SCOPE Obesity is associated with gut microbiome dysbiosis. Mannose oligosaccharide (MOS) has been reported to be a potential prebiotic. The present study was aimed to determine the effects of MOS on Western diet-induced obesity and to uncover the mediating roles of the gut microbiota and microbial metabolites. METHODS AND RESULTS Three-month-old male ICR mice were fed with a high-fat and high-fructose diet for eight weeks. The diet-induced obese mice were then orally administrated with MOS (100 mg/kg/day and 200 mg/kg/day) for four weeks. MOS significantly reduced bodyweight gain, insulin resistance, fatty liver, and inflammatory responses in obese mice. MOS also stimulated lipolysis and inhibited lipogenesis in the adipose tissues. Moreover, MOS restructured the gut microbiome by enhancing the abundance of Bifidobacterium and Lactobacillus in obese mice. The microbial metabolites short-chain fatty acids (SCFAs) were also increased in the feces and serum. Correlation analysis indicated that the appetite suppression and lipid-lowering effects of MOS were highly correlated with the butyrate levels. CONCLUSION MOS suppressed the appetite, which resulted in less lipid deposition. The lower appetite was likely due to an altered gut microbiome and elevated SCFAs production. MOS might be a potential nutraceutical used in bodyweight management and gut health improvement. This article is protected by copyright. All rights reserved.
Mannan Oligosaccharide Suppresses Lipid Accumulation and Appetite in Western Diet-Induced Obese Mice Via Reshaping Gut Microbiome and Enhancing Short-Chain Fatty Acids Production.
Shikai Yan,Renjie Shi,Ling Li,Shaobo Ma,Hongbo Zhang,Jin Ye,Jiamin Wang,Junru Pan,Qianxu Wang,Xiang Jin,Xuebo Liu,Zhigang Liu
Published 2019 in Molecular Nutrition & Food Research
ABSTRACT
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- Publication year
2019
- Venue
Molecular Nutrition & Food Research
- Publication date
2019-12-01
- Fields of study
Biology, Medicine, Chemistry, Environmental Science
- Identifiers
- External record
- Source metadata
Semantic Scholar, PubMed
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