Abstract
The potential of resveratrol to mimic beneficial effects of calorie restriction (CR) was investigated. We compared the effects of both CR (70% of ad libitum energy intake) or resveratrol (2 g/kg or 4 g/kg food) on high-fat diet-induced obesity and fatty liver formation in C57Bl/6J mice, and we examined their effects on calorimetry, metabolic performance, and the expressions of inflammatory genes and SIRT proteins. We found that resveratrol with 4 g/kg dose partially prevented hepatic steatosis and hepatocyte ballooning and induced skeletal muscle SIRT1 and SIRT4 expression while other examined parameter were unaffected by resveratrol. In contrast, CR provided superior protection against diet-induced obesity and fatty liver formation as compared to resveratrol, and the effects were associated with increased physical activity and ameliorated adipose tissue inflammation. CR increased expressions of SIRT3 in metabolically important tissues, suggesting that the beneficial effects of CR are mediated, at least in part, via SIRT3-dependent pathways.
Highlights
Obesity, the worldwide increasing problem, associates with several metabolic abnormalities and increases the risk of chronic diseases such as type 2 diabetes, cardiovascular diseases, and certain forms of cancer [1]
We compared the effects of both calorie restriction (CR) (70% of ad libitum energy intake) or resveratrol (2 g/kg or 4 g/kg food) on high-fat diet-induced obesity and fatty liver formation in C57Bl/6J mice, and we examined their effects on calorimetry, metabolic performance, and the expressions of inflammatory genes and SIRT proteins
We found that resveratrol with 4 g/kg dose partially prevented hepatic steatosis and hepatocyte ballooning and induced skeletal muscle SIRT1 and SIRT4 expression while other examined parameter were unaffected by resveratrol
Summary
The worldwide increasing problem, associates with several metabolic abnormalities and increases the risk of chronic diseases such as type 2 diabetes, cardiovascular diseases, and certain forms of cancer [1]. Obesity is the major risk factor for nonalcoholic fatty liver disease (NAFLD), a disease spectrum that includes hepatic steatosis, steatohepatitis, fibrosis, and liver cirrhosis [2, 3]. CR extends lifespan by up to 50% [7]. The mechanisms underlying the beneficial effects of CR is not well understood; accumulating evidence indicates an important role for sirtuins, a highly conserved family of NAD+-dependent enzymes regulating lifespan in lower organisms, as metabolic sensors and mediators of the cellular effects of CR [8]
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