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

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-in...

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Autores principales: Huang, Hsiu-Chen, Chen, Chiung-Ju, Lai, Yu-Heng, Lin, Yu-Chun, Chiou, Wei-Chung, Lu, Hsu-Feng, Chen, Ying-Fang, Chen, Yu-Hsin, Huang, Cheng
Formato: Online Artículo Texto
Lenguaje:English
Publicado: MDPI 2021
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7961723/
https://www.ncbi.nlm.nih.gov/pubmed/33808007
http://dx.doi.org/10.3390/ijms22052640
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author Huang, Hsiu-Chen
Chen, Chiung-Ju
Lai, Yu-Heng
Lin, Yu-Chun
Chiou, Wei-Chung
Lu, Hsu-Feng
Chen, Ying-Fang
Chen, Yu-Hsin
Huang, Cheng
author_facet Huang, Hsiu-Chen
Chen, Chiung-Ju
Lai, Yu-Heng
Lin, Yu-Chun
Chiou, Wei-Chung
Lu, Hsu-Feng
Chen, Ying-Fang
Chen, Yu-Hsin
Huang, Cheng
author_sort Huang, Hsiu-Chen
collection PubMed
description 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.
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spelling pubmed-79617232021-03-17 Momordica cochinchinensis Aril Ameliorates Diet-Induced Metabolic Dysfunction and Non-Alcoholic Fatty Liver by Modulating Gut Microbiota Huang, Hsiu-Chen Chen, Chiung-Ju Lai, Yu-Heng Lin, Yu-Chun Chiou, Wei-Chung Lu, Hsu-Feng Chen, Ying-Fang Chen, Yu-Hsin Huang, Cheng Int J Mol Sci Article 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. MDPI 2021-03-05 /pmc/articles/PMC7961723/ /pubmed/33808007 http://dx.doi.org/10.3390/ijms22052640 Text en © 2021 by the authors. Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (http://creativecommons.org/licenses/by/4.0/).
spellingShingle Article
Huang, Hsiu-Chen
Chen, Chiung-Ju
Lai, Yu-Heng
Lin, Yu-Chun
Chiou, Wei-Chung
Lu, Hsu-Feng
Chen, Ying-Fang
Chen, Yu-Hsin
Huang, Cheng
Momordica cochinchinensis Aril Ameliorates Diet-Induced Metabolic Dysfunction and Non-Alcoholic Fatty Liver by Modulating Gut Microbiota
title Momordica cochinchinensis Aril Ameliorates Diet-Induced Metabolic Dysfunction and Non-Alcoholic Fatty Liver by Modulating Gut Microbiota
title_full Momordica cochinchinensis Aril Ameliorates Diet-Induced Metabolic Dysfunction and Non-Alcoholic Fatty Liver by Modulating Gut Microbiota
title_fullStr Momordica cochinchinensis Aril Ameliorates Diet-Induced Metabolic Dysfunction and Non-Alcoholic Fatty Liver by Modulating Gut Microbiota
title_full_unstemmed Momordica cochinchinensis Aril Ameliorates Diet-Induced Metabolic Dysfunction and Non-Alcoholic Fatty Liver by Modulating Gut Microbiota
title_short Momordica cochinchinensis Aril Ameliorates Diet-Induced Metabolic Dysfunction and Non-Alcoholic Fatty Liver by Modulating Gut Microbiota
title_sort momordica cochinchinensis aril ameliorates diet-induced metabolic dysfunction and non-alcoholic fatty liver by modulating gut microbiota
topic Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7961723/
https://www.ncbi.nlm.nih.gov/pubmed/33808007
http://dx.doi.org/10.3390/ijms22052640
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