Exogenous galanin alleviates hepatic steatosis by promoting autophagy via the AMPK-mTOR pathway

作者全名："Zhu, Shuyuan; Wang, Shuai; Luo, Tao"

作者地址："[Zhu, Shuyuan; Wang, Shuai; Luo, Tao] Chongqing Med Univ, Dept Geriatr, Affiliated Hosp 1, Chongqing 400016, Peoples R China"

通信作者："Luo, T (通讯作者)，Chongqing Med Univ, Dept Geriatr, Affiliated Hosp 1, Chongqing 400016, Peoples R China."

来源：ARCHIVES OF BIOCHEMISTRY AND BIOPHYSICS

ESI学科分类：BIOLOGY & BIOCHEMISTRY

WOS号：WOS:001044319400001

JCR分区：Q1

影响因子：3.8

年份：2023

卷号：744

期号：　

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结束页：　

文献类型：Article

关键词：NAFLD; AMPK; & beta;-Oxidation; Autophagy; Galanin

摘要："Defective autophagy-induced intracellular lipid degradation is causally associated with non-alcoholic fatty liver disease (NAFLD) development. Therefore, agents that can restore autophagy may have potential clinical application prospects on this public health issue. Galanin (GAL) is a pleiotropic peptide that regulates autophagy and is a potential drug for the treatment of NAFLD. In this study, we used an MCD-induced NAFLD mouse model in vivo and an FFA-induced HepG2 hepatocyte model in vitro to evaluate the anti-NAFLD effect of GAL. Exogenous GAL supplementation significantly attenuated lipid droplet accumulation and suppressed hepatocyte TG levels in mice and cell models. Mechanistically, Galanin-mediated reduction of lipid accumulation was positively correlated with upregulated p-AMPK, as evidenced by upregulated protein expressions of fatty acid oxidation-related gene markers (PPAR-a and CPT1A), upregulated expressions of the autophagy-related marker (LC3B), and downregulated autophagic substrate p62 levels. In FFA-treated HepG2 cells, activation of fatty acid oxidation and autophagy-related proteins by galanin was reversed by autophagy inhibitors, chloroquine, and the AMPK inhibitor. Galanin ameliorates hepatic fat accumulation by inducing autophagy and fatty acid oxidation via the AMPK/mTOR pathway."

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