Experimental and Molecular Medicine (Dec 2018)

Sodium butyrate reduces high-fat diet-induced non-alcoholic steatohepatitis through upregulation of hepatic GLP-1R expression

  • Da Zhou,
  • Yuan-Wen Chen,
  • Ze-Hua Zhao,
  • Rui-Xu Yang,
  • Feng-Zhi Xin,
  • Xiao-Lin Liu,
  • Qin Pan,
  • Huiping Zhou,
  • Jian-Gao Fan

DOI
https://doi.org/10.1038/s12276-018-0183-1
Journal volume & issue
Vol. 50, no. 12
pp. 1 – 12

Abstract

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Fatty liver disease: A gutsy way to prevent disease progression A treatment for non-alcoholic fatty liver disease that incorporates a metabolite found in the gut could prevent progression to a more serious liver condition. Drugs that enhance the activity of glucagon-like peptide-1 (GLP-1), a protein involved in regulating metabolic processes, have shown promise in targeting non-alcoholic fatty liver disease and the more serious condition, steatohepatitis. However, some patients appear resistant to treatment. Jian-Gao Fan at Shanghai Jiao Tong University in China, Huiping Zhou at McGuire VA Medical Center in Richmond, USA, and co-workers demonstrated that a gut metabolite called sodium butyrate may help encourage responsiveness to GLP-1 treatment. The team found that liver GLP-1R expression was considerably reduced in patients with liver disease compared with healthy controls. Experiments on mouse models showed that treatment incorporating sodium butyrate improved GLP-1R levels and reduced fatty liver deposits.