Abstract

Fish are carbohydrates-intolerant, thus generally exhibiting metabolic disorders and mitochondrial dysfunctions to high-carbohydrate (HC) diets. Benfotiamine is a lipid-soluble derivative of vitamin B 1 , which can reduce oxidative stress , improve the function of glycolysis, and play a high biological effect, while the underlying mechanisms still remains unclear. This study aimed to investigate the effects of benfotiamine on the mitochondrial oxidative stress of carp Megalobrama amblycephala subjected to HC treatment both in vivo and in vitro. In vivo, fish were randomly fed a control diet , a HC diet, and a HC diet supplemented with benfotiamine respectively for 12 weeks. In the first vitro study, primary hepatocytes were cultured with media, high-glucose (HG), and HG supplemented with benfotiamine, respectively. In the second vitro study, hepatocytes were treated by media, vehicle, HG, HG +  honokiol (the agonist of SIRT3), respectively. HC/HG induced mitochondrial oxidative stress of fish, as was evidenced by the increased ROS and MDA contents coupled with the decreased CAT , GSH-Px and MnSOD activities, and the decreased SIRT3 and SOD 2 contents. However, benfotiamine supplementation exhibited opposite effects, as also held true after the treatment of honokiol. Overall, the results suggested that benfotiamine could alleviate the mitochondrial oxidative stress of fish subjected to HG/HC treatment by activating SIRT3.