Abstract
Backgroundl-Fucose (Fuc), a six-deoxy hexose monosaccharide, is present endogenously in humans and animals and has a wide range of biological functions. In the present study, we aimed to examine the effect of Fuc on obesity and hepatic steatosis in mice fed a high-fat diet (HFD).MethodsC57BL/6 mice were fed a normal chow (NC) or HFD for 18 weeks to induce obesity and fatty liver. Fuc was administered intragastrically from the 8th week to the end of the experiment (18 weeks).ResultsMetagenomic analysis showed that HFD altered the genomic profile of gut microbiota in the mice; specifically, expression of alpha-l-fucosidase, the gene responsible for Fuc generation, was markedly reduced in the HFD group compared with that in the NC group. Fuc treatment decreased body weight gain, fat accumulation, and hepatic triglyceride elevation in HFD-fed mice. In addition, Fuc decreased the levels of endotoxin-producing bacteria of the Desulfovibrionaceae family and restored HFD-induced enteric dysbiosis at both compositional and functional levels.ConclusionOur findings suggest that Fuc might be a novel strategy to treat HFD-induced obesity and fatty liver.
Highlights
The epidemic of obesity and obesity-associated liver diseases in particular are a major cause of death worldwide and their prevalence is at unprecedentedly high levels [1, 2]
Metagenomics analysis showed that high-fat diet (HFD) altered the gut microbial functional profile To characterize the effect of HFD on the gut microbiome, we first performed metagenomics analysis using DNA extracted from cecal contents of mice fed with normal chow (NC) or HFD for 18 weeks
Volcano plot showed that the abundance of some genes was enriched in the NC group while that of others was enriched in the HFD group (Fig. 1b)
Summary
The epidemic of obesity and obesity-associated liver diseases in particular are a major cause of death worldwide and their prevalence is at unprecedentedly high levels [1, 2]. It has been widely shown that gut microbiota is associated with development of liver disease in mice, including acetaminophen-induced acute liver injury [3, 4], ethanol-induced liver injury [5, 6], and high-fat diet (HFD)-induced non-alcoholic fatty liver disease (NAFLD) [7, 8]. Studies conducted over the last decade have shown that HFD feeding leads to accumulation of adipose tissue and NAFLD development, which is related to compositional and functional dysbiosis of gut microbiota [11, 12]. Through using metagenomic analysis, we found that expression of the alpha-l-fucosidase gene (fuca), which is responsible for l-Fucose (Fuc) generation, was markedly
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