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Insulin resistance in morbid obesity: reversal with intramyocellular fat depletion

机译:病态肥胖中的胰岛素抵抗:逆转肌内脂肪减少

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Obesity is frequent cause of insulin resistance and poses a major risk for diabetes. Abnormal fat deposition within skeletal muscle has been identified as a mecha- nism of obesity-associated insulin resistance. We tested the hypothesis that dietary lipid deprivation may selec- tively deplete intramyocellular lipids, thereby reversing insulin resistance. Whole-body insulin sensitivity(by the insulin clamp technique), intramyocellular lipids (by quantitative histochemistry on quadriceps muscle biopsies), muscle insulin action(as the expression of Glut4 glucose transporters), and postprandial lipemia Were measured in 20 morbidly obese patients(BMI = 49±8[mean ± SD]kg.mQ-2)and 7 nonobese control subjects.
机译:肥胖是胰岛素抵抗的常见原因,对糖尿病构成重大风险。骨骼肌中异常脂肪沉积已被认为是与肥胖相关的胰岛素抵抗的机制。我们检验了以下假设:饮食中的脂质剥夺可选择性地消耗肌细胞内脂质,从而逆转胰岛素抵抗。在20例病态肥胖患者中测量了全身胰岛素敏感性(通过胰岛素钳技术),肌内脂质(通过对股四头肌肌肉活组织检查的定量组织化学),肌肉胰岛素作用(作为Glut4葡萄​​糖转运蛋白的表达)和餐后血脂。 = 49±8 [mean±SD] kg.mQ-2)和7位非肥胖对照受试者。

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