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lüll Lipid-induced insulin resistance: unravelling the mechanism Samuel VT; Petersen KF; Shulman GILancet 2010[Jun]; 375 (9733): 2267-77Insulin resistance has long been associated with obesity. More than 40 years ago, Randle and colleagues postulated that lipids impaired insulin-stimulated glucose use by muscles through inhibition of glycolysis at key points. However, work over the past two decades has shown that lipid-induced insulin resistance in skeletal muscle stems from defects in insulin-stimulated glucose transport activity. The steatotic liver is also resistant to insulin in terms of inhibition of hepatic glucose production and stimulation of glycogen synthesis. In muscle and liver, the intracellular accumulation of lipids-namely, diacylglycerol-triggers activation of novel protein kinases C with subsequent impairments in insulin signalling. This unifying hypothesis accounts for the mechanism of insulin resistance in obesity, type 2 diabetes, lipodystrophy, and ageing; and the insulin-sensitising effects of thiazolidinediones.|Animals[MESH]|Diabetes Mellitus, Type 2/metabolism[MESH]|Diglycerides[MESH]|Fatty Acids/metabolism[MESH]|Fatty Liver/metabolism[MESH]|Glucose/metabolism[MESH]|Humans[MESH]|Insulin Resistance/*physiology[MESH]|Insulin/metabolism[MESH]|Lipids/*physiology[MESH]|Muscle, Skeletal/metabolism[MESH]|Obesity/*metabolism[MESH]|Protein Kinase C/metabolism[MESH] |