IRS2 takes center stage in the development of type 2 diabetes.
The etiology of type 2 diabetes is characterized by obesity, insulin and leptin resistance, and compensatory beta cell hyperplasia followed by islet degeneration, resulting in the eventual dysregulation of glucose and lipid homeostasis. The recent identification of insulin receptor substrate 2 (IRS2) as a central player in the pathophysiology of many of these processes suggests a potentially unifying molecular link underlying the initiation and progression of type 2 diabetes.
Department of Medicine, Committee on Molecular Metabolism and Nutrition, University of Chicago, Chicago, Illinois 60637, USA. mbrady@medicine.bsd.uchicago.edu
Matthew J
MJ
Brady
D000818:Animals; D003924:Diabetes Mellitus, Type 2 / Q000209:etiology / Q000378:metabolism* / Q000503:physiopathology; D006801:Humans; D007328:Insulin / Q000378:metabolism; D055504:Insulin Receptor Substrate Proteins; D047908:Intracellular Signaling Peptides and Proteins; D051379:Mice; D010641:Phenotype; D010750:Phosphoproteins / Q000378:metabolism*; D011972:Receptor, Insulin / Q000378:metabolism; D015398:Signal Transduction / Q000502:physiology
C526297:IRS2 protein, human; D007328:Insulin; D055504:Insulin Receptor Substrate Proteins; D047908:Intracellular Signaling Peptides and Proteins; C526298:Irs2 protein, mouse; D010750:Phosphoproteins; D011972:Receptor, Insulin