Anthocyanins Improved Mitochondrial Dysfunction in Mice of Non‐alcoholic Fatty Liver Disease Induced by High Fat Diet

Abstract

Recent studies indicate that mitochondrial dysfunction plays a critical role in the pathogenesis of non‐alcoholic fatty liver disease (NAFLD. The goal of this study is to investigate whether anthocyanins (ACNs) from bilberries and blackcurrants possess a protective effect on mitochondrial dysfunction and eventually contribute to attenuation of NAFLD in mice induced by feeding a high fat (HF) diet. Twenty‐four male C57BL6/J mice were randomly divided into three groups with different diets respectively for sixteen weeks: the control group was fed a low‐fat diet and the other two groups were fed a HF diet with ACNs or not. Our results illustrated that ACNs administration at a dosage of 100 mg in 1 kg diet significantly inhibited HF diet‐induced hepatic steatosis and inflammatory cell infiltration. In addition, increase of mitochondrial swelling, decrease of mitochondrial content and damage of mitochondrial biogenesis, oxidative phosphorylation and β‐oxidation were observed in mice fed with a HF diet, which were significantly normalized through ACNs supplementation. This appears to be attributed to activation of phosphorylated AMP‐activated protein kinase (p‐AMPK) and its downstream peroxisome proliferator‐activated receptor‐gamma coactivator‐1α (PGC‐1α). Our work presents the beneficial effects of ACNs on mitochondrial dysfunction in HF‐induced NAFLD mice by promoting activation of AMPK/PGC1α signaling axis, signifying that ACNs may be a useful nutrient for the treatment of NAFLD.All animal procedures were approved by the Animal Care and Protection Committee of Sun Yat‐Sen University (2013–10).Support or Funding InformationThis research was funded by grants from the National Basic Research Program (973 Program, 2012CB517506) and the National Nature Science Foundation (81172655, 81372994).