Huth Claire, Pigeon Étienne, Riou Marie-Ève, St-Onge Josée, Arguin Hélène, Couillard Erick, Dubois Marie-Julie, Marette André, Tremblay Angelo, Weisnagel S John, Lacaille Michel, Mauriège Pascale, Joanisse Denis R
Department of Kinesiology, Université Laval, Québec, Québec, Canada.
Centre de Recherche de l'Institut Universitaire de Cardiologie et de Pneumologie de Québec (CRIUCPQ), Université Laval, Québec, Québec, Canada.
J Physiol Biochem. 2016 Sep;72(3):435-44. doi: 10.1007/s13105-016-0488-2. Epub 2016 May 2.
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.
脂肪组织病变,即病态脂肪,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。脂肪组织病变在预测胰岛素抵抗方面的相对作用尚不清楚。我们在53名年龄在34 - 53岁的男性中,研究了以低血浆脂联素/瘦素比值评估的脂肪组织病变与人体测量学、身体成分(水下称重)、胰岛素敏感性(高胰岛素正常血糖钳夹)、炎症和体能水平(功率自行车最大摄氧量,毫升/千克去脂体重/分钟)之间的关系。这53名男性分为四组:无肥胖的久坐对照组(体重指数[BMI]<25千克/米²)、肥胖的久坐组(BMI>30千克/米²)、肥胖且糖耐量异常的久坐组以及无肥胖的耐力训练活跃组。脂联素/瘦素比值在训练有素的男性中最高(4.75±0.82),在肥胖且糖耐量异常的受试者中最低(0.27±0.06;方差分析p<0.0001),表明肥胖者的脂肪组织病变增加。该比值与肥胖程度呈负相关(例如,腰围,r = -0.59,p<0.01),与最大摄氧量呈正相关(r = 0.67,p<0.01)以及与胰岛素敏感性(M/I,r = 0.73,p<0.01)呈正相关。多元回归分析显示体能是胰岛素敏感性最强的独立预测因素(偏R² = 0.61)。虽然脂肪组织病变也是一个独立且显著的因素(偏R² = 0.10),但腰围对模型的贡献很小(偏R² = 0.024)。当将训练有素的受试者排除在模型之外时,这三个变量仍然是显著的独立预测因素。血浆脂质未保留在模型中。我们得出结论,低体能、脂肪组织病变以及肥胖(尤其是腹型肥胖)是无糖尿病男性胰岛素抵抗的独立影响因素。