In Drosophila, as in other invertebrates, multiple insulin-like peptides (ILPs) are encoded by a family of related genes (see gene group report FBgg0000048).
A small deficiency that removes Ilp1, Ilp2, Ilp3, Ilp4, and Ilp5 has been generated and assessed. Animals homozygous for the deficiency are small and severely growth-delayed; they exhibit reduced metabolic activity, decreased triglyceride levels and prematurely activate autophagy; circulating sugar levels are elevated during eating and fasting. Although these phenotypes recapitulate many of the phenotypes of type 1 diabetes, they are less severe than phenotypes observed for untreated insulin deficiency in mammals (which is fatal). A model using RNAi targeted to Ilp2 has also been developed.
Animals homozygous for separate deficiencies that remove Ilp6 or Ilp7 exhibit no major metabolic defects.
Ilp1, Ilp2, Ilp3, and Ilp5 are expressed in clusters of median neurosecretory cells called insulin producing cells (IPCs) of the brain. See the human disease model report 'diabetes mellitus, insulin-dependent, IPC-ablation models' (FBhh0000478).
[updated Jan. 2023 by FlyBase; FBrf0222196]
Type 1 diabetes occurs when the body's immune system attacks the insulin-producing beta cells in the pancreas and destroys them, resulting in the production of little or no insulin. (https://www.ncbi.nlm.nih.gov/pubmedhealth/PMHT0024702/)
Low-scoring ortholog of human INS (proinsulin).
Low-scoring ortholog of human INS (proinsulin).
Low-scoring ortholog of human INS (proinsulin).
