Fitness, adiposopathy, and adiposity are independent predictors of insulin sensitivity in middle-aged men without diabetes
Fitness, adiposopathy, and adiposity are independent predictors of insulin sensitivity in middle-aged men without diabetes
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DOI：
10.1007/s13105-016-0488-2
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发表时间：
2016-09-01
影响因子：
3.4
通讯作者：
Joanisse, Denis R.
中科院分区：
文献类型：
--
作者：
Huth, Claire;Pigeon, Etienne;Joanisse, Denis R.
脂肪病或病态脂肪是指脂肪组织功能障碍，可导致多种并发症，如血脂异常、胰岛素抵抗和高血糖症。脂肪病在预测胰岛素抵抗中的相对作用尚不清楚。我们研究了脂肪病，如血浆脂联素/瘦素比值低，与人体测量，身体成分，（静水压重量）、胰岛素敏感性（高胰岛素-正常血糖钳夹）、炎症和健身水平53名男性的最大氧耗量（单位：mL/kgFFM/min）（34-53岁），分为四组：不肥胖的久坐对照组（身体质量指数[BMI] < 25 kg/m2）、久坐伴肥胖（BMI > 30 kg/m2）、久坐伴肥胖和葡萄糖耐受不良以及耐力训练活跃但不肥胖。脂联素/瘦素比率在受过训练的男性中最高（4.75 +/- 0.82），在患有肥胖症的葡萄糖不耐受受试者中最低（0.27 +/- 0.06; ANOVA p < 0.0001），表明肥胖症患者中脂肪病增加。该比率与肥胖呈负相关（例如，腰围与最大摄氧量（r = 0.67，p <0.01）和胰岛素敏感性（M/I，r = 0.73，p < 0.01）呈正相关。多元回归分析显示，健身是胰岛素敏感性最强的独立预测因子（部分R（2）= 0.61）。虽然脂肪病也是一个独立的和重要的贡献者（部分R（2）= 0.10），腰围增加的权力模型（部分R（2）= 0.024）。所有这三个变量仍然是显着的独立预测因素时，训练的对象被排除在模型之外。模型中未保留血浆脂质。我们的结论是，低健身，肥胖症，以及肥胖（特别是腹部肥胖）是独立的贡献者胰岛素抵抗的男性无糖尿病。
Adiposopathy, or sick fat, refers to adipose tissue dysfunction that can lead to several complications such as dyslipidemia, insulin resistance, and hyperglycemia. The relative contribution of adiposopathy in predicting insulin resistance remains unclear. We investigated the relationship between adiposopathy, as assessed as a low plasma adiponectin/leptin ratio, with anthropometry, body composition (hydrostatic weighing), insulin sensitivity (hyperinsulinemic-euglycemic clamp), inflammation, and fitness level (ergocycle VO2max, mL/kgFFM/min) in 53 men (aged 34-53 years) from four groups: sedentary controls without obesity (body mass index [BMI] < 25 kg/m(2)), sedentary with obesity (BMI > 30 kg/m(2)), sedentary with obesity and glucose intolerance, and endurance trained active without obesity. The adiponectin/leptin ratio was the highest in trained men (4.75 +/- 0.82) and the lowest in glucose intolerant subjects with obesity (0.27 +/- 0.06; ANOVA p < 0.0001) indicating increased adiposopathy in those with obesity. The ratio was negatively associated with adiposity (e.g., waist circumference, r = -0.59, p < 0.01) and positively associated with VO2max (r = 0.67, p < 0.01) and insulin sensitivity (M/I, r = 0.73, p < 0.01). Multiple regression analysis revealed fitness as the strongest independent predictor of insulin sensitivity (partial R (2) = 0.61). While adiposopathy was also an independent and significant contributor (partial R (2) = 0.10), waist circumference added little power to the model (partial R (2) = 0.024). All three variables remained significant independent predictors when trained subjects were excluded from the model. Plasma lipids were not retained in the model. We conclude that low fitness, adiposopathy, as well as adiposity (and in particular abdominal obesity) are independent contributors to insulin resistance in men without diabetes.