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首页> 外文期刊>Cellular Physiology and Biochemistry >Akt2-Dependent Beneficial Effect of Galanin on Insulin-Induced Glucose Uptake in Adipocytes of Diabetic Rats
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Akt2-Dependent Beneficial Effect of Galanin on Insulin-Induced Glucose Uptake in Adipocytes of Diabetic Rats

机译：甘丙肽对糖尿病大鼠脂肪细胞中胰岛素诱导的葡萄糖摄取的依赖于Akt2的有益作用。

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>Background/Aims: Glucose uptake occurs via the activation of an insulin-signaling cascade, resulting in the translocation of glucose transporter 4 (GLUT4) to the plasma membrane of adipocytes and myocytes. Recent research found that galanin could boost insulin-induced glucose uptake. This study aimed to explore whether activation of Akt2 mediates the beneficial effects of galanin on insulin-induced glucose uptake in the adipocytes of diabetic rats. Method: In this experiment, insulin, galanin and MK-2206, an Akt inhibitor, were injected individually or in combination into diabetic rats once a day for ten days. Then, glucose uptake and pAkt2 and its downstream proteins were examined in adipocytes. Results: Administration of galanin significantly enhanced insulin-induced 2-Deoxy-D-[3H]glucose uptake; GLUT4 and vesicle-associated membrane protein 2 contents in plasma membranes; and pAkt2Thr308/Ser473 and Akt2 mRNA expression levels in adipocytes. In addition, Akt2 downstream proteins including phosphorylated AS160 were increased, but the levels of phosphorylated forkhead box O1 and glycogen synthase kinase-3?2 were reduced. Treatment with MK-2206 may block the beneficial effects of galanin on these insulin-induced events. Conclusions: The results of this study suggest that phosphorylation of Akt2 mediates the beneficial effects of galanin on insulin-induced glucose uptake in the adipocytes of diabetic rats.
机译：> 背景/目的： 葡萄糖摄取是通过激活胰岛素信号级联反应发生的，从而导致葡萄糖转运蛋白4（GLUT4）转运到CYP的质膜上。脂肪细胞和肌细胞。最近的研究发现甘丙肽可以促进胰岛素诱导的葡萄糖摄取。这项研究旨在探讨Akt2的激活是否介导甘丙肽对糖尿病大鼠脂肪细胞中胰岛素诱导的葡萄糖摄取的有益作用。 方法： 在该实验中，胰岛素，甘丙肽和一种Akt抑制剂MK-2206每天一次或联合注射到糖尿病大鼠中，持续10天。然后，检查脂肪细胞中的葡萄糖摄取和pAkt2及其下游蛋白。 结果： 甘丙肽的给药显着增强了胰岛素诱导的2-Deoxy-D-[ 3 H]葡萄糖的摄取;质膜中GLUT4和囊泡相关膜蛋白2的含量;脂肪细胞中pAkt2 Thr308 / Ser473 和Akt2 mRNA的表达水平。此外，包括磷酸化的AS160的Akt2下游蛋白增加了，但是磷酸化的叉头盒O1和糖原合酶激酶-3β2的水平降低了。用MK-2206治疗可能会阻断甘丙肽对这些胰岛素诱导的事件的有益作用。 结论： 这项研究的结果表明，Akt2的磷酸化介导甘丙肽对胰岛素诱导的糖尿病大鼠脂肪细胞摄取葡萄糖的有益作用。

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