期刊
LANCET
卷 375, 期 9733, 页码 2267-2277出版社
ELSEVIER SCIENCE INC
DOI: 10.1016/S0140-6736(10)60408-4
关键词
-
资金
- Veterans Administration
- US Public Health Service [R01 AG-23686, R01 DK-49230, P01 DK-068229, R01 DK-40936, P30 DK-45735, U24 DK-59635, UL1 RR-024139, K23 RR17404, UL1 RR024139]
- American Diabetes Association
- NATIONAL CENTER FOR RESEARCH RESOURCES [K23RR017404, UL1RR024139] Funding Source: NIH RePORTER
- NATIONAL INSTITUTE OF DIABETES AND DIGESTIVE AND KIDNEY DISEASES [P01DK068229, P30DK045735, R01DK049230, R01DK040936, U24DK059635] Funding Source: NIH RePORTER
- NATIONAL INSTITUTE ON AGING [R56AG023686, R01AG023686] Funding Source: NIH RePORTER
Insulin 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.
作者
我是这篇论文的作者
点击您的名字以认领此论文并将其添加到您的个人资料中。
推荐
暂无数据