Desensitization of beta-adrenergic receptors in adipocytes causes increased insulin sensitivity of glucose transport.
Desensitization of beta-adrenergic receptors in adipocytes causes increased insulin sensitivity of glucose transport.
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脂肪细胞中β-肾上腺素能受体的脱敏导致葡萄糖转运的胰岛素敏感性增加。
DOI：
10.1152/ajpendo.1996.271.2.e271
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发表时间：
1996
期刊：
影响因子：
--
通讯作者：
Dobias,SB
中科院分区：
文献类型：
--
作者：
Green,A;Carroll,RM;Dobias,SB
为探讨脂肪细胞β-肾上腺素能受体脱敏对胰岛素敏感性的影响，用渗透压微泵连续给大鼠注射异丙肾上腺素(50或100微克·kg~(-1)·h~(-1))3d。分离附睾腺脂肪细胞。根据脂肪分解反应(甘油释放)，来自处理动物的细胞对异丙肾上腺素不敏感。经处理的大鼠脂肪细胞质膜上[125I]碘氰基吲哚结合量减少约80%，表明β-肾上腺素能受体下调。Gnα和Giα的细胞浓度没有改变。通过测量胰岛素对葡萄糖转运(2-脱氧-[~3H]葡萄糖摄取)的影响来确定胰岛素敏感性。注入异丙肾上腺素的大鼠细胞对胰岛素的敏感性明显高于对照组。高剂量异丙肾上腺素处理的大鼠细胞的最大葡萄糖转运速率增加了约50%，两组胰岛素的半最大有效浓度降低了约40%，证明了这一点。注射异丙肾上腺素不改变~(125)I标记的胰岛素与脂肪细胞的结合，表明β-肾上腺素能受体的脱敏导致胰岛素受体与葡萄糖转运刺激之间更紧密的偶联。
To determine the effect of desensitization of adipocyte beta-adrenergic receptors on insulin sensitivity, rats were continuously infused with isoproterenol (50 or 100 micrograms.kg-1.h-1) for 3 days by osmotic minipumps. Epididymal adipocytes were isolated. The cells from treated animals were desensitized to isoproterenol, as determined by response of lipolysis (glycerol release). Binding of [125I]iodocyanopindolol was decreased by approximately 80% in adipocyte plasma membranes isolated from treated rats, indicating that beta-adrenergic receptors were downregulated. Cellular concentrations of Gn alpha and Gi alpha were not altered. Insulin sensitivity was determined by measuring the effect of insulin on glucose transport (2-deoxy-[3H]glucose uptake). Cells from the isoproterenol-infused rats were markedly more sensitive to insulin than those from control rats. This was evidenced by an approximately 50% increase in maximal glucose transport rate in cells from the high-dose isoproterenol-treated rats and by an approximately 40% decrease in the half-maximal effective concentration of insulin in both groups. 125I-labeled insulin binding to adipocytes was not altered by the isoproterenol infusions, indicating that desensitization of beta-adrenergic receptors results in tighter coupling between insulin receptors and stimulation of glucose transport.