Skip to main page content
U.S. flag

An official website of the United States government

Dot gov

The .gov means it’s official.
Federal government websites often end in .gov or .mil. Before sharing sensitive information, make sure you’re on a federal government site.

Https

The site is secure.
The https:// ensures that you are connecting to the official website and that any information you provide is encrypted and transmitted securely.

Access keys NCBI Homepage MyNCBI Homepage Main Content Main Navigation
Review
. 2018 Jan;7(1):R38-R46.
doi: 10.1530/EC-17-0347. Epub 2017 Nov 30.

On type 1 diabetes mellitus pathogenesis

Stavroula A Paschou  1 , Nektaria Papadopoulou-Marketou  1 , George P Chrousos  1 , Christina Kanaka-Gantenbein  2
Affiliations
Review

On type 1 diabetes mellitus pathogenesis

Stavroula A Paschou et al. Endocr Connect. 2018 Jan.

Abstract

Type 1 diabetes mellitus (T1DM) results from the autoimmune destruction of β cells of the endocrine pancreas. Pathogenesis of T1DM 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 occur after a long latency period, which reflects the large percentage of β cells that need to be destroyed before overt diabetes become evident.

Keywords: autoimmunity; genetics; microbiota; pathogenesis; type 1 diabetes.

PubMed Disclaimer

References

    1. Paschou SA, Petsiou A, Chatzigianni K, Tsatsoulis A, Papadopoulos GK. Type 1 diabetes as an autoimmune disease: the evidence. Diabetologia 2014. 57 1500–1501. ( 10.1007/s00125-014-3229-5) - DOI - PubMed
    1. Atkinson MA, Maclaren NK. The pathogenesis of insulin-dependent diabetes mellitus. New England Journal of Medicine 1994. 331 1428 ( 10.1056/NEJM199411243312107) - DOI - PubMed
    1. Beyan H, Riese H, Hawa MI, Beretta G, Davidson HW, Hutton JC, Burger H, Schlosser M, Snieder H, Boehm BO, et al Glycotoxin and autoantibodies are additive environmentally determined predictors of type 1 diabetes: a twin and population study. Diabetes 2012. 61 1192–1198. ( 10.2337/db11-0971) - DOI - PMC - PubMed
    1. Redondo MJ, Rewers M, Yu L, Garg S, Pilcher CC, Elliott RB, Eisenbarth GS. Genetic determination of islet cell autoimmunity in monozygotic twin, dizygotic twin, and non-twin siblings of patients with type 1 diabetes: prospective twin study. BMJ 1999. 318 698 ( 10.1136/bmj.318.7185.698) - DOI - PMC - PubMed
    1. Størling J, Pociot F. Type 1 diabetes candidate genes linked to pancreatic islet cell inflammation and beta-cell apoptosis. Genes 2017. 8 E72. - PMC - PubMed