Sinha M K, Raineri-Maldonado C, Buchanan C, Pories W J, Carter-Su C, Pilch P F, Caro J F
Department of Medicine, School of Medicine, East Carolina University, Greenville, North Carolina 27858.
Diabetes. 1991 Apr;40(4):472-7. doi: 10.2337/diab.40.4.472.
We investigated the mechanism of peripheral insulin resistance in the adipose tissue of obese and non-insulin-dependent diabetes mellitus (NIDDM) patients at the level of the glucose-transport effector system. Freshly isolated adipocytes from obese nondiabetic and obese NIDDM subjects had decreased insulin sensitivity and responsiveness for glucose-transport stimulation compared with control subjects, with more pronounced changes associated with obese NIDDM patients. The relative abundance of muscle/fat glucose-transporter isoform in the three groups of subjects was determined by Western-blot analysis of detergent-soluble adipose tissue extracts with monoclonal antibody 1F8. Obesity per se had no effect on adipose tissue muscle/fat glucose-transporter isoform (3150 +/- 660 vs. 4495 +/- 410 counts/min [cpm]/mg protein). Furthermore, decreased levels of muscle/fat isoform in adipose tissue of NIDDM patients were also reflected in isolated adipocytes. Our results demonstrate that insulin resistance in isolated adipocytes of NIDDM patients could at least partly be due to a significant depletion of adipose tissue muscle/fat glucose-transporter isoform.
我们在葡萄糖转运效应系统水平上研究了肥胖和非胰岛素依赖型糖尿病（NIDDM）患者脂肪组织中周围胰岛素抵抗的机制。与对照受试者相比，来自肥胖非糖尿病和肥胖NIDDM受试者的新鲜分离脂肪细胞对葡萄糖转运刺激的胰岛素敏感性和反应性降低，肥胖NIDDM患者的变化更为明显。通过用单克隆抗体1F8对去污剂可溶的脂肪组织提取物进行蛋白质免疫印迹分析，确定了三组受试者中肌肉/脂肪葡萄糖转运异构体的相对丰度。肥胖本身对脂肪组织肌肉/脂肪葡萄糖转运异构体没有影响（3150±660对4495±410计数/分钟[cpm]/毫克蛋白质）。此外，NIDDM患者脂肪组织中肌肉/脂肪异构体水平的降低在分离的脂肪细胞中也有体现。我们的结果表明，NIDDM患者分离脂肪细胞中的胰岛素抵抗至少部分可能是由于脂肪组织肌肉/脂肪葡萄糖转运异构体的显著减少。
