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阿屈生源肽通过改变 PI3K/Akt 和胰岛素信号通路在链脲佐菌素诱导的糖尿病大鼠中的抗糖尿病作用。

Anti-diabetic Role of Adropin in Streptozotocin Induced Diabetic Rats via Alteration of PI3K/Akt and Insulin Signaling Pathway.

机构信息

Department of Endocrinology, Zhengzhou Central Hospital Affiliated to Zhengzhou University.

出版信息

J Oleo Sci. 2021;70(5):657-664. doi: 10.5650/jos.ess21019.

DOI:10.5650/jos.ess21019
PMID:33952790
Abstract

Diabetes mellitus (DM) is a hyperglycemia-related multifactorial condition with an elevated risk of microvascular and microvascular complications associated with this disease. The current experimental study was to examine the antidiabetic activity of streptozotocin (STZ)-induced adropin against diabetic rats by altering the PI3K/Akt and insulin signaling pathways. STZ (60 mg/kg) was used for the induction of DM and rats were divided into different groups and received the adropin (20, 40 and 80 mg/kg) and glibenclamide (10 mg/kg) till 28 days. Body weight, plasma insulin, blood glucose and food intake were estimated, respectively. Biochemical enzymes, carbohydrate enzymes, lipid parameters, AMPK and insulin signalling pathway parameters were estimated. GLUT4 and PPARγ expression were also estimated. Oral administration of adropin significantly (p < 0.001) increased the glycogen, glucose-6-phosphatase dehydrogenase, insulin, hexokinase and belittled the blood glucose level, fructose 1-6-biphosphatase, glucose-6-phosphatase at dose dependent manner. Adropin significantly (p < 0.001) reduced the level of triglyceride, cholesterol, low density lipoprotein, very low density lipoprotein and increased the level of high density lipoprotein at dose dependent manner. Adropin significantly (p < 0.001) activated the Akt, IRS-2, IRS-1, IR, p-AKT and PI3k, which are the key modulator molecules of PI3K/Akt, AMPK and insulin signalling pathway in DM rats. The current experimental study confirms the anti-diabetic effect of adropin on DM rats induced by AMPK and insulin signalling pathway against STZ.

摘要

糖尿病(DM)是一种与高血糖相关的多因素疾病,存在与该疾病相关的微血管和微血管并发症的风险增加。本实验研究旨在通过改变 PI3K/Akt 和胰岛素信号通路来研究链脲佐菌素(STZ)诱导的 adropin 对糖尿病大鼠的抗糖尿病活性。使用 STZ(60mg/kg)诱导 DM,将大鼠分为不同组,并给予 adropin(20、40 和 80mg/kg)和格列本脲(10mg/kg)直至 28 天。分别估计体重、血浆胰岛素、血糖和食物摄入量。估计生化酶、碳水化合物酶、脂质参数、AMPK 和胰岛素信号通路参数。还估计了 GLUT4 和 PPARγ 的表达。口服 adropin 显著(p<0.001)增加了糖原、葡萄糖-6-磷酸脱氢酶、胰岛素、己糖激酶,并降低了血糖水平、果糖 1-6-二磷酸酶、葡萄糖-6-磷酸酶的水平,呈剂量依赖性。adropin 显著(p<0.001)降低了甘油三酯、胆固醇、低密度脂蛋白、极低密度脂蛋白的水平,并呈剂量依赖性增加了高密度脂蛋白的水平。adropin 显著(p<0.001)激活了 Akt、IRS-2、IRS-1、IR、p-AKT 和 PI3k,这些都是 PI3K/Akt、AMPK 和胰岛素信号通路在 DM 大鼠中的关键调节分子。本实验研究证实了 adropin 对 STZ 诱导的 DM 大鼠的抗糖尿病作用,其作用机制是通过 AMPK 和胰岛素信号通路。

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