In an animal study, sodium butyrate (NaB) was demonstrated to correct gut microbiota imbalance induced by a high fat diet (HFD), while considerably elevating the magnitude of the beneficial bacteria Christensenellaceae, Blautia and Lactobacillus. These bacteria characteristically produce high amounts of butyric acid. Butyrate in turn served to restore the intestinal mucosa damage induced by the high fat diet, increase the expression of the gastrointestinal barrier indicator zonula occluden-1 (ZO-1) in the small intestine, and decreased the level of gut endotoxin in both the serum and liver, as compared to the high fat group. NaB also served to downregulate multiple genes, including endotoxin-associated genes such as Toll-like receptor 4 (TLR4) and Myd88, and numerous pro- inflammatory genes such as MCP-1, TNF-α, IL-1, IL-2, IL-6 and IFN-γ in liver or epididymal fat. Other benefits of NaB administration were also observed, including the amelioration of liver inflammation and fat accumulation, decreased levels of triglycerides and cholesterol in liver, and a significantly decreased nonalcoholic fatty liver activity (NAS) score. Metabolic indices (FBG and HOMA-IR) and liver function indicators (ALT and AST) were also improved compared to the high fat group. It was concluded that NaB may restore the dysbiosis of gut microbiota to attenuate steatohepatitis, which may be therapeutic for non-alcoholic fatty liver disease (NAFLD).
“NaB was able to correct the HFD-induced gut microbiota imbalance in mice, while it considerably elevated the abundance of beneficial bacteria. These bacteria can produce butyric acid in what seems like a virtuous circle, and butyrate restored HFD induced symptoms.”
Zhou D, Pan Q, Xin F-Z, Zhang, R.-N., He, C.-X., Chen, G.-Y, Liu C, Chen Y-W, Fanet J-G. Sodium butyrate attenuates high-fat diet-induced steatohepatitis in mice by improving gut microbiota and gastrointestinal barrier. World Journal of Gastroenterology. 2017;23(1):60-75. doi:10.3748/wjg.v23.i1.60.