Momordica cochinchinensis Aril Ameliorates Diet-Induced Metabolic Dysfunction and Non-Alcoholic Fatty Liver by Modulating Gut Microbiota

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Title:	Momordica cochinchinensis Aril Ameliorates Diet-Induced Metabolic Dysfunction and Non-Alcoholic Fatty Liver by Modulating Gut Microbiota
Authors:	Huang, HC (Huang, Hsiu-Chen) Chen, CJ (Chen, Chiung-Ju) Lai, YH (Lai, Yu-Heng) Lin, YC (Lin, Yu-Chun) Chiou, WC (Chiou, Wei-Chung) Lu, HF (Lu, Hsu-Feng) Chen, YF (Chen, Ying-Fang) Chen, YH (Chen, Yu-Hsin) Huang, C (Huang, Cheng)
Contributors:	化學系
Keywords:	adiposity gut microbiota insulin resistance Momordica cochinchinensis aril nonalcoholic fatty liver
Date:	2021-03
Issue Date:	2021-04-14 14:08:32 (UTC+8)
Abstract:	Obesity and its associated conditions, such as type 2 diabetes mellitus (T2DM) and nonalcoholic fatty liver disease (NAFLD), are a particular worldwide health problem at present. Momordica cochinchinensis (MC) is consumed widely in Southeast Asia. However, whether it has functional effects on fat-induced metabolic syndrome remains unclear. This study was conducted to examine the prevention effect of Momordica cochinchinensis aril (MCA) on obesity, non-alcoholic fatty liver and insulin resistance in mice. MCA protected the mice against high-fat diet (HFD)-induced body weight gain, hyperlipidemia and hyperglycemia, compared with mice that were not treated. MCA inhibited the expansion of adipose tissue and adipocyte hypertrophy. In addition, the insulin sensitivity-associated index that evaluates insulin function was also significantly restored. MCA also regulated the secretion of adipokines in HFD-induced obese mice. Moreover, hepatic fat accumulation and liver damage were reduced, which suggested that fatty liver was prevented by MCA. Furthermore, MCA supplementation suppressed hepatic lipid accumulation by activation of the AMP-activated protein kinase (AMPK) and peroxisome proliferator-activated receptor-alpha (PPAR-alpha) signaling pathway in the human fatty liver HuS-E/2 cell model. Our data indicate that MCA altered the microbial contents of the gut and modulated microbial dysbiosis in the host, and consequently is involved in the prevention of HFD-induced adiposity, insulin resistance and non-alcoholic fatty liver disease.
Relation:	INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES 卷冊: 22 期: 5 文獻號碼: 2640
Appears in Collections:	[Department of Chemistry & Graduate Institute of Applied Chemistry ] journal articles

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