Effects of long-term caloric restriction on early steps of the insulin-signaling system in mouse skeletal muscle
Effects of long-term caloric restriction on early steps of the insulin-signaling system in mouse skeletal muscle
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DOI：
10.1093/gerona/60.1.28
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发表时间：
2005-01-01
影响因子：
5.1
通讯作者：
Turyn, D
中科院分区：
文献类型：
--
作者：
Argentino, DP;Dominici, FP;Turyn, D
在这项研究中，我们分析了长期(14个月)热量限制(CR)对正常小鼠骨骼肌胰岛素信号系统第一步的影响。CR可显著降低血清胰岛素和血糖水平，提示胰岛素敏感性增强。CR使体内胰岛素诱导的胰岛素受体底物(IRS)-1的磷酸化降低了27%，但这一差异并不显著(p=.298)。CR使胰岛素受体(IR)丰度比随机值减少了34%，但这种差异没有达到显著意义(p=.246)。CR后PI3K的P85调节亚基和葡萄糖转运蛋白4的丰度没有改变。然而，接触CR的小鼠肌肉中IRS-1的丰度显著增加了42%。这些结果表明，CR诱导的小鼠胰岛素作用的改善与葡萄糖转运蛋白4、PI3K的P85调节亚基或骨骼肌中IR丰度的变化无关，但可能与该组织中IRS-1丰度的增加有关。
In this study, we analyzed the effects of long-term (14 months) caloric restriction (CR) on the first steps of the insulin signaling system in skeletal muscle of normal mice. CR induced a significant decrease in serum insulin and glucose levels, indicating an enhancernent of insulin sensitivity. CR reduced the in vivo insulin-induced phosphorylation of the insulin receptor substrate (IRS)-1 by 27%, but this difference was not significant (p = .298). CR reduced insulin receptor(IR) abundance by 34% from the ad libitum values, but this difference did not reach significance (p = .246). The abundance of the p85 regulatory subunit of PI3K and glucose transporter 4 was unaltered after CR. However, IRS-1 abundance was significantly increased by 42% in muscle of mice exposed to CR. These findings indicate that the CR-induced improvement of insulin action in mice is not related to changes in glucose transporter 4, the p85 regulatory subunit of PI3K, or IR abundance in skeletal muscle but might be related to an increase in IRS-1 abundance in this tissue.