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Disruption of IRS-2 causes type 2 diabetes in mice.

Nature | Feb 26, 1998

http://www.ncbi.nlm.nih.gov/pubmed/9495343

Human type 2 diabetes is characterized by defects in both insulin action and insulin secretion. It has been difficult to identify a single molecular abnormality underlying these features. Insulin-receptor substrates (IRS proteins) may be involved in type 2 diabetes: they mediate pleiotropic signals initiated by receptors for insulin and other cytokines. Disruption of IRS-1 in mice retards growth, but diabetes does not develop because insulin secretion increases to compensate for the mild resistance to insulin. Here we show that disruption of IRS-2 impairs both peripheral insulin signalling and pancreatic beta-cell function. IRS-2-deficient mice show progressive deterioration of glucose homeostasis because of insulin resistance in the liver and skeletal muscle and a lack of beta-cell compensation for this insulin resistance. Our results indicate that dysfunction of IRS-2 may contribute to the pathophysiology of human type 2 diabetes.

Pubmed ID: 9495343 RIS Download

Mesh terms: Animals | Blood Glucose | Cloning, Molecular | Diabetes Mellitus, Type 2 | Female | Gene Targeting | Humans | Insulin | Insulin Receptor Substrate Proteins | Insulin Resistance | Intracellular Signaling Peptides and Proteins | Islets of Langerhans | Liver | Male | Mice | Mice, Inbred C57BL | Muscle, Skeletal | Phosphatidylinositol 3-Kinases | Phosphoproteins | Phosphorylation | Receptor, Insulin | Recombination, Genetic | Signal Transduction

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Associated grants

  • Agency: NIDDK NIH HHS, Id: R01 DK040936

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