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首页> 美国卫生研究院文献>Age >Calorie restriction initiated at a young age activates the Akt/PKCζ/λ-Glut4 pathway in rat white adipose tissue in an insulin-independent manner
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Calorie restriction initiated at a young age activates the Akt/PKCζ/λ-Glut4 pathway in rat white adipose tissue in an insulin-independent manner

机译：从年轻时开始的热量限制以胰岛素非依赖方式激活大鼠白色脂肪组织中的Akt /PKCζ/λ-Glut4途径

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Calorie restriction (CR) may exert an anti-aging effect through a metabolic adaptation to limited energy intake. The present study investigated the effect of CR on insulin signaling in response to glucose load in the epididymal adipose tissue of male F344 rats at 7 and 22 months of age. Young and middle-aged rats were fed ad libitum (AL) or 30% CR diets for 4 months, underwent glucose tolerance tests and were sacrificed 15 min after an intraperitoneal glucose or saline injection to evaluate glucose-stimulated insulin response and subsequent activation of insulin signaling molecules in the adipose tissue. In the 7- and 22- month AL groups, glucose administration increased serum insulin levels and also increased phosphorylated (p) levels of the insulin receptor (IR), v-akt murine thymoma viral oncogene homolog (Akt), protein kinase C (PKC) ζ/λ and the membrane fraction of glucose transporter 4 (mGlut4). In contrast, in the 7-month CR group, p-Akt, p-PKCζ/λ and mGlut4 levels were upregulated without glucose stimulation; the glucose load augmented the p-IR level but there was no additional activation of the downstream molecules. In the 22-month CR group, these unexpected findings were not observed. In summary, basal levels of insulin signaling molecules such as p-Akt, p-PKCζ/λ, and mGlut4 were significantly increased with a low insulin response in the 7-month CR group. The present results suggest the presence of an age-specific insulin-independent mechanism that is induced by CR to regulate energy metabolism in white adipose tissue.Electronic supplementary materialThe online version of this article (doi:10.1007/s11357-008-9071-2) contains supplementary material, which is available to authorized users.
机译：热量限制（CR）可能通过代谢适应有限的能量摄入而发挥抗衰老作用。本研究调查了7和22个月大的雄性F344大鼠附睾脂肪组织中CR对胰岛素信号响应葡萄糖负荷的影响。幼鼠和中年大鼠自由喂食（AL）或30％CR饮食4个月，进行葡萄糖耐量试验，并在腹膜内注射葡萄糖或盐水后15分钟处死大鼠以评估葡萄糖刺激的胰岛素反应和随后的胰岛素活化脂肪组织中的信号分子。在7和22个月的AL组中，葡萄糖给药增加了血清胰岛素水平，并且还增加了胰岛素受体（IR），v-akt鼠胸腺瘤病毒致癌基因同源物（Akt），蛋白激酶C（PKC）的磷酸化（p）水平。 ）ζ/λ和葡萄糖转运蛋白4（mGlut4）的膜分数。相反，在7个月的CR组中，在没有葡萄糖刺激的情况下，p-Akt，p-PKCζ/λ和mGlut4的水平上调。葡萄糖负荷增加了p-IR水平，但下游分子没有其他激活。在22个月的CR组中，未观察到这些意外的发现。总而言之，在7个月的CR组中，胰岛素信号响应分子（例如p-Akt，p-PKCζ/λ和mGlut4）的基础水平显着提高，而胰岛素响应却很低。目前的结果表明，CR可以诱导特定年龄的胰岛素非依赖性机制来调节白色脂肪组织中的能量代谢。电子补充材料本文的在线版本（doi：10.1007 / s11357-008-9071-2）包含补充材料，授权用户可以使用。

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