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Alleviates Liver Steatosis and Steatohepatitis by Increasing Fibroblast Growth Factor 21 Sensitivity. | LitMetric

Alleviates Liver Steatosis and Steatohepatitis by Increasing Fibroblast Growth Factor 21 Sensitivity.

Front Endocrinol (Lausanne)

Department of Endocrinology and Metabolism, Shanghai Jiao Tong University Affiliated Sixth People's Hospital, Shanghai Diabetes Institute, Shanghai Clinical Center for Diabetes, Shanghai, China.

Published: February 2022

AI Article Synopsis

  • The gut microbiota, specifically a certain species, has been linked to the development of non-alcoholic fatty liver disease (NAFLD) and can improve liver health by reducing liver fat and inflammation.
  • The study explored whether this gut microbiota treatment works by enhancing the effects of a protein called fibroblast growth factor 21 (FGF21), known to protect against NAFLD.
  • Results showed that this treatment not only improved liver conditions but also strengthened the gut barrier and increased the liver's responsiveness to FGF21, indicating it could be a potential therapy for NAFLD.

Article Abstract

The gut microbiota is a newly identified contributor to the development of non-alcoholic fatty liver disease (NAFLD). Previous studies of (), a species of that is common in the human intestinal tract, have demonstrated that it can alleviate liver steatosis and steatohepatitis. Fibroblast growth factor 21 (FGF21) has long been considered as a biomarker of NAFLD, and recent studies have shown the protective effect of FGF21 analogs on NAFLD. We wondered whether treatment would alleviate NAFLD via the interaction with FGF21. To this end, male C57BL/6J mice on a choline-deficient high-fat diet (CDHFD) were treated with drinking water supplemented with for 8 weeks, followed by the acute administration of recombinant mouse FGF21 protein (rmFGF21) to conduct the FGF21 response test. Consistent with previous studies, supplementation reversed the CDHFD-induced liver steatosis and steatohepatitis. This was evaluated on the NAFLD activity score (NAS), reduced liver enzymes, and lipid accumulation. Further studies demonstrated that supplementation preserved the gut barrier, reduced the gut microbiota-derived lipopolysaccharide (LPS), and inhibited the hepatic TLR4/NF-κB pathway. This was accompanied by the elevated expressions of the receptors of FGF21, fibroblast growth factor receptor 1 (FGFR1) and β-klotho (KLB), in the liver and the decreased expression of FGF21. The results of FGF21 response test showed that supplementation alleviated the CDHFD-induced FGF21 resistance. In vivo experiments suggested that LPS could suppress the expression of FGF21 and KLB in a dose-dependent manner. Collectively, this study showed that supplementation could alleviate NAFLD by increasing FGF21 sensitivity.

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Source
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC8756294PMC
http://dx.doi.org/10.3389/fendo.2021.773340DOI Listing

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