Oral Supplementation of Sodium Butyrate Attenuates the Progression of Non-Alcoholic Steatohepatitis [14.04.20]
Sodium butyrate (SoB) is the salt of butyric acid, a short-chain fatty acid being built by microbial anaerobic fermentation of non-digestible polysaccharides in the intestinal tract. The compound is used as an additive in animal feed, but also in human medicine because of its positive effects on the regeneration of the intestinal mucosa. In a recent study, a German-Austrian research team including Sascha Venturelli and Markus Burkard from the University of Hohenheim investigated SoB effects in a mouse model for NAFLD (Non-Alcoholic Fatty Liver Disease). In a current paper the team discusses treatment options and the underlying molecular mechanisms.
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Original Paper
Baumann A1, Jin CJ2, Brandt A1, Sellmann C2, Nier A1, Burkard M3,4, Venturelli S3,4, Bergheim I1.(2020) Oral Supplementation of Sodium Butyrate Attenuates the Progression of Non-Alcoholic Steatohepatitis. Nutrients. 2020 Mar 30;12(4). pii: E951. doi: 10.3390/nu12040951.
Author information
- Department of Nutritional Sciences, Molecular Nutritional Science, University of Vienna, Althanstraße 14, UZA II, 1090 Vienna, Austria.
- Institute of Nutritional Sciences, SD Model Systems of Molecular Nutrition, Friedrich-Schiller-University Jena, Dornburger Straße 22-25, 07743 Jena, Germany.
- Institute of Physiology, Department of Vegetative and Clinical Physiology, University Hospital Tuebingen, Wilhelmstraße 56, 72074 Tuebingen, Germany.
- Institute of Biological Chemistry and Nutrition, University of Hohenheim, Garbenstraße 30, 70599 Stuttgart, Germany.
Abstract
Sodium butyrate (SoB) supplementation has been suggested to attenuate the development of non-alcoholic fatty liver disease (NAFLD). Here, we determined the therapeutic potential of SoB on NAFLD progression and molecular mechanism involved. Eight-week old C57BL/6J mice were pair-fed a fat-, fructose- and cholesterol-rich diet (FFC) or control diet (C). After 8 weeks, some mice received 0.6g SoB/kg bw in their respective diets (C+SoB; FFC+SoB) or were maintained on C or FFC for the next 5 weeks of feeding. Liver damage, markers of glucose metabolism, inflammation, intestinal barrier function and melatonin metabolism were determined. FFC-fed mice progressed from simple steatosis to early non-alcoholic steatohepatitis, along with significantly higher TNFα and IL-6 protein levels in the liver and impaired glucose tolerance. In FFC+SoB-fed mice, disease was limited to steatosis associated with protection against the induction of Tlr4 mRNA and iNOS protein levels in livers. SoB supplementation had no effect on FFC-induced loss of tight junction proteins in the small intestine but was associated with protection against alterations in melatonin synthesis and receptor expression in the small intestine and livers of FFC-fed animals. Our results suggest that the oral supplementation of SoB may attenuate the progression of simple steatosis to steatohepatitis.
KEYWORDS: inducible nitric oxide synthase; melatonin synthesis; non-alcoholic steatohepatitis; sodium butyrate; toll-like receptor 4
