Heart Emma, Sung Chin K
Department of Physiology and Biophysics, University of Southern California, Los Angeles, California 90089-9142, USA.
Biochem Biophys Res Commun. 2002 Mar 29;292(2):308-11. doi: 10.1006/bbrc.2002.6663.
In 3T3-L1 adipocytes, we previously reported that glucosamine impairs insulin stimulation of glucose transport, which is accompanied by impaired insulin stimulation of serine/threonine kinase Akt. To examine the role of Akt in glucosamine-induced insulin resistance, we investigated time course for insulin stimulation of Akt activity and glucose transport during recovery from glucosamine-induced insulin resistance. After induction of insulin resistance by glucosamine, we washed cells to remove glucosamine and incubated them for various times. After one hour, insulin stimulated-glucose transport was significantly increased and continued to increase up to 6-24 h. Insulin stimulation of Akt, however, did not increase after 1-3 h and began to slightly increase after 6 h. Next, we investigated effects of osmotic shock and vanadate on glucose transport in glucosamine-treated cells and found that glucosamine completely inhibited their actions in these cells. These data suggest that an Akt-independent mechanism is operative in glucosamine-induced insulin resistance and glucosamine impairs glucose transport stimulated by various stimuli involving and not involving Akt activation.
在3T3-L1脂肪细胞中，我们之前报道过氨基葡萄糖会损害胰岛素对葡萄糖转运的刺激作用，同时伴随着胰岛素对丝氨酸/苏氨酸激酶Akt刺激作用的受损。为了研究Akt在氨基葡萄糖诱导的胰岛素抵抗中的作用，我们调查了从氨基葡萄糖诱导的胰岛素抵抗恢复过程中胰岛素刺激Akt活性和葡萄糖转运的时间进程。在用氨基葡萄糖诱导胰岛素抵抗后，我们洗涤细胞以去除氨基葡萄糖，并将它们孵育不同时间。一小时后，胰岛素刺激的葡萄糖转运显著增加，并持续增加至6 - 24小时。然而，胰岛素对Akt的刺激在1 - 3小时后没有增加，在6小时后才开始略有增加。接下来，我们研究了渗透休克和钒酸盐对氨基葡萄糖处理细胞中葡萄糖转运的影响，发现氨基葡萄糖完全抑制了它们在这些细胞中的作用。这些数据表明，一种不依赖Akt的机制在氨基葡萄糖诱导的胰岛素抵抗中起作用，并且氨基葡萄糖会损害由各种涉及和不涉及Akt激活的刺激所引发的葡萄糖转运。
