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烷基酰胺改善链脲佐菌素诱导的糖尿病大鼠的蛋白质代谢紊乱。

alkylamides ameliorate protein metabolism disorder in STZ-induced diabetic rats.

作者信息

Ren Tingyuan, Zhu Yuping, Xia Xuejuan, Ding Yongbo, Guo Jing, Kan Jianquan

机构信息

College of Food ScienceSouthwest University, Chongqing, China.

Laboratory of Quality & Safety Risk Assessment for Agro-products on Storage and Preservation (Chongqing)Ministry of Agriculture, Chongqing, China.

出版信息

J Mol Endocrinol. 2017 Apr;58(3):113-125. doi: 10.1530/JME-16-0218. Epub 2017 Jan 18.

DOI:10.1530/JME-16-0218
PMID:28100702
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC5424265/
Abstract

This study aimed to evaluate the protein metabolism effect of alkylamides and to explore the potential mechanism in streptozotocin (STZ)-induced diabetic rats. Diabetic rats were orally treated with 2, 4 and 8 mg per kg bw of alkylamides daily for 28 days. Alkylamides decreased the relative weight of the liver and food intake, significantly increased the relative skeletal muscle weight and significantly decreased the blood urea nitrogen levels. Insulin, insulin-like growth factor 1, total protein (TP) and albumin (ALB), globular proteins and ALB proteins/globulin protein levels in serum significantly increased. TP, RNA content and RNA/DNA ratio significantly increased in the skeletal muscle of diabetic rats. Real-time quantitative polymerase chain reaction results indicated that alkylamides significantly increased the mRNA expression of insulin receptor (InR), IGF1 and insulin-like growth factor 1 receptor (IGF1R) in the liver and skeletal muscle. Moreover, the mRNA and protein expression levels of PI3K, PKB and mTOR significantly increased, whereas those of atrogin-1, muscle ring finger 1 and FOXO in the skeletal muscle significantly decreased. Alkylamides may advance protein synthesis by the PI3K/PKB/mTOR signalling pathway and attenuate the catabolism of protein through the ubiquitin-proteasome pathway. Therefore, it was possible that alkylamides ameliorate protein metabolism disorders in diabetic rats by activating the mTOR pathway.

摘要

本研究旨在评估烷基酰胺对蛋白质代谢的影响,并探讨其在链脲佐菌素(STZ)诱导的糖尿病大鼠中的潜在作用机制。将糖尿病大鼠每日按每千克体重2、4和8毫克的剂量口服给予烷基酰胺,持续28天。烷基酰胺降低了肝脏相对重量和食物摄入量,显著增加了骨骼肌相对重量,并显著降低了血尿素氮水平。血清中的胰岛素、胰岛素样生长因子1、总蛋白(TP)、白蛋白(ALB)、球蛋白以及ALB蛋白/球蛋白蛋白水平均显著升高。糖尿病大鼠骨骼肌中的TP、RNA含量以及RNA/DNA比值显著增加。实时定量聚合酶链反应结果表明,烷基酰胺显著增加了肝脏和骨骼肌中胰岛素受体(InR)、IGF1和胰岛素样生长因子1受体(IGF1R)的mRNA表达。此外,PI3K、PKB和mTOR的mRNA和蛋白表达水平显著增加,而骨骼肌中atrogin-1、肌肉环形指蛋白1和FOXO的表达水平显著降低。烷基酰胺可能通过PI3K/PKB/mTOR信号通路促进蛋白质合成,并通过泛素-蛋白酶体途径减弱蛋白质分解代谢。因此,烷基酰胺有可能通过激活mTOR途径改善糖尿病大鼠的蛋白质代谢紊乱。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2ba7/5424265/81c8f41ba75b/jme-58-113-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2ba7/5424265/b95453a3ab2c/jme-58-113-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2ba7/5424265/b19a26f09e46/jme-58-113-g002.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2ba7/5424265/1165a94bacd2/jme-58-113-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2ba7/5424265/81c8f41ba75b/jme-58-113-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2ba7/5424265/b95453a3ab2c/jme-58-113-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2ba7/5424265/b19a26f09e46/jme-58-113-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2ba7/5424265/b4eebcf3e2bb/jme-58-113-g003.jpg
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