Azevedo J L, Carey J O, Pories W J, Morris P G, Dohm G L
Department of Biochemistry, School of Medicine, East Carolina University, Greenville, NC 27858, USA.
Diabetes. 1995 Jun;44(6):695-8. doi: 10.2337/diab.44.6.695.
Insulin and muscle contraction stimulate glucose transport into muscle cells by separate signaling pathways, and hypoxia has been shown to operate via the contraction signaling pathway. To elucidate the mechanism of insulin resistance in human skeletal muscle, strips of rectus abdominis muscle from lean (body mass index [BMI] < 25), obese (BMI > 30), and obese non-insulin-dependent diabetes mellitus (NIDDM) (BMI > 30) patients were incubated under basal and insulin-, hypoxia-, and hypoxia + insulin-stimulated conditions. Insulin significantly stimulated 2-deoxyglucose transport approximately twofold in muscle from lean (P < 0.05) patients, but not in muscle from obese or obese NIDDM patients. Furthermore, maximally insulin-stimulated transport rates in muscle from obese and diabetic patients were significantly lower than rates in muscle from lean patients (P < 0.05). Hypoxia significantly stimulated glucose transport in muscle from lean and obese patients. There were no significant differences in hypoxia-stimulated glucose transport rates among lean, obese, and obese NIDDM groups. Hypoxia + insulin significantly stimulated glucose transport in lean, obese, and diabetic muscle. The results of the present study suggest that the glucose transport effector system is intact in diabetic human muscle when stimulated by hypoxia.
胰岛素和肌肉收缩通过不同的信号通路刺激葡萄糖转运进入肌肉细胞，并且缺氧已被证明是通过收缩信号通路起作用的。为了阐明人类骨骼肌中胰岛素抵抗的机制，将来自瘦（体重指数[BMI]<25）、肥胖（BMI>30）和肥胖非胰岛素依赖型糖尿病（NIDDM）（BMI>30）患者的腹直肌条在基础、胰岛素、缺氧和缺氧+胰岛素刺激条件下进行孵育。胰岛素显著刺激瘦患者（P<0.05）肌肉中的2-脱氧葡萄糖转运约两倍，但在肥胖或肥胖NIDDM患者的肌肉中则不然。此外，肥胖和糖尿病患者肌肉中最大胰岛素刺激的转运速率显著低于瘦患者肌肉中的速率（P<0.05）。缺氧显著刺激瘦和肥胖患者肌肉中的葡萄糖转运。瘦、肥胖和肥胖NIDDM组之间缺氧刺激的葡萄糖转运速率没有显著差异。缺氧+胰岛素显著刺激瘦、肥胖和糖尿病肌肉中的葡萄糖转运。本研究结果表明，当受到缺氧刺激时，糖尿病患者肌肉中的葡萄糖转运转效应器系统是完整的。
