Pendergrass M, Fazioni E, Collins D, DeFronzo R A
Diabetes Division, Department of Medicine, University of Texas Health Science Center, San Antonio, Texas 78284, USA.
Am J Physiol. 1998 Aug;275(2):E345-50. doi: 10.1152/ajpendo.1998.275.2.E345.
Decreased insulin-mediated muscle glucose uptake is a characteristic feature of non-insulin-dependent diabetes mellitus and other insulin-resistant states. It has been suggested that an impairment in the ability of insulin to augment limb blood flow, resulting in diminished glucose delivery to muscle, may contribute to this abnormality. In this study, we used human insulin-like growth factor (IGF) I in conjunction with the forearm balance technique to determine whether forearm glucose uptake could be stimulated by increasing blood flow without directly stimulating the intrinsic ability of the muscle to extract glucose. IGF-I was infused intra-arterially in healthy controls at a rate of either 0.4 microg . kg-1 . min-1 (high IGF) or 0.04 microg . kg-1 . min-1 (low IGF) for 140 min. With high IGF, forearm blood flow increased approximately twofold (34 +/- 3 vs. 64 +/- 8 ml . min-1 . l forearm volume-1, P < 0.01), and arteriovenous glucose concentration difference (a-v difference) increased modestly (0.19 +/- 0.05 vs. 0.31 +/- 0.08 mM, P = 0.32), resulting in an increased forearm glucose uptake (6.4 +/- 1.7 vs. 21.7 +/- 7.4 micromol . min-1 . l forearm volume-1, P = 0.09 vs. basal). With low IGF, forearm blood flow increased by 59% (29 +/- 4 vs. 46 +/- 9 ml . min-1 . l forearm volume-1, P < 0.05) and was associated with a proportional decrease in the a-v difference (0. 29 +/- 0.04 vs. 0.18 +/- 0.05 mM, P < 0.05). Forearm glucose uptake therefore was not significantly different from basal values (7.6 +/- 0.6 vs. 6.9 +/- 1.8 micromol . min-1 . kg-1). These data demonstrate that increasing blood flow without increasing the intrinsic ability of the muscle to extract glucose does not increase forearm muscle glucose uptake.
胰岛素介导的肌肉葡萄糖摄取减少是非胰岛素依赖型糖尿病和其他胰岛素抵抗状态的一个特征。有人提出,胰岛素增加肢体血流的能力受损,导致输送到肌肉的葡萄糖减少,可能是导致这种异常的原因。在本研究中,我们将人胰岛素样生长因子(IGF)I与前臂平衡技术结合使用,以确定增加血流而不直接刺激肌肉摄取葡萄糖的内在能力是否能刺激前臂葡萄糖摄取。在健康对照者中,以0.4微克·千克-1·分钟-1(高IGF)或0.04微克·千克-1·分钟-1(低IGF)的速率动脉内输注IGF-I 140分钟。高IGF组前臂血流增加约两倍(34±3对64±8毫升·分钟-1·升前臂容积-1,P<0.01),动静脉葡萄糖浓度差(a-v差)适度增加(0.19±0.05对0.31±0.08毫摩尔,P=0.32),导致前臂葡萄糖摄取增加(6.4±1.7对21.7±7.4微摩尔·分钟-1·升前臂容积-1,与基础值相比P=0.09)。低IGF组前臂血流增加59%(29±4对46±9毫升·分钟-1·升前臂容积-1,P<0.05),并与a-v差成比例下降相关(0.29±0.04对0.18±0.05毫摩尔,P<0.05)。因此,前臂葡萄糖摄取与基础值无显著差异(7.6±0.6对6.9±1.8微摩尔·分钟-1·千克-1)。这些数据表明,在不增加肌肉摄取葡萄糖内在能力的情况下增加血流不会增加前臂肌肉葡萄糖摄取。