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鸡肌管中自噬的调节:胰岛素、胰岛素样生长因子-I和氨基酸的作用

Regulation of Autophagy in Chick Myotubes: Effects of Insulin, Insulin-Like Growth Factor-I, and Amino Acids.

作者信息

Nakashima Kazuki, Ishida Aiko

机构信息

Division of Animal Metabolism and Nutrition, Institute of Livestock and Grassland Science, NARO, Tsukuba 305-0901, Japan.

出版信息

J Poult Sci. 2018;55(4):257-262. doi: 10.2141/jpsa.0170196. Epub 2018 Mar 25.

DOI:10.2141/jpsa.0170196
PMID:32055183
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC6756409/
Abstract

Autophagy, an intracellular bulk protein degradation system in skeletal muscle, is increased under catabolic conditions resulting in muscle atrophy. This study aimed to investigate the effects of insulin, insulin-like growth factor (IGF)-I, and amino acids on autophagy (LC3-II content and expression of autophagy-related genes) in chick myotubes. Chick myotubes were incubated with insulin (1 g/m), IGF-I (100 ng/m), and amino acids for 3 h. The LC3-II content, an index of autophagosome formation, and mRNA expression of LC3B and GABARAPL1 were significantly decreased by insulin. The LC3-II content, but not mRNA expression of autophagy-related genes, was also significantly decreased by IGF-I. The LC3-II content and LC3B mRNA level were also significantly decreased by amino acids. The mRNA expression of atrogin-1/MAFbx, a muscle-specific ubiquitin ligase, was also significantly decreased by insulin, IGF-I, and amino acids in chick myotubes. These results indicated that insulin, IGF-I, and amino acids regulate autophagy as well as the ubiquitin-proteasome proteolytic pathway in chick myotubes.

摘要

自噬是骨骼肌中的一种细胞内大量蛋白质降解系统,在分解代谢条件下会增强,导致肌肉萎缩。本研究旨在探讨胰岛素、胰岛素样生长因子(IGF)-I和氨基酸对鸡肌管自噬(LC3-II含量及自噬相关基因表达)的影响。将鸡肌管用胰岛素(1 μg/ml)、IGF-I(100 ng/ml)和氨基酸孵育3小时。胰岛素显著降低了自噬体形成指标LC3-II的含量以及LC3B和GABARAPL1的mRNA表达。IGF-I也显著降低了LC3-II的含量,但未降低自噬相关基因的mRNA表达。氨基酸同样显著降低了LC3-II的含量和LC3B的mRNA水平。鸡肌管中的肌肉特异性泛素连接酶atrogin-1/MAFbx的mRNA表达也因胰岛素、IGF-I和氨基酸而显著降低。这些结果表明,胰岛素、IGF-I和氨基酸在鸡肌管中既调节自噬,也调节泛素-蛋白酶体蛋白水解途径。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2ae0/6756409/9dfe90ac1b9d/1349-0486-55-257-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2ae0/6756409/46344a4bea3f/1349-0486-55-257-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2ae0/6756409/0b26affcd060/1349-0486-55-257-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2ae0/6756409/9dfe90ac1b9d/1349-0486-55-257-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2ae0/6756409/46344a4bea3f/1349-0486-55-257-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2ae0/6756409/0b26affcd060/1349-0486-55-257-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2ae0/6756409/9dfe90ac1b9d/1349-0486-55-257-g003.jpg

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