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On type 1 diabetes mellitus pathogenesis
Division of Endocrinology and Diabetes, "Aghia Sophia" Hospital, National and Kapodistrian University of Athens - Faculty of Medicine, Athens, Greece.
Division of Endocrinology and Diabetes, "Aghia Sophia" Hospital, National and Kapodistrian University of Athens - Faculty of Medicine, Athens, Greece.
Division of Endocrinology and Diabetes, "Aghia Sophia" Hospital, National and Kapodistrian University of Athens - Faculty of Medicine, Athens, Greece.
Division of Endocrinology and Diabetes, "Aghia Sophia" Hospital, National and Kapodistrian University of Athens - Faculty of Medicine, Athens, Greece.
2017 (English)In: Endocrine Connections, ISSN 2049-3614, E-ISSN 2049-3614, article id EC-17-0347Article in journal (Refereed) Epub ahead of print
Abstract [en]

Type 1 diabetes mellitus (T1DM) results from the autoimmune destruction of β cells of the endocrine pancreas. Pathogenesis of type 1 diabetes mellitus is different from that of type 2 diabetes mellitus, where both insulin resistance and reduced secretion of insulin by the β cells play a synergistic role. We will present genetic, environmental and immunologic factors that destroy β cells of the endocrine pancreas and lead to insulin deficiency. The process of autoimmune destruction takes place in genetically susceptible individuals under the triggering effect of one or more environmental factors and usually progresses over a period of many months to years, during which period patients are asymptomatic and euglycemic, but positive for relevant autoantibodies. Symptomatic hyperglycemia and frank diabetes occurs after a long latency period, which reflects the large percentage of β cells that need to be destroyed before overt diabetes become evident.

Place, publisher, year, edition, pages
Bioscientifica, 2017. article id EC-17-0347
Keywords [en]
type 1 diabetes, pathogenesis, genetics, autoimmunity, microbiota
National Category
Endocrinology and Diabetes
Identifiers
URN: urn:nbn:se:liu:diva-144192DOI: 10.1530/EC-17-0347ISI: 000426045300003PubMedID: 29191919Scopus ID: 2-s2.0-85041307344OAI: oai:DiVA.org:liu-144192DiVA, id: diva2:1172305
Available from: 2018-01-09 Created: 2018-01-09 Last updated: 2018-04-27Bibliographically approved

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