Proposed mechanism for increased insulin-mediated glucose transport in adipose cells from young, obese Zucker rats. Large intracellular pool of glucose transporters.
Proposed mechanism for increased insulin-mediated glucose transport in adipose cells from young, obese Zucker rats. Large intracellular pool of glucose transporters.
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提出了增加年轻肥胖 Zucker 大鼠脂肪细胞中胰岛素介导的葡萄糖转运的机制。
DOI：
10.1016/s0021-9258(18)89537-0
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发表时间：
1985
期刊：
影响因子：
--
通讯作者：
Wardzalag
中科院分区：
文献类型：
--
作者：
M. Guerre;M. Lavau;S. Horne;Lawrence;Wardzalag
研究了30日龄肥胖Zucker大鼠脂肪细胞中胰岛素介导的高反应性葡萄糖转运机制。葡萄糖转运通过测量3- o -甲基葡萄糖转运来检测，葡萄糖转运体浓度通过测量特异性d -葡萄糖抑制细胞松弛素B结合来估计。胰岛素使肥胖大鼠细胞的葡萄糖转运活性增加了约17 fmol/细胞/分钟，而瘦鼠的细胞转运活性为3 fmol/细胞/分钟。胰岛素使两组的膜蛋白中葡萄糖转运体浓度增加约15 pmol/mg。胰岛素介导的低密度微粒体部分转运蛋白浓度下降，肥胖大鼠为30 pmol/mg膜蛋白，而瘦对照组为15 pmol/mg膜蛋白。利用膜蛋白和酶回收率计算各组葡萄糖转运蛋白的估计数量。胰岛素使肥胖大鼠的质膜转运蛋白数量增加了3 × 10(6)个位点/细胞，而瘦肉对照组的转运蛋白数量仅增加了0.6 × 10(6)个位点/细胞。此外，胰岛素使肥胖大鼠的细胞膜内转运蛋白/细胞数量减少约4 × 10(6)个位点/细胞，瘦大鼠的转运蛋白/细胞数量减少约0.9 × 10(6)个位点/细胞。肥胖动物的转运蛋白总数约为7 × 10(6)个位点/细胞，而瘦弱对照组的转运蛋白总数约为1.6 × 10(6)个位点/细胞。在基础状态下，超过80%的这些转运蛋白位于瘦鼠和肥胖大鼠的细胞内池。因此，在30日龄肥胖Zucker大鼠的脂肪细胞中观察到的胰岛素介导的葡萄糖转运的高反应性可能是细胞内葡萄糖转运体数量显著增加的结果。
The mechanism for hyperresponsive insulin-mediated glucose transport in adipose cells from 30-day-old obese Zucker rats was examined. Glucose transport was assayed by measuring 3-O-methylglucose transport, and the concentration of glucose transporters was estimated by measuring specific D-glucose-inhibitable cytochalasin B binding. Insulin increased glucose transport activity by approximately 17 fmol/cell/min in cells from obese rats compared to 3 fmol/cell/min in lean littermates. Insulin increased the concentration of glucose transporters in the plasma membrane fraction by about 15 pmol/mg of membrane protein in both groups. The insulin-mediated decrease in the concentration of transporters in the low-density microsomal fraction was 30 pmol/mg of membrane protein for the obese rats compared to 15 pmol/mg of membrane protein for the lean controls. An estimated number of glucose transporters was calculated using membrane protein and enzyme recoveries for each group. Insulin increased the number of transporters in the plasma membrane by 3 X 10(6) sites/cell for the obese rats and only 0.6 X 10(6) sites/cell for the lean controls. In addition, insulin decreased the number of transporters/cell in the intracellular membrane pool by approximately 4 X 10(6) sites/cell for the obese rats and 0.9 X 10(6) sites/cells for the lean rats. The total number of transporters/cell was about 7 X 10(6) sites/cell for the obese animals and 1.6 X 10(6) sites/cell for the lean controls. In the basal state, more than 80% of these transporters were located in the intracellular pool for both the lean and obese rats. Thus, the marked hyperresponsive insulin-mediated glucose transport observed in adipose cells from 30-day-old obese Zucker rats may be the consequence of a marked increase in the number of glucose transporters in the intracellular pool.