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.
Highlights
Studies suggest that the global prevalence of non-alcoholic fatty liver disease (NAFLD) in the general population is ~25% [1]
The signs of NAFLD had progressed to early steatohepatitis
ALT and AST activity in plasma, as well as the number of neutrophils in liver tissue, were significantly higher in FFC+Sodium butyrate (SoB)-fed when compared with control animals and did not differ from
Summary
Studies suggest that the global prevalence of non-alcoholic fatty liver disease (NAFLD) in the general population is ~25% [1]. Overnutrition and certain dietary patterns like the so-called. Western-style dietary pattern, as well as a lack of physical activity and changes in the intestinal microbiota and barrier function, are thought to be critical in the development of NAFLD [4,5,6,7,8]. Butyric acid is a short-chain fatty acid being built by microbial anaerobic fermentation of non-digestible polysaccharides. It is found in foods like milk and milk-products and in the oral cavity and intestinal tract of humans and mammals [10]. The short-chain fatty acid has various other biological effects such as the regulation of metabolism and maintenance of intestinal homeostasis [11]
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