Metabolic fluxes in skeletal muscle in relation to obesity and insulin resistance
Metabolic fluxes in skeletal muscle in relation to obesity and insulin resistance
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DOI：
10.1016/j.beem.2005.04.001
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发表时间：
2005-09-01
影响因子：
7.4
通讯作者：
Blaak, EE
中科院分区：
文献类型：
--
作者：
Blaak, EE
本文提出了骨骼肌脂质利用效率低下可能与肥胖和胰岛素抵抗的发展有关的假设。在实践中，有证据表明肥胖状态下肌肉脂肪酸利用受损，研究表明肌肉脂肪酸氧化能力的差异可能在肥胖的发病机制中发挥作用。肥胖和胰岛素抵抗之间的联系已经被认识了很多年。越来越多的证据表明，肌肉脂肪氧化能力紊乱会导致脂质中间体二酰基甘油和脂肪酸酰基辅酶a （CoA）的积累，这可能会干扰胰岛素信号传导并导致胰岛素介导的葡萄糖摄取抑制。脂肪酸处理紊乱的潜在机制可能与脂肪组织脂肪分解受损、肌肉脂肪酸摄取异常和脂肪氧化能力降低有关。这些异常在肥胖和2型糖尿病患者中都有报道。肥胖本身在这些紊乱中的作用是一个需要解决的重要问题。
The present article addresses the hypothesis that inefficient skeletal muscle lipid utilization may relate to the development of obesity and insulin resistance. In practice, there is evidence of impaired muscle fatty acid utilization in the obese state, and studies indicate that differences in muscle fatty acid oxidative capacity might play a role in the pathogenesis of obesity. The link between obesity and insulin resistance has been recognized for many years. There is accumulating evidence that a disturbed muscle fat oxidative capacity results in the accumulation of the lipid intermediates diacylglycerol and Fatty acid acyl coenzyme A (CoA), which may interfere with insulin signaling and result in an inhibition of insulin-mediated glucose uptake. Underlying mechanisms for disturbed fatty acid handling may relate to impaired adipose tissue lipolysis, abnormal muscle fatty acid uptake and a reduced ability to oxidize fat. Many of these abnormalities have been reported both in the obese and the type 2 diabetic state. The role of obesity per se in these disturbances is an important question that needs to be addressed.