The insulin-like effect of sodium vanadate on adipocyte glucose transport is mediated at a post-insulin-receptor level.
The insulin-like effect of sodium vanadate on adipocyte glucose transport is mediated at a post-insulin-receptor level.
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钒酸钠对脂肪细胞葡萄糖转运的胰岛素样作用是在胰岛素受体后水平介导的。
DOI：
10.1042/bj2380663
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发表时间：
1986
期刊：
影响因子：
--
通讯作者：
Green,A
中科院分区：
文献类型：
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作者：
Green,A
钒酸钠有几种类似胰岛素的作用。为了确定钒酸盐是否通过胰岛素受体起作用，我研究了钒酸盐对脂肪细胞中葡萄糖运输（2-脱氧葡萄糖摄取）的影响，这些脂肪细胞被处理以减少胰岛素受体的数量。胰蛋白酶（100微克/毫升）导致超过95%的125i -胰岛素结合丧失，并使葡萄糖转运对胰岛素和抗胰岛素受体抗体都产生抗性。然而，钒酸盐导致转运率增加了8倍[EC50 (concern)]。在对照和胰蛋白酶处理的细胞中，给予最大效应的50% (0.2 mM)，表明胰岛素受体不必是完整的，钒酸盐刺激葡萄糖运输。在Tris存在的情况下，胰岛素（100 ng/ml）处理脂肪细胞，胰岛素受体被耗尽（Tris阻断受体循环）。2小时的处理导致60%的受体丢失，胰岛素刺激葡萄糖转运的剂量-反应曲线向右偏移（对照组为0.3 ng/ml胰岛素，处理细胞为1.2 ng/ml）。对钒酸盐的反应同样不受影响。胰岛素治疗4小时导致胰岛素结合减少67%，除了胰岛素剂量-反应曲线向右移动外，基础转运率和最大转运率也下降（这不能用胰岛素受体数量减少来解释）。在对照组和处理过的细胞中，钒酸盐的EC50同样相等，但在最大有效浓度（1mm）的情况下，葡萄糖转运减少。我的结论是，钒酸盐对葡萄糖转运的影响与胰岛素受体无关。长期暴露于胰岛素诱导受体后缺陷（可能是细胞葡萄糖转运体总数的减少）降低了最大有效浓度的钒酸盐的效力。研究结果表明，钒酸盐通过远端胰岛素受体水平的影响刺激葡萄糖运输。
Sodium vanadate has several insulin-like effects. To determine whether vanadate acts via the insulin receptor, I investigated the effect of vanadate on glucose transport (2-deoxyglucose uptake) in adipocytes that had been treated to decrease the number of insulin receptors. Trypsin (100 micrograms/ml) caused greater than 95% loss of 125I-insulin binding and rendered glucose transport resistant to both insulin and an anti-insulin-receptor antibody. However, vanadate caused an 8-fold increase in the transport rate [EC50 (concn. giving 50% of maximum effect) 0.2 mM] in both control and trypsin-treated cells, demonstrating that the insulin receptor does not have to be intact for vanadate to stimulate glucose transport. Insulin receptors were depleted by treatment of adipocytes with insulin (100 ng/ml) in the presence of Tris (which blocks receptor recycling). A 2 h treatment caused 60% loss of receptors, and a shift to the right in the dose-response curve for insulin stimulation of glucose transport (EC50 0.3 ng of insulin/ml in controls, 1.2 ng/ml in treated cells). The response to vanadate was again unaffected. Treatment with insulin for 4 h caused a 67% decrease in insulin binding and, in addition to the rightward shift in the insulin dose-response curve, a decrease in basal and maximal transport rates (which cannot be explained by decreased insulin receptor number). The EC50 of vanadate was again equal in control and treated cells, but glucose transport in the presence of a maximally effective concentration of vanadate (1 mM) was decreased. I conclude that the effect of vanadate on glucose transport is independent of the insulin receptor. Induction of a post-receptor defect (which may be a decrease in the total number of cellular glucose transporters) by prolonged exposure to insulin decreases the potency of a maximally effective concentration of vanadate. The findings demonstrate that vanadate stimulates glucose transport by an effect at a level distal to the insulin receptor.