Magnesium deficiency and glucose metabolism in rat adipocytes
Magnesium deficiency and glucose metabolism in rat adipocytes
复制标题
DOI：
10.1016/s0026-0495(96)90156-0
复制
发表时间：
1996-07-01
影响因子：
9.8
通讯作者：
Nadler, JL
中科院分区：
文献类型：
--
作者：
Kandeel, FR;Balon, E;Nadler, JL
我们研究了降低环境和细胞内游离Mg离子（[Mg](i)）浓度对雄性Sprague-Dawley大鼠附睾脂肪细胞中胰岛素作用的影响，包括：(1)不可代谢的2-脱氧葡萄糖的细胞运输，(2)[U-C-14]葡萄糖氧化为CO2，以及(3)D-[H-3]葡萄糖掺入甘油三酯。在生理（1.24 mmol）和低（0.16 mmol） Mg环境下培养长达24小时的脂肪细胞之间，基础或胰岛素刺激的a-脱氧葡萄糖运输没有显著差异。相比之下，在低Mg环境下培养的脂肪细胞中，胰岛素刺激的[U-C-14]葡萄糖氧化成CO2显著减少（P < 0.05 ~ 0.01），而不是基础[U-C-14]葡萄糖氧化成CO2显著减少。同样，在低Mg或生理Mg培养基中培养长达24小时的细胞之间，基础葡萄糖并入甘油三酯的情况也没有差异。然而，长期（24小时）而非短期（2小时）暴露于低Mg的细胞与胰岛素刺激的D-[3H]葡萄糖并入甘油三酯的显著减少30%相关。低Mg条件下培养的脂肪细胞在高Mg条件下（1.24或5 mmol）培养30分钟后，胰岛素刺激的D-[H-3]葡萄糖融入甘油三酯恢复正常。脂肪细胞在低Mg （0.16 mmol）条件下孵育24小时，其[Mg](i) （264 +/- 89 v 437 +/- 125 mu mol/ cells[平均+/- SEM]）比在生理Mg （1.24 mmol, P < 0.01）条件下孵育的细胞显著降低。这些数据支持细胞内镁缺乏在胰岛素抵抗发展中的作用，并表明这种影响发生在葡萄糖进入细胞的远端。镁缺乏对胰岛素作用的影响似乎是可逆的。版权所有(C) 1996年由W.B.桑德斯公司
We examined the effect of reducing ambient and intracellular free Mg ion ([Mg](i)) concentrations on insulin action in epididymal adipocytes from male Sprague-Dawley rats in terms of (1) cellular transport of nonmetabolizable 2-deoxyglucose, (2) [U-C-14]glucose oxidation to CO2, and (3) D-[H-3]glucose incorporation into triglycerides. There were no significant differences in basal or insulin-stimulated transport of a-deoxyglucose between adipocytes cultured in physiologic (1.24 mmol) or low (0.16 mmol) Mg for up to 24 hours. In contrast, insulin-stimulated but not basal [U-C-14]glucose oxidation to CO2 was significantly reduced in adipocytes cultured in low versus physiologic Mg (P < .05 to .01). Similarly, there were no differences in basal glucose incorporation into triglycerides between cells cultured in low or physiologic Mg media for up to 24 hours. However, long-term (24-hour) but not short-term (2-hour) exposure of cells to low Mg was associated with a significant 30% reduction in insulin-stimulated D-[3H]glucose incorporation into triglycerides. When adipocytes incubated in low Mg were reincubated in high Mg (1.24 or 5 mmol) for 30 minutes, normal insulin-stimulated D-[H-3]glucose incorporation into triglycerides was restored. Incubation of adipocytes in low Mg (0.16 mmol) for 24 hours resulted in a significant decrease in [Mg](i) (264 +/- 89 v 437 +/- 125 mu mol/cell [mean +/- SEM]) as compared with cells incubated in physiologic Mg (1.24 mmol; P < .01). These data support a role for intracellular Mg deficiency in the development of insulin resistance and suggest that the effect occurs at a site(s) distal to glucose entry into the cell. The effect of Mg deficiency on insulin action appears to be reversible. Copyright (C) 1996 by W.B. Saunders Company