Golay A, Defronzo R A, Thorin D, Jequier E, Felber J P
Department of Internal Medicine, CHUV, Lausanne, Switzerland.
Diabete Metab. 1988 Jul-Aug;14(4):443-51.
Insulin resistance is a characteristic finding in obesity and in non insulin dependent (Type II) diabetes mellitus. However, the interaction between diabetes and obesity has been poorly characterized and the metabolic disturbances contributing to the defect in insulin-mediated glucose uptake have not been defined. To examine these questions euglycemic and hyperinsulinemic clamp studies (40 mU/m2/min) were performed in 10 control non-obese subjects, 10 non diabetic obese subjects, 8 normal weight Type II diabetics, and 12 obese Type II diabetics. During the insulin clamp study total body glucose uptake in the obese non diabetics (157 +/- 18 mg/m2.min, p less than 0.01), the normal weight diabetics (159 +/- 21, p less than 0.01) and the obese diabetics (125 +/- 11, p less than 0.001) was significantly reduced compared to the non-obese non diabetic control group (249 +/- 22 mg/m2.min). The impairment in total body glucose uptake was the result mainly of a defect in non-oxidative glucose disposal. Indeed non-oxidative glucose disposal was blunted by 50% in the obese groups (p less than 0.01), somewhat less significantly in the non-obese diabetic group (p less than 0.05) but more when obesity and diabetes mellitus were combined (p less than 0.001). Total glucose oxidation was significantly diminished (p less than 0.01) in both diabetic groups but not in the obese non diabetic group when compared to lean control. A significant inverse correlation between the fasting free fatty acids levels and total glucose uptake (r = -0.453, p less than 0.001) and total glucose oxidation (r = -0.446, p less than 0.001) during the clamp was observed.(ABSTRACT TRUNCATED AT 250 WORDS)
胰岛素抵抗是肥胖症和非胰岛素依赖型(II型)糖尿病的典型特征。然而,糖尿病与肥胖症之间的相互作用尚未得到充分描述,导致胰岛素介导的葡萄糖摄取缺陷的代谢紊乱也尚未明确。为了研究这些问题,对10名非肥胖对照受试者、10名非糖尿病肥胖受试者、8名正常体重的II型糖尿病患者和12名肥胖的II型糖尿病患者进行了正常血糖和高胰岛素钳夹研究(40 mU/m2/分钟)。在胰岛素钳夹研究期间,与非肥胖非糖尿病对照组(249±22 mg/m2·分钟)相比,肥胖非糖尿病患者(157±18 mg/m2·分钟,p<0.01)、正常体重糖尿病患者(159±21,p<0.01)和肥胖糖尿病患者(125±11,p<0.001)的全身葡萄糖摄取显著降低。全身葡萄糖摄取受损主要是由于非氧化葡萄糖处理缺陷。事实上,肥胖组的非氧化葡萄糖处理减少了50%(p<0.01),非肥胖糖尿病组减少幅度稍小(p<0.05),但肥胖与糖尿病合并时减少幅度更大(p<0.001)。与瘦对照组相比,两个糖尿病组的总葡萄糖氧化均显著降低(p<0.01),而肥胖非糖尿病组则未降低。在钳夹期间,观察到空腹游离脂肪酸水平与总葡萄糖摄取(r = -0.453,p<0.001)和总葡萄糖氧化(r = -0.446,p<0.001)之间存在显著负相关。(摘要截断于250字)