Segal S, Lloyd S, Sherman N, Sussman K, Draznin B
Department of Medicine, Veterans Administration Medical Center, Denver, Colo.
Horm Res. 1990;34(1):39-44. doi: 10.1159/000181793.
We evaluated the possible relationship between [Ca2+]i and glucose uptake in the postabsorptive state and postprandially in adipocytes obtained from normal and obese subjects, as well as from patients with non-insulin-dependent diabetes mellitus (NIDDM). Adipocytes isolated from overnight-fasted obese and NIDDM patients revealed high levels of [Ca2+]i (p less than 0.05 vs. control) in association with a decreased insulin-stimulated glucose uptake (p less than 0.05 vs. controls). In obese and NIDDM patients treated with oral hypoglycemic agents, the overnight fasting levels of [Ca2+]i were increased postprandially (p less than 0.05), concomitantly with a further decrease in insulin-stimulated 2-deoxyglucose uptake. Although the precise nature of the relationship between [Ca2+]i in specific insulin target tissues and diminished insulin action remains unknown, it is clear that high levels of [Ca2+]i may contribute to the development of insulin resistance.
我们评估了正常和肥胖受试者以及非胰岛素依赖型糖尿病(NIDDM)患者的脂肪细胞在吸收后状态和餐后状态下细胞内钙离子浓度([Ca2+]i)与葡萄糖摄取之间的可能关系。从禁食过夜的肥胖患者和NIDDM患者分离出的脂肪细胞显示,[Ca2+]i水平较高(与对照组相比,p<0.05),同时胰岛素刺激的葡萄糖摄取减少(与对照组相比,p<0.05)。在用口服降糖药治疗的肥胖和NIDDM患者中,餐后[Ca2+]i的过夜空腹水平升高(p<0.05),同时胰岛素刺激的2-脱氧葡萄糖摄取进一步减少。虽然特定胰岛素靶组织中[Ca2+]i与胰岛素作用减弱之间关系的确切性质尚不清楚,但很明显,高水平的[Ca2+]i可能导致胰岛素抵抗的发生。