerance test">Insulin tolerance test</a></li> <li><a href="/wiki/Metabolic_Score_for_Insulin_Resistance" title="Metabolic Score for Insulin Resistance">Metabolic Score for Insulin Resistance (METS-IR)</a></li> <li><a href="/wiki/Homeostatic_model_assessment" title="Homeostatic model assessment">Homeostatic model assessment</a></li> <li><a href="/wiki/SPINA-GBeta" title="SPINA-GBeta">SPINA-GBeta</a></li> <li><a href="/wiki/SPINA-GR" title="SPINA-GR">SPINA-GR</a></li> <li><a href="/wiki/Disposition_index" title="Disposition index">Disposition index</a></li></ul> </div></td></tr><tr><th scope="row" class="navbox-group" style="background-color:turquoise;width:1%"><a href="/wiki/Diabetes_management" title="Diabetes management">Management</a></th><td class="navbox-list-with-group navbox-list navbox-odd hlist" style="width:100%;padding:0"><div style="padding:0 0.25em"> <ul><li><a href="/wiki/Prevention_of_type_2_diabetes" title="Prevention of type 2 diabetes">Prevention</a></li> <li>Metabolic assessment and monitoring <ul><li><a href="/wiki/Blood_glucose_monitoring" title="Blood glucose monitoring">Blood glucose monitoring</a></li> <li><a href="/wiki/Ambulatory_glucose_profile" title="Ambulatory glucose profile">Ambulatory glucose profile</a></li></ul></li> <li><a href="/wiki/Diet_in_diabetes" title="Diet in diabetes">Diet in diabetes</a></li> <li><a href="/wiki/Diabetes_medication" title="Diabetes medication">Diabetes medication</a></li> <li><a href="/wiki/Insulin_(medication)" title="Insulin (medication)">Insulin therapy</a> <ul><li><a href="/wiki/Intensive_insulin_therapy" title="Intensive insulin therapy">intensive</a></li> <li><a href="/wiki/Conventional_insulin_therapy" title="Conventional insulin therapy">conventional</a></li> <li><a href="/wiki/Pulsatile_insulin" title="Pulsatile insulin">pulsatile</a></li></ul></li> <li><a href="/wiki/Diabetic_shoe" title="Diabetic shoe">Diabetic shoes</a></li> <li>Cure <ul><li><a href="/wiki/Embryonic_stem_cell" title="Embryonic stem cell">Embryonic stem cells</a></li> <li><a href="/wiki/Automated_insulin_delivery_system" title="Automated insulin delivery system">Artificial pancreas</a></li></ul></li> <li>Other <ul><li><a href="/wiki/Gastric_bypass_surgery#Results_and_health_benefits_of_gastric_bypass" title="Gastric bypass surgery">Gastric bypass surgery</a></li></ul></li></ul> </div></td></tr><tr><th scope="row" class="navbox-group" style="background-color:turquoise;width:1%"><a href="/wiki/Complications_of_diabetes" title="Complications of diabetes">Complications</a></th><td class="navbox-list-with-group navbox-list navbox-even hlist" style="width:100%;padding:0"><div style="padding:0 0.25em"> <ul><li><a href="/wiki/Diabetic_coma" title="Diabetic coma">Diabetic comas</a> <ul><li><a href="/wiki/Diabetic_hypoglycemia" title="Diabetic hypoglycemia">Hypoglycemia</a></li> <li><a href="/wiki/Diabetic_ketoacidosis" title="Diabetic ketoacidosis">Ketoacidosis</a></li> <li><a href="/wiki/Hyperosmolar_hyperglycemic_state" title="Hyperosmolar hyperglycemic state">Hyperosmolar hyperglycemic state</a></li></ul></li> <li><a href="/wiki/Diabetic_foot" title="Diabetic foot">Diabetic foot</a> <ul><li><a href="/wiki/Diabetic_foot_ulcer" title="Diabetic foot ulcer">ulcer</a></li> <li><a href="/wiki/Neuropathic_arthropathy" title="Neuropathic arthropathy">Neuropathic arthropathy</a></li></ul></li> <li>Organs in diabetes <ul><li><a href="/wiki/Diabetic_angiopathy" title="Diabetic angiopathy">Blood vessels</a></li> <li><a href="/wiki/Diabetic_myonecrosis" title="Diabetic myonecrosis">Muscle</a></li> <li><a href="/wiki/Diabetic_nephropathy" title="Diabetic nephropathy">Kidney</a></li> <li><a href="/wiki/Diabetic_neuropathy" title="Diabetic neuropathy">Nerves</a></li> <li><a href="/wiki/Diabetic_retinopathy" title="Diabetic retinopathy">Retina</a></li> <li><a href="/wiki/Diabetic_cardiomyopathy" title="Diabetic cardiomyopathy">Heart</a></li></ul></li> <li><a href="/wiki/Diabetic_dermadrome" title="Diabetic dermadrome">Diabetes-related skin disease</a> <ul><li><a href="/wiki/Diabetic_dermopathy" title="Diabetic dermopathy">Diabetic dermopathy</a></li> <li><a href="/wiki/Diabetic_bulla" title="Diabetic bulla">Diabetic bulla</a></li> <li><a href="/wiki/Diabetic_cheiroarthropathy" title="Diabetic cheiroarthropathy">Diabetic cheiroarthropathy</a></li> <li><a href="/wiki/Diabetic_foot_ulcer" title="Diabetic foot ulcer">Diabetic foot ulcer</a></li></ul></li> <li><a href="/wiki/Hyperglycemia" title="Hyperglycemia">Hyperglycemia</a></li> <li><a href="/wiki/Hypoglycemia" title="Hypoglycemia">Hypoglycemia</a></li></ul> </div></td></tr><tr><th scope="row" class="navbox-group" style="background-color:turquoise;width:1%">Advocacy & Organizations</th><td class="navbox-list-with-group navbox-list navbox-odd hlist" style="width:100%;padding:0"><div style="padding:0 0.25em"> <ul><li><a href="/wiki/T1International" title="T1International">T1International</a></li> <li><a href="/wiki/Open_Insulin_Project" title="Open Insulin Project">Open Insulin Project</a></li> <li><a href="/wiki/Breakthrough_T1D" title="Breakthrough T1D">Breakthrough T1D</a></li> <li><a href="/wiki/International_Diabetes_Federation" title="International Diabetes Federation">International Diabetes Federation</a></li> <li><a href="/wiki/World_Diabetes_Day" title="World Diabetes Day">World Diabetes Day</a></li> <li><a href="/wiki/Diabetes_UK" title="Diabetes UK">Diabetes UK</a></li></ul> </div></td></tr><tr><th scope="row" class="navbox-group" style="background-color:turquoise;width:1%">Other</th><td class="navbox-list-with-group navbox-list navbox-even hlist" style="width:100%;padding:0"><div style="padding:0 0.25em"> <ul><li><a href="/wiki/Outline_of_diabetes" title="Outline of diabetes">Outline of diabetes</a></li> <li><a href="/wiki/Glossary_of_diabetes" title="Glossary of diabetes">Glossary of diabetes</a></li> <li><a href="/wiki/Epidemiology_of_diabetes" title="Epidemiology of diabetes">Epidemiology of diabetes</a></li> <li><a href="/wiki/History_of_diabetes" title="History of diabetes">History of diabetes</a></li> <li><a href="/wiki/List_of_people_with_type_1_diabetes" title="List of people with type 1 diabetes">Notable people with type 1 diabetes</a></li></ul> </div></td></tr></tbody></table></div> <div class="navbox-styles"><link rel="mw-deduplicated-inline-style" href="mw-data:TemplateStyles:r1129693374"><link rel="mw-deduplicated-inline-style" href="mw-data:TemplateStyles:r1236075235"></div><div role="navigation" class="navbox" aria-labelledby="Disease_of_the_pancreas_and_glucose_metabolism" style="padding:3px"><table class="nowraplinks mw-collapsible autocollapse navbox-inner" style="border-spacing:0;background:transparent;color:inherit"><tbody><tr><th scope="col" class="navbox-title" colspan="2"><link rel="mw-deduplicated-inline-style" href="mw-data:TemplateStyles:r1129693374"><link rel="mw-deduplicated-inline-style" href="mw-data:TemplateStyles:r1239400231"><div class="navbar plainlinks hlist navbar-mini"><ul><li class="nv-view"><a href="/wiki/Template:Disease_of_the_pancreas_and_glucose_metabolism" title="Template:Disease of the pancreas and glucose metabolism"><abbr title="View this template">v</abbr></a></li><li class="nv-talk"><a href="/wiki/Template_talk:Disease_of_the_pancreas_and_glucose_metabolism" title="Template talk:Disease of the pancreas and glucose metabolism"><abbr title="Discuss this template">t</abbr></a></li><li class="nv-edit"><a href="/wiki/Special:EditPage/Template:Disease_of_the_pancreas_and_glucose_metabolism" title="Special:EditPage/Template:Disease of the pancreas and glucose metabolism"><abbr title="Edit this template">e</abbr></a></li></ul></div><div id="Disease_of_the_pancreas_and_glucose_metabolism" style="font-size:114%;margin:0 4em">Disease of the <a href="/wiki/Pancreatic_disease" title="Pancreatic disease">pancreas</a> and <a href="/wiki/Glucose_metabolism_disorder" class="mw-redirect" title="Glucose metabolism disorder">glucose metabolism</a></div></th></tr><tr><th scope="row" class="navbox-group" style="width:1%"><a href="/wiki/Diabetes_mellitus" class="mw-redirect" title="Diabetes mellitus">Diabetes</a></th><td class="navbox-list-with-group navbox-list navbox-odd hlist" style="width:100%;padding:0"><div style="padding:0 0.25em"> <ul><li>Types <ul><li><a class="mw-selflink selflink">type 1</a></li> <li><a href="/wiki/Type_2_diabetes" title="Type 2 diabetes">type 2</a></li> <li><a href="/wiki/Gestational_diabetes" title="Gestational diabetes">gestational</a></li> <li><a href="/wiki/Maturity_onset_diabetes_of_the_young" class="mw-redirect" title="Maturity onset diabetes of the young">MODY</a> <a href="/wiki/MODY_1" title="MODY 1">1</a> <a href="/wiki/MODY_2" title="MODY 2">2</a> <a href="/wiki/MODY_3" title="MODY 3">3</a> <a href="/wiki/MODY_4" title="MODY 4">4</a> <a href="/wiki/MODY_5" class="mw-redirect" title="MODY 5">5</a> <a href="/wiki/MODY_6" title="MODY 6">6</a></li></ul></li> <li><a href="/wiki/Complications_of_diabetes_mellitus" class="mw-redirect" title="Complications of diabetes mellitus">Complications</a> <ul><li>See <a href="/wiki/Template:Diabetes" title="Template:Diabetes">Template:Diabetes</a></li></ul></li></ul> </div></td></tr><tr><th scope="row" class="navbox-group" style="width:1%">Abnormal <a href="/wiki/Blood_glucose" class="mw-redirect" title="Blood glucose">blood glucose</a> levels</th><td class="navbox-list-with-group navbox-list navbox-even hlist" style="width:100%;padding:0"><div style="padding:0 0.25em"> <ul><li><a href="/wiki/Hyperglycemia" title="Hyperglycemia">Hyperglycemia</a> <ul><li><a href="/wiki/Oxyhyperglycemia" title="Oxyhyperglycemia">Oxyhyperglycemia</a></li></ul></li> <li><a href="/wiki/Hypoglycemia" title="Hypoglycemia">Hypoglycemia</a> <ul><li><a href="/wiki/Whipple%27s_triad" title="Whipple's triad">Whipple's triad</a></li></ul></li></ul> </div></td></tr><tr><th scope="row" class="navbox-group" style="width:1%"><a href="/wiki/Insulin" title="Insulin">Insulin</a> disorders</th><td class="navbox-list-with-group navbox-list navbox-odd hlist" style="width:100%;padding:0"><div style="padding:0 0.25em"> <ul><li><a href="/wiki/Insulin_resistance" title="Insulin resistance">Insulin resistance</a></li> <li><a href="/wiki/Hyperinsulinism" title="Hyperinsulinism">Hyperinsulinism</a> <ul><li><a href="/wiki/Congenital_hyperinsulinism" title="Congenital hyperinsulinism">Congenital hyperinsulinism</a></li></ul></li> <li><a href="/wiki/Rabson%E2%80%93Mendenhall_syndrome" title="Rabson–Mendenhall syndrome">Rabson–Mendenhall syndrome</a></li></ul> </div></td></tr><tr><th scope="row" class="navbox-group" style="width:1%">Other pancreatic disorders and conditions</th><td class="navbox-list-with-group navbox-list navbox-even hlist" style="width:100%;padding:0"><div style="padding:0 0.25em"> <ul><li><a href="/wiki/Pancreatic_beta_cell_function" title="Pancreatic beta cell function">Pancreatic beta cell function</a></li> <li><a href="/wiki/Insulinoma" title="Insulinoma">Insulinoma</a></li> <li><a href="/wiki/Insulitis" title="Insulitis">Insulitis</a></li></ul> </div></td></tr></tbody></table></div> <div class="navbox-styles"><link rel="mw-deduplicated-inline-style" href="mw-data:TemplateStyles:r1129693374"><link rel="mw-deduplicated-inline-style" href="mw-data:TemplateStyles:r1236075235"></div><div role="navigation" class="navbox" aria-labelledby="Hypersensitivity_and_autoimmune_diseases" style="padding:3px"><table class="nowraplinks hlist mw-collapsible autocollapse navbox-inner" style="border-spacing:0;background:transparent;color:inherit"><tbody><tr><th scope="col" class="navbox-title" colspan="2"><link rel="mw-deduplicated-inline-style" href="mw-data:TemplateStyles:r1129693374"><link rel="mw-deduplicated-inline-style" href="mw-data:TemplateStyles:r1239400231"><div class="navbar plainlinks hlist navbar-mini"><ul><li class="nv-view"><a href="/wiki/Template:Hypersensitivity_disease_by_cause" title="Template:Hypersensitivity disease by cause"><abbr title="View this template">v</abbr></a></li><li class="nv-talk"><a href="/wiki/Template_talk:Hypersensitivity_disease_by_cause" title="Template talk:Hypersensitivity disease by cause"><abbr title="Discuss this template">t</abbr></a></li><li class="nv-edit"><a href="/wiki/Special:EditPage/Template:Hypersensitivity_disease_by_cause" title="Special:EditPage/Template:Hypersensitivity disease by cause"><abbr title="Edit this template">e</abbr></a></li></ul></div><div id="Hypersensitivity_and_autoimmune_diseases" style="font-size:114%;margin:0 4em"><a href="/wiki/Hypersensitivity" title="Hypersensitivity">Hypersensitivity</a> and <a href="/wiki/Autoimmune_disease" title="Autoimmune disease">autoimmune diseases</a></div></th></tr><tr><th scope="row" class="navbox-group" style="width:1%"><a href="/wiki/Type_I_hypersensitivity" title="Type I hypersensitivity">Type I</a>/<a href="/wiki/Allergy" title="Allergy">allergy</a>/<a href="/wiki/Atopy" title="Atopy">atopy</a> (<a href="/wiki/Immunoglobulin_E" title="Immunoglobulin E">IgE</a>)</th><td class="navbox-list-with-group navbox-list navbox-odd" style="width:100%;padding:0"><div style="padding:0 0.25em"></div><table class="nowraplinks navbox-subgroup" style="border-spacing:0"><tbody><tr><th scope="row" class="navbox-group" style="width:1%">Foreign</th><td class="navbox-list-with-group navbox-list navbox-odd" style="width:100%;padding:0"><div style="padding:0 0.25em"> <ul><li><a href="/wiki/Allergic_asthma" class="mw-redirect" title="Allergic asthma">Allergic asthma</a></li> <li><a href="/wiki/Allergic_urticaria" class="mw-redirect" title="Allergic urticaria">Allergic urticaria</a></li> <li><a href="/wiki/Allergic_rhinitis" title="Allergic rhinitis">Allergic rhinitis</a> (Hay fever)</li> <li><a href="/wiki/Anaphylaxis" title="Anaphylaxis">Anaphylaxis</a></li> <li><a href="/wiki/Atopic_dermatitis" title="Atopic dermatitis">Atopic dermatitis</a></li> <li><a href="/wiki/Food_allergy" title="Food allergy">Food allergy</a> <ul><li>common allergies include: <a href="/wiki/Egg_allergy" title="Egg allergy">Egg</a></li> <li><a href="/wiki/Milk_allergy" title="Milk allergy">Milk</a></li> <li><a href="/wiki/Peanut_allergy" title="Peanut allergy">Peanut</a></li> <li><a href="/wiki/Seafood_allergy" class="mw-redirect" title="Seafood allergy">Seafood</a></li> <li><a href="/wiki/Soy_allergy" title="Soy allergy">Soy</a></li> <li><a href="/wiki/Tree_nut_allergy" title="Tree nut allergy">Tree nut</a></li> <li><a href="/wiki/Wheat_allergy" title="Wheat allergy">Wheat</a></li></ul></li> <li><a href="/wiki/Side_effects_of_penicillin" title="Side effects of penicillin">Penicillin allergy</a></li></ul> </div></td></tr><tr><th scope="row" class="navbox-group" style="width:1%">Autoimmune</th><td class="navbox-list-with-group navbox-list navbox-even" style="width:100%;padding:0"><div style="padding:0 0.25em"> <ul><li><a href="/wiki/Autoimmune_urticaria" title="Autoimmune urticaria">Autoimmune urticaria</a></li> <li><a href="/wiki/Eosinophilic_esophagitis" title="Eosinophilic esophagitis">Eosinophilic esophagitis</a></li></ul> </div></td></tr></tbody></table><div></div></td></tr><tr><th scope="row" class="navbox-group" style="width:1%"><a href="/wiki/Type_II_hypersensitivity" title="Type II hypersensitivity">Type II</a>/<a href="/wiki/Antibody-dependent_cellular_cytotoxicity" title="Antibody-dependent cellular cytotoxicity">ADCC</a> <ul><li><ul><li><a href="/wiki/Immunoglobulin_G" title="Immunoglobulin G">IgG</a></li> <li><a href="/wiki/Immunoglobulin_M" title="Immunoglobulin M">IgM</a></li></ul></li></ul></th><td class="navbox-list-with-group navbox-list navbox-odd" style="width:100%;padding:0"><div style="padding:0 0.25em"></div><table class="nowraplinks navbox-subgroup" style="border-spacing:0"><tbody><tr><th scope="row" class="navbox-group" style="width:1%">Foreign</th><td class="navbox-list-with-group navbox-list navbox-odd" style="width:100%;padding:0"><div style="padding:0 0.25em"> <li><a href="/wiki/Hemolytic_disease_of_the_newborn" title="Hemolytic disease of the newborn">Hemolytic disease of the newborn</a></li> </div></td></tr><tr><th scope="row" class="navbox-group" style="width:1%">Autoimmune</th><td class="navbox-list-with-group navbox-list navbox-odd" style="width:100%;padding:0"><div style="padding:0 0.25em"></div><table class="nowraplinks navbox-subgroup" style="border-spacing:0"><tbody><tr><th scope="row" class="navbox-group" style="width:1%"><a href="/wiki/Cytotoxicity" title="Cytotoxicity">Cytotoxic</a></th><td class="navbox-list-with-group navbox-list navbox-even" style="width:100%;padding:0"><div style="padding:0 0.25em"> <ul><li><a href="/wiki/Autoimmune_hemolytic_anemia" title="Autoimmune hemolytic anemia">Autoimmune hemolytic anemia</a></li> <li><a href="/wiki/Bullous_pemphigoid" title="Bullous pemphigoid">Bullous pemphigoid</a></li> <li><a href="/wiki/Goodpasture_syndrome" title="Goodpasture syndrome">Goodpasture syndrome</a></li> <li><a href="/wiki/Guillain%E2%80%93Barr%C3%A9_syndrome" title="Guillain–Barré syndrome">Guillain–Barré syndrome</a></li> <li><a href="/wiki/Immune_thrombocytopenic_purpura" title="Immune thrombocytopenic purpura">Immune thrombocytopenic purpura</a></li> <li><a href="/wiki/Pemphigus_vulgaris" title="Pemphigus vulgaris">Pemphigus vulgaris</a></li> <li><a href="/wiki/Rheumatic_fever" title="Rheumatic fever">Rheumatic fever</a></li></ul> </div></td></tr><tr><th scope="row" class="navbox-group" style="width:1%">"<a href="/wiki/Hypersensitivity#Type_V" title="Hypersensitivity">Type V</a>"/<a href="/wiki/Receptor_(biochemistry)" title="Receptor (biochemistry)">receptor</a></th><td class="navbox-list-with-group navbox-list navbox-odd" style="width:100%;padding:0"><div style="padding:0 0.25em"> <ul><li><a href="/wiki/Graves%27_disease" title="Graves' disease">Graves' disease</a></li> <li><a href="/wiki/Myasthenia_gravis" title="Myasthenia gravis">Myasthenia gravis</a></li> <li><a href="/wiki/Pernicious_anemia" title="Pernicious anemia">Pernicious anemia</a></li></ul> </div></td></tr></tbody></table><div></div></td></tr></tbody></table><div></div></td></tr><tr><th scope="row" class="navbox-group" style="width:1%"><a href="/wiki/Type_III_hypersensitivity" title="Type III hypersensitivity">Type III</a> (<a href="/wiki/Immune_complex" title="Immune complex">Immune complex</a>)</th><td class="navbox-list-with-group navbox-list navbox-odd" style="width:100%;padding:0"><div style="padding:0 0.25em"></div><table class="nowraplinks navbox-subgroup" style="border-spacing:0"><tbody><tr><th scope="row" class="navbox-group" style="width:1%">Foreign</th><td class="navbox-list-with-group navbox-list navbox-even" style="width:100%;padding:0"><div style="padding:0 0.25em"> <ul><li><a href="/wiki/Arthus_reaction" title="Arthus reaction">Arthus reaction</a></li> <li><a href="/wiki/Farmer%27s_lung" title="Farmer's lung">Farmer's lung</a></li> <li><a href="/wiki/Henoch%E2%80%93Sch%C3%B6nlein_purpura" title="Henoch–Schönlein purpura">Henoch–Schönlein purpura</a></li> <li><a href="/wiki/Cutaneous_small-vessel_vasculitis" title="Cutaneous small-vessel vasculitis">Hypersensitivity vasculitis</a></li> <li><a href="/wiki/Acute_proliferative_glomerulonephritis" title="Acute proliferative glomerulonephritis">Post-streptococcal glomerulonephritis</a></li> <li><a href="/wiki/Reactive_arthritis" title="Reactive arthritis">Reactive arthritis</a></li> <li><a href="/wiki/Serum_sickness" title="Serum sickness">Serum sickness</a></li></ul> </div></td></tr><tr><th scope="row" class="navbox-group" style="width:1%">Autoimmune</th><td class="navbox-list-with-group navbox-list navbox-odd" style="width:100%;padding:0"><div style="padding:0 0.25em"> <ul><li><a href="/wiki/Lupus" title="Lupus">Lupus</a></li> <li><a href="/wiki/Rheumatoid_arthritis" title="Rheumatoid arthritis">Rheumatoid arthritis</a></li> <li><a href="/wiki/Subacute_bacterial_endocarditis" title="Subacute bacterial endocarditis">Subacute bacterial endocarditis</a></li></ul> </div></td></tr></tbody></table><div></div></td></tr><tr><th scope="row" class="navbox-group" style="width:1%"><a href="/wiki/Type_IV_hypersensitivity" title="Type IV hypersensitivity">Type IV</a>/<a href="/wiki/Cell-mediated_immunity" title="Cell-mediated immunity">cell-mediated</a> (<a href="/wiki/T_cell" title="T cell">T cells</a>)</th><td class="navbox-list-with-group navbox-list navbox-odd" style="width:100%;padding:0"><div style="padding:0 0.25em"></div><table class="nowraplinks navbox-subgroup" style="border-spacing:0"><tbody><tr><th scope="row" class="navbox-group" style="width:1%">Foreign</th><td class="navbox-list-with-group navbox-list navbox-even" style="width:100%;padding:0"><div style="padding:0 0.25em"> <ul><li><a href="/wiki/Allergic_contact_dermatitis" title="Allergic contact dermatitis">Allergic contact dermatitis</a></li> <li><a href="/wiki/Mantoux_test" title="Mantoux test">Mantoux test</a></li></ul> </div></td></tr><tr><th scope="row" class="navbox-group" style="width:1%">Autoimmune</th><td class="navbox-list-with-group navbox-list navbox-odd" style="width:100%;padding:0"><div style="padding:0 0.25em"> <ul><li><a href="/wiki/Coeliac_disease" title="Coeliac disease">Coeliac disease</a></li> <li><a href="/wiki/Giant_cell_arteritis" title="Giant cell arteritis">Giant cell arteritis</a></li> <li><a href="/wiki/Hashimoto%27s_thyroiditis" title="Hashimoto's thyroiditis">Hashimoto's thyroiditis</a></li> <li><a href="/wiki/Multiple_sclerosis" title="Multiple sclerosis">Multiple sclerosis</a></li> <li><a href="/wiki/Postorgasmic_illness_syndrome" title="Postorgasmic illness syndrome">Postorgasmic illness syndrome</a></li> <li><a href="/wiki/Reactive_arthritis" title="Reactive arthritis">Reactive arthritis</a></li> <li><a class="mw-selflink selflink">Type 1 diabetes</a></li></ul> </div></td></tr><tr><th scope="row" class="navbox-group" style="width:1%"><a href="/wiki/Graft-versus-host_disease" title="Graft-versus-host disease">GVHD</a></th><td class="navbox-list-with-group navbox-list navbox-even" style="width:100%;padding:0"><div style="padding:0 0.25em"> <ul><li><a href="/wiki/Transfusion-associated_graft-versus-host_disease" title="Transfusion-associated graft-versus-host disease">Transfusion-associated graft-versus-host disease</a></li></ul> </div></td></tr></tbody></table><div></div></td></tr><tr><th scope="row" class="navbox-group" style="width:1%">Unknown/ multiple</th><td class="navbox-list-with-group navbox-list navbox-odd" style="width:100%;padding:0"><div style="padding:0 0.25em"></div><table class="nowraplinks navbox-subgroup" style="border-spacing:0"><tbody><tr><th scope="row" class="navbox-group" style="width:1%">Foreign</th><td class="navbox-list-with-group navbox-list navbox-odd" style="width:100%;padding:0"><div style="padding:0 0.25em"> <ul><li><a href="/wiki/Hypersensitivity_pneumonitis" title="Hypersensitivity pneumonitis">Hypersensitivity pneumonitis</a> <ul><li><a href="/wiki/Allergic_bronchopulmonary_aspergillosis" title="Allergic bronchopulmonary aspergillosis">Allergic bronchopulmonary aspergillosis</a></li></ul></li> <li><a href="/wiki/Latex_allergy" title="Latex allergy">Latex allergy</a> (I+IV)</li> <li><a href="/wiki/Transplant_rejection" title="Transplant rejection">Transplant rejection</a></li></ul> </div></td></tr><tr><th scope="row" class="navbox-group" style="width:1%">Autoimmune</th><td class="navbox-list-with-group navbox-list navbox-even" style="width:100%;padding:0"><div style="padding:0 0.25em"> <ul><li><a href="/wiki/Addison%27s_disease" title="Addison's disease">Autoimmune adrenalitis</a></li> <li><a href="/wiki/Autoimmune_hepatitis" title="Autoimmune hepatitis">Autoimmune hepatitis</a></li> <li><a href="/wiki/Autoimmune_polyendocrine_syndrome" title="Autoimmune polyendocrine syndrome">Autoimmune polyendocrine syndrome</a> <ul><li><a href="/wiki/Autoimmune_polyendocrine_syndrome_type_1" title="Autoimmune polyendocrine syndrome type 1">APS1</a></li> <li><a href="/wiki/Autoimmune_polyendocrine_syndrome_type_2" title="Autoimmune polyendocrine syndrome type 2">APS2</a></li></ul></li> <li><a href="/wiki/Sj%C3%B6gren_syndrome" title="Sjögren syndrome">Sjögren syndrome</a></li> <li><a href="/wiki/Autoimmune_disease" title="Autoimmune disease">Systemic autoimmune disease</a></li></ul> </div></td></tr></tbody></table><div></div></td></tr></tbody></table></div>    </div><noscript><img src="https://login.wikimedia.org/wiki/Special:CentralAutoLogin/start?type=1x1" alt="" width="1" height="1" style="border: none; position: absolute;"></noscript> <div class="printfooter" data-nosnippet="">Retrieved from "<a dir="ltr" href="https://en.wikipedia.org/w/index.php?title=Type_1_diabetes&oldid=1260000036">https://en.wikipedia.org/w/index.php?title=Type_1_diabetes&oldid=1260000036</a>"</div></div> <div id="catlinks" class="catlinks" data-mw="interface"><div id="mw-normal-catlinks" class="mw-normal-catlinks"><a href="/wiki/Help:Category" title="Help:Category">Categories</a>: <ul><li><a href="/wiki/Category:Autoimmune_diseases" title="Category:Autoimmune diseases">Autoimmune diseases</a></li><li><a href="/wiki/Category:Types_of_diabetes" title="Category:Types of diabetes">Types of diabetes</a></li></ul></div><div id="mw-hidden-catlinks" class="mw-hidden-catlinks mw-hidden-cats-hidden">Hidden categories: <ul><li><a href="/wiki/Category:Source_attribution" title="Category:Source attribution">Source attribution</a></li><li><a href="/wiki/Category:CS1_maint:_DOI_inactive_as_of_November_2024" title="Category:CS1 maint: DOI inactive as of November 2024">CS1 maint: DOI inactive as of November 2024</a></li><li><a href="/wiki/Category:Wikipedia_articles_needing_page_number_citations_from_October_2022" title="Category:Wikipedia articles needing page number citations from October 2022">Wikipedia articles needing page number citations from October 2022</a></li><li><a href="/wiki/Category:Articles_with_short_description" title="Category:Articles with short description">Articles with short description</a></li><li><a href="/wiki/Category:Short_description_is_different_from_Wikidata" title="Category:Short description is different from Wikidata">Short description is different from Wikidata</a></li><li><a href="/wiki/Category:Use_dmy_dates_from_January_2023" title="Category:Use dmy dates from January 2023">Use dmy dates from January 2023</a></li><li><a href="/wiki/Category:Webarchive_template_wayback_links" title="Category:Webarchive template wayback links">Webarchive template wayback links</a></li></ul></div></div> </div> </main> </div> 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Template:Infobox_medical_condition"," 5.29% 106.992 1 Template:Infobox"," 4.88% 98.788 1 Template:Medical_resources"," 4.74% 95.891 15 Template:Cite_book"," 4.55% 92.129 22 Template:Cite_web"]},"scribunto":{"limitreport-timeusage":{"value":"1.323","limit":"10.000"},"limitreport-memusage":{"value":9495904,"limit":52428800},"limitreport-logs":"anchor_id_list = table#1 {\n [\"CITEREFAanstootAndersonDanemanDanne2007\"] = 1,\n [\"CITEREFAl-AwarKupaiVeszelkaSzűcs2016\"] = 1,\n [\"CITEREFAlarcón-GómezChulvi-MedranoMartin-RiveraCalatayud2021\"] = 1,\n [\"CITEREFAmerican_Diabetes_Association2021\"] = 1,\n [\"CITEREFAmerican_Diabetes_Association_(6)2021\"] = 1,\n [\"CITEREFArffmanHakkarainenKeskimäkiOksanen2023\"] = 1,\n [\"CITEREFAtkinsonMcgillDassauLaffel2020\"] = 1,\n [\"CITEREFAustralian_Institute_of_Health_and_Welfare2015\"] = 1,\n [\"CITEREFBanarerMcGregorCryer2002\"] = 1,\n [\"CITEREFBluestoneHeroldEisenbarth2010\"] = 1,\n [\"CITEREFBoneEvans-Molina2017\"] = 1,\n [\"CITEREFBottazzoFlorin-ChristensenDoniach1974\"] = 1,\n [\"CITEREFBoughtonHovorka2020\"] = 1,\n [\"CITEREFBrownSinaiiRother2008\"] = 1,\n [\"CITEREFBrownleeAielloSunCooper2020\"] = 1,\n [\"CITEREFButlerMisselbrook2020\"] = 1,\n [\"CITEREFCashenPetersen2019\"] = 1,\n [\"CITEREFChangGurley2012\"] = 1,\n [\"CITEREFChellappanSivamTeohLeong2018\"] = 1,\n [\"CITEREFChenDuZou2020\"] = 1,\n [\"CITEREFChenSuLinSung2012\"] = 1,\n [\"CITEREFChenThayerWenWong2020\"] = 1,\n [\"CITEREFChiangKirkmanLaffelPeters2014\"] = 1,\n [\"CITEREFChristofferssonFlodström-Tullberg2020\"] = 1,\n [\"CITEREFCodnerEscobar-Morreale2007\"] = 1,\n [\"CITEREFCooperbergCryer2009\"] = 1,\n [\"CITEREFDaneman2006\"] = 1,\n [\"CITEREFDayanKorahTatovicBundy2019\"] = 1,\n [\"CITEREFDeanKuklaStegallKudva2017\"] = 1,\n [\"CITEREFDeanMcEntyre2004\"] = 1,\n [\"CITEREFDelliLernmark2016\"] = 1,\n [\"CITEREFDevarajGlaserGriffenWang-Polagruto2006\"] = 1,\n [\"CITEREFDiMeglioEvans-MolinaOram2018\"] = 1,\n [\"CITEREFElfströmSundströmLudvigsson2014\"] = 1,\n [\"CITEREFErlichValdesNobleCarlson2008\"] = 1,\n [\"CITEREFEscobar-MorrealeRoldánBarrioAlonso2000\"] = 1,\n [\"CITEREFEspositoToniTasciniSanti2019\"] = 1,\n [\"CITEREFFangWangEchouffo-TcheuguiSelvin2023\"] = 1,\n [\"CITEREFFarhyMcCall2015\"] = 1,\n [\"CITEREFGarcía-HermosoEzzatvarHuerta-UribeAlonso-Martínez2023\"] = 1,\n [\"CITEREFGargTylerYangCutler2012\"] = 1,\n [\"CITEREFGoswamiVishwanathGangadarappaRazdan2014\"] = 1,\n [\"CITEREFGranbergEjskjaerPeakmanSundkvist2005\"] = 1,\n [\"CITEREFGrantHakonarson2009\"] = 1,\n [\"CITEREFHeroldVignaliCookeBluestone2013\"] = 1,\n [\"CITEREFHuxleyPetersMishraWoodward2015\"] = 1,\n [\"CITEREFIsaacsFoskettMaxwellWard2021\"] = 1,\n [\"CITEREFJamesHijaz2014\"] = 1,\n [\"CITEREFJerramDangLeslie2017\"] = 1,\n [\"CITEREFJohnson2008\"] = 1,\n [\"CITEREFKamrathMönkemöllerBiesterRohrer2020\"] = 1,\n [\"CITEREFKatsarouGudbjörnsdottirRawshaniDabelea2017\"] = 1,\n [\"CITEREFKing2012\"] = 1,\n [\"CITEREFKing2020\"] = 1,\n [\"CITEREFKingEstil_LesMontanya2020\"] = 1,\n [\"CITEREFKnipVeijolaVirtanenHyöty2005\"] = 1,\n [\"CITEREFKostopoulouSinopidisFouzasGkentzi2023\"] = 1,\n [\"CITEREFLeeCollettBergfordHartnell2023\"] = 1,\n [\"CITEREFLenzen2017\"] = 1,\n [\"CITEREFLenzenArndtElsnerWedekind2020\"] = 1,\n [\"CITEREFLenzenTiedgeElsnerLortz2001\"] = 1,\n [\"CITEREFLeslieEvans-MolinaFreund-BrownBuzzetti2021\"] = 1,\n [\"CITEREFLivingstoneLevinLookerLindsay2015\"] = 1,\n [\"CITEREFLumb2014\"] = 1,\n [\"CITEREFLy2015\"] = 1,\n [\"CITEREFMartín-TimónDel_Cañizo-Gómez2015\"] = 1,\n [\"CITEREFMcNulty2023\"] = 1,\n [\"CITEREFMeierKjemsVeldhuisLefèbvre2006\"] = 1,\n [\"CITEREFMittalCamickLemosHirani2024\"] = 1,\n [\"CITEREFMundingerMeiFoulisFligner2016\"] = 1,\n [\"CITEREFMundingerTaborsky2016\"] = 1,\n [\"CITEREFNobleErlich2012\"] = 1,\n [\"CITEREFNorrisJohnsonStene2020\"] = 1,\n [\"CITEREFPandeyDvorakova2020\"] = 1,\n [\"CITEREFPaolissoSgambatoTorellaVarricchio1988\"] = 1,\n [\"CITEREFPetschnigWagnerRobubiBaron2020\"] = 1,\n [\"CITEREFRadenkovićStojanovićProstran2016\"] = 1,\n [\"CITEREFRajuCryer2005\"] = 1,\n [\"CITEREFRamliReddyOliver2019\"] = 1,\n [\"CITEREFRedondoSteckPugliese2018\"] = 1,\n [\"CITEREFRenoLitvinClarkFisher2013\"] = 1,\n [\"CITEREFRepaske2016\"] = 1,\n [\"CITEREFRickelsRobertson2019\"] = 1,\n [\"CITEREFRobertsonDavisLarsenStratta2006\"] = 1,\n [\"CITEREFRoep2003\"] = 1,\n [\"CITEREFRoyLloyd2012\"] = 1,\n [\"CITEREFSadeharjuHämäläinenKnipLönnrot2003\"] = 1,\n [\"CITEREFSalpeaCosentinoIgoillo-Esteve2020\"] = 1,\n [\"CITEREFSeckoldFisherde_BockKing2019\"] = 1,\n [\"CITEREFSeeKaukinenMakhariaGibson2015\"] = 1,\n [\"CITEREFShapiroPokrywczynskaRicordi2017\"] = 1,\n [\"CITEREFShaw2012\"] = 1,\n [\"CITEREFSiaWeinem2005\"] = 1,\n [\"CITEREFSkyler2012\"] = 1,\n [\"CITEREFSmithHarris2018\"] = 1,\n [\"CITEREFSteckRewers2011\"] = 1,\n [\"CITEREFTEDDY_Study_Group2008\"] = 1,\n [\"CITEREFTesfayeSeaquist2010\"] = 1,\n [\"CITEREFThe_Diabetes_Research_in_Children_Network_(DirecNet)_Study_Group2006\"] = 1,\n [\"CITEREFTodd2010\"] = 1,\n [\"CITEREFTorpyLynmGlass2007\"] = 1,\n [\"CITEREFTosurHuangInglisAguirre2024\"] = 1,\n [\"CITEREFUngerCherrington2012\"] = 1,\n [\"CITEREFVaarala2012\"] = 1,\n [\"CITEREFVangMileticBottiniMustelin2007\"] = 1,\n [\"CITEREFWeissDonnachieBeyerleinZiegler2023\"] = 1,\n [\"CITEREFWolsdorfGarvey2016\"] = 1,\n [\"CITEREFXieChangHuangZhou2020\"] = 1,\n [\"CITEREFYosten2018\"] = 1,\n [\"CITEREFZhengPermanyerCanudas-RomoAburto2023\"] = 1,\n [\"CITEREFvon_ScholtenKreinerGoughvon_Herrath2021\"] = 1,\n}\ntemplate_list = table#1 {\n [\"!\"] = 3,\n [\"CS1 config\"] = 1,\n [\"Citation\"] = 1,\n [\"Cite book\"] = 15,\n [\"Cite journal\"] = 95,\n [\"Cite news\"] = 1,\n [\"Cite press release\"] = 1,\n [\"Cite web\"] = 22,\n [\"DEFAULTSORT:Diabetes Mellitus Type 1\"] = 1,\n [\"Diabetes\"] = 1,\n [\"Disease of the pancreas and glucose metabolism\"] = 1,\n [\"Further\"] = 3,\n [\"Harvid\"] = 1,\n [\"Hypersensitivity disease by cause\"] = 1,\n [\"ICD10\"] = 1,\n [\"ICD9\"] = 1,\n [\"IPAc-en\"] = 1,\n [\"Infobox medical condition\"] = 1,\n [\"Main\"] = 1,\n [\"Medical resources\"] = 1,\n [\"Page needed\"] = 1,\n [\"ProQuest\"] = 1,\n [\"Refbegin\"] = 1,\n [\"Refend\"] = 1,\n [\"Reflist\"] = 1,\n [\"See also\"] = 1,\n [\"Sfn\"] = 123,\n [\"Short description\"] = 1,\n [\"Source-attribution\"] = 1,\n [\"TOC limit\"] = 1,\n [\"Use dmy dates\"] = 1,\n [\"Webarchive\"] = 2,\n}\narticle_whitelist = table#1 {\n}\n","limitreport-profile":[["?","220","15.9"],["MediaWiki\\Extension\\Scribunto\\Engines\\LuaSandbox\\LuaSandboxCallback::callParserFunction","220","15.9"],["MediaWiki\\Extension\\Scribunto\\Engines\\LuaSandbox\\LuaSandboxCallback::find","200","14.5"],["MediaWiki\\Extension\\Scribunto\\Engines\\LuaSandbox\\LuaSandboxCallback::match","140","10.1"],["dataWrapper \u003Cmw.lua:672\u003E","100","7.2"],["recursiveClone \u003CmwInit.lua:45\u003E","100","7.2"],["MediaWiki\\Extension\\Scribunto\\Engines\\LuaSandbox\\LuaSandboxCallback::getAllExpandedArguments","40","2.9"],["MediaWiki\\Extension\\Scribunto\\Engines\\LuaSandbox\\LuaSandboxCallback::unstripNoWiki","40","2.9"],["\u003Cmw.lua:694\u003E","40","2.9"],["(for generator)","20","1.4"],["[others]","260","18.8"]]},"cachereport":{"origin":"mw-api-int.codfw.main-b87644b56-s4fx9","timestamp":"20241128072349","ttl":2592000,"transientcontent":false}}});});</script> <script type="application/ld+json">{"@context":"https:\/\/schema.org","@type":"Article","name":"Type 1 diabetes","url":"https:\/\/en.wikipedia.org\/wiki\/Type_1_diabetes","sameAs":"http:\/\/www.wikidata.org\/entity\/Q124407","mainEntity":"http:\/\/www.wikidata.org\/entity\/Q124407","author":{"@type":"Organization","name":"Contributors to Wikimedia projects"},"publisher":{"@type":"Organization","name":"Wikimedia Foundation, Inc.","logo":{"@type":"ImageObject","url":"https:\/\/www.wikimedia.org\/static\/images\/wmf-hor-googpub.png"}},"datePublished":"2005-10-02T02:30:10Z","dateModified":"2024-11-28T07:23:31Z","image":"https:\/\/upload.wikimedia.org\/wikipedia\/commons\/4\/43\/Blue_circle_for_diabetes.svg","headline":"autoimmune disease, a form of diabetes mellitus that occurs when insulin-producing cells are destroyed by the immune system"}</script> </body> </html>