Butyrate Improves the Metabolic Disorder and Gut Microbiome Dysbiosis in Mice Induced by a High-Fat Diet

Abstract

Background: Metabolic syndrome (MS) is one of the major causes of coronary artery diseases (CAD). Gut microbiome diversity and its natural fermentation products are not only correlated with MS and CAD, but their correlations also appear to be stronger than the associations with traditional risk factors. Therefore, the aim of this study was to provide a new potential pathway for the natural fermentation product butyrate to improve MS and to examine whether it is associated with serum metabolic profiles and gut flora composition. Methods: C57BL/6J mice fed a high-fat diet (HFD) were treated with 400 mg/kg of sodium butyrate for 16 weeks. Blood and fecal samples were collected, and the metabolite concentrations and 16s rRNA were measured with liquid chromatography–MS and Illumina platform, respectively. The plasma differential metabolites and gut microbiome composition were analyzed with XCMS online and QIIME 2, respectively. Results: Gut microbiome-derived butyrate reduced glucose intolerance and insulin resistance, resisting HFD-induced increase in the relative abundance of f_Lachnospiraceae, f_Rikenellaceae, and f_Paraprevotellaceae. Meanwhile, sodium butyrate increased the levels of α-linolenate, all-trans-retinal, resolvin E1, and leukotriene in the plasma, and the differential pathways showed enrichment in mainly resolvin E biosynthesis, histidine degradation, lipoxin biosynthesis, and leukotriene biosynthesis. Moreover, sodium butyrate increased the levels of phosphorylated-adenosine 5′-monophosphate-activated protein kinase (p-AMPK) and facilitated glucose transporter member 4 (GLUT4) in the adipose tissue. Conclusion: Butyrate can induce AMPK activation and GLUT4 expression in the adipose tissue, improving cardiovascular disease (CVD)-related metabolic disorder, resisting HFD-induced gut microbiome dysbiosis, and promoting resolvin E1 and lipoxin biosynthesis. Oral supplement of the natural fermentation product butyrate can be a potential strategy for preventing CVD.

Codium fragile Ameliorates High-Fat Diet-Induced Metabolism by Modulating the Gut Microbiota in Mice

“…Previous study reported that fucoidan from Laminaria japonica significantly increased the relative abundance of Ruminococcaceae while the abundance of Verrucomicrobia decreased, which is consistent with our current results [69]. Ruminococcaceae and Lachnospiraceae are predominant families of intestinal bacteria involved in carbohydrate metabolisms [70,71]. Many SCFA-producing bacteria also belong to these families.…”

Effects of dietary fibres on gut microbial metabolites and liver lipid metabolism in growing pigs

“…Several mechanisms may explain the changes in hepatic lipid content. The butyrate produced in intestinal lumen, which is an energy source for colonocytes, can activate the AMPK signalling pathway in intestinal epithelium, inhibiting hepatic cholesterol and fatty acids synthesis (Gao et al., 2019; Rumberger, Arch, & Green, 2014; Song et al., 2019). In our study, a combined wheat bran fibre and inulin diet feeding tended to reduce the butyrate concentrations in colon, which may lead to a reduced inhibition of hepatic lipid accumulation.…”

Adipokines and Adipose Tissue-Related Metabolites, Nuts and Cardiovascular Disease

“…In rats on a high-fat diet, butyrate supplementation induced the activation of AMP-activated 5 Protein Kinase (AMPK) and glucose transporter 4 (GLUT4) in the adipose tissue, attenuated diet-induced dysbiosis, promoted biosynthesis of resolvin E1 and lipoxin (anti-inflammatory lipid mediators) [175], attenuated weight gain, adiposity, adipocyte hypertrophy, inflammation, and leptin secretion [176]. In the same animal model, butyrate supplementation appears to induce lipolysis in WAT mediated by activation of β3-adrenergic receptors [177] and regulates gene expression related to intestinal cholesterol absorption resulting in attenuation of atherosclerosis [178].…”