Berberine alleviates nonalcoholic fatty liver induced by a high‐fat diet in mice by activating SIRT3

What is it about?

NAFLD is a burgeoning health problem that starts with the aberrant accumulation of triglyceride in the liver and is associated with insulin resistance as well as abnormal glucose metabolism. Lipid accumulation is a typical characteristic of NAFLD. The mitochondrial dysfunction is a typical feature of NAFLD, companying with the decline of β-OX, which further aggravates the progress of NAFLD. BBR is a natural isoquinoline alkaloid isolated from Coptischinensis, which has been previously used in the treatment of diarrhea in China and possessed a hypoglycemic effect in the metabolic diseases. Post-translational modifications of the metabolic proteins are indispensable manner of metabolic regulation. One way is the alteration of the acetylation state. The sirtuins (SIRT1-SIRT7), a family of nicotinamide adenine dinucleotide (NAD+)-dependent protein deacetylases, regulate multiple cellular processes, attracting much attentions in the metabolic homeostasis field in recent years. SIRT3 is the main deacetylase localized in mitochondria and regulates the activities of metabolic enzymes through its deacetylatic activity, taking part in a variety of metabolic process. SIRT3 can regulate the mitochondrial β-OX through regulating the enzymatic activity of LCAD. In this manuscript, it is the first time found that BBR alleviate HFD-induced inhibition of fatty acid β-OX through SIRT3-mediated LCAD deacetylation and SIRT3 is essential for the metabolic effects of BBR on β-OX in NAFLD mice, which provides a novel mechanism, supporting BBR as a promising therapeutics for NAFLD.

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