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FB2026_01
,
released March 12, 2026
This report includes links to reviews and general information on diabetes mellitus, insulin-dependent (IDDM) also known as diabetes mellitus, type 1. Both genetic and environmental factors are important in determining IDDM disease risk. A very active area of current study is the identification and characterization of genes that confer susceptibility to type 1 diabetes.
The Drosophila insulin-like peptide genes are expressed in a small clusters of cells, insulin-producing cells (IPCs), in the brain. The IPCs appear to be functionally analogous to the human pancreatic islet beta cells. Ablation of these insulin-producing cells causes developmental delay, growth retardation, and elevated carbohydrate levels in larval hemolymph; in adults, increased fasting glucose levels in the hemolymph is observed, similar to that found in diabetic mammals. See the FlyBase gene group report for Insulin-like Peptides (FBgg0000048) and the pathway report for Insulin-Like Receptor Signaling (FBgg0000904).
References describing biology of this Drosophila system, methods and assays: Owusu-Ansah and Perrimon, 2014 (FBrf0224368); Alfa and Kim, 2016 (FBrf0231859); Graham and Pick, 2017 (FBrf0234320); Murillo-Maldonado and Riesgo-Escovar, 2017 (FBrf0235584); Li and Tennessen, 2017 (FBrf0236417); Inoue et al., 2018 (FBrf0239288). See also Vinayagam et al., 2016 (FBrf0233454), which describes a comprehensive analysis of the InR/PI3K/AKT network in Drosophila.
The obesity epidemic is widely blamed for a rise in the incidence of type 2 diabetes among children; it has been proposed that it is also to blame for a similar increase in type 1 diabetes. Children who develop type 1 diabetes are genetically predisposed to get the disease, but being overweight appears to accelerate the process (https://www.webmd.com/diabetes/news/20030926/obesity-linked-to-type-1-diabetes#1). See also human disease models listed in the report 'obesity, susceptibility to (fly models overview)' (FBhh0000492).
For a listing of Drosophila models of insulin-dependent diabetes mellitus see the "Related Diseases" section, below, or go to the FlyBase Human Disease Model Report Index (http://flybase.org/lists/FBhh/).
[updated Sep. 2019 by FlyBase; FBrf0222196]
[TYPE 1 DIABETES MELLITUS; T1D](https://omim.org/entry/222100)
[TYPE 1 DIABETES MELLITUS; T1D](https://omim.org/entry/222100)
[INTERLEUKIN 6; IL6](https://omim.org/entry/147620)
[HNF1 HOMEOBOX A; HNF1A](https://omim.org/entry/142410)
Diabetes mellitus is classified clinically into 2 major forms of the primary illness, insulin-dependent diabetes mellitus (IDDM) and noninsulin-dependent diabetes mellitus (NIDDM), and secondary forms related to gestation or medical disorders. The type of diabetes mellitus called IDDM is a disorder of glucose homeostasis that is characterized by susceptibility to ketoacidosis in the absence of insulin therapy. Long-term complications that affect the eyes, kidneys, nerves, and blood vessels. [from MIM:222100; 2017.01.23]
Both genetic and environmental factors are important in defining IDDM disease risk; this is supported by observations showing that the proband-wise concordance for monozygotic (MZ) twins is estimated to be ~50%, compared with ~8% for dizygotic [DZ] twins. The highly polymorphic HLA class II genes clearly play the most important single role in susceptibility to type 1 diabetes. Multiple additional non-HLA genes and regions have been identified, including regions based on GWAS analyses. (Pociot, et al. 2010; pubmed:20587799)
Candidate gene and genome-wide association studies have identified > 50 susceptibility loci for common type 1 diabetes (T1D) and approximately 100 susceptibility loci for type 2 diabetes (T2D). About 1-5% of all cases of diabetes result from single-gene mutations and are termed monogenic diabetes (Yang and Chan, 2016; pubmed:27035557).
Both animal model and human studies indicate that an autoimmune response to the β-cells of the pancreatic islets occurs in type 1 diabetes (Pociot, et al. 2010; pubmed:20587799).