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Article

Oral Supplementation of Sodium Butyrate Attenuates the Progression of Non-Alcoholic Steatohepatitis

1
Department of Nutritional Sciences, Molecular Nutritional Science, University of Vienna, Althanstraße 14, UZA II, 1090 Vienna, Austria
2
Institute of Nutritional Sciences, SD Model Systems of Molecular Nutrition, Friedrich-Schiller-University Jena, Dornburger Straße 22-25, 07743 Jena, Germany
3
Institute of Physiology, Department of Vegetative and Clinical Physiology, University Hospital Tuebingen, Wilhelmstraße 56, 72074 Tuebingen, Germany
4
Institute of Biological Chemistry and Nutrition, University of Hohenheim, Garbenstraße 30, 70599 Stuttgart, Germany
*
Author to whom correspondence should be addressed.
These authors contributed equally to this work.
Nutrients 2020, 12(4), 951; https://doi.org/10.3390/nu12040951
Received: 20 February 2020 / Revised: 23 March 2020 / Accepted: 27 March 2020 / Published: 30 March 2020
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. View Full-Text
Keywords: inducible nitric oxide synthase; melatonin synthesis; non-alcoholic steatohepatitis; sodium butyrate; toll-like receptor 4 inducible nitric oxide synthase; melatonin synthesis; non-alcoholic steatohepatitis; sodium butyrate; toll-like receptor 4
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MDPI and ACS Style

Baumann, A.; Jin, C.J.; Brandt, A.; Sellmann, C.; Nier, A.; Burkard, M.; Venturelli, S.; Bergheim, I. Oral Supplementation of Sodium Butyrate Attenuates the Progression of Non-Alcoholic Steatohepatitis. Nutrients 2020, 12, 951. https://doi.org/10.3390/nu12040951

AMA Style

Baumann A, Jin CJ, Brandt A, Sellmann C, Nier A, Burkard M, Venturelli S, Bergheim I. Oral Supplementation of Sodium Butyrate Attenuates the Progression of Non-Alcoholic Steatohepatitis. Nutrients. 2020; 12(4):951. https://doi.org/10.3390/nu12040951

Chicago/Turabian Style

Baumann, Anja, Cheng J. Jin, Annette Brandt, Cathrin Sellmann, Anika Nier, Markus Burkard, Sascha Venturelli, and Ina Bergheim. 2020. "Oral Supplementation of Sodium Butyrate Attenuates the Progression of Non-Alcoholic Steatohepatitis" Nutrients 12, no. 4: 951. https://doi.org/10.3390/nu12040951

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