Hepatic lipid metabolic pathways modified by resveratrol in rats fed an obesogenic diet

Objective: The scientific community is on the look-out for safe biomolecules useful in the prevention of obesity and related aberrations such as fatty liver. This study analyzed the influence of resveratrol on hepatic triacylglycerol metabolism. Methods: Male Sprague-Dawley rats were divided into control and resveratrol-treated groups (30 mg/kg of body weight per day) and fed a commercial obesogenic diet for 6 wk. Liver triacylglycerol content and the activity of carnitine palmitoyl transferase-la (CPT-Ia), acyl-coenzyme A oxydase (ACO), fatty acid synthase (FAS), glucose-6-phosphate dehydrogenase (G6PDH), malic enzyme (ME), acetyl-coenzyme A carboxylase (ACC), adenosine monophosphate-activated protein kinase (AMPK), and peroxisome proliferator-activated receptor-gamma coactivator-1 alpha (PGC-1 alpha) activation were measured. Mitochondrial protein cytochrome C oxidase subunit 2 (COXII), mitochondrial transcription factor A (TFAM), sterol regulatory element-binding protein-1c (SREBP-1c), peroxisome proliferator-activated receptor-alpha (PPAR-alpha), sirtuin-1 (SIRT1), hepatocyte nuclear factor receptor-4 alpha (HNF-4 alpha), and PGC-1 alpha mRNA levels were also analyzed. Serum insulin was quantified. Results: Resveratrol decreased liver fat accumulation, increased CPT-I alpha and ACO, and decreased ACC activities. Other lipogenic enzymes, FAS, ME, and G6PDH were not modified. The polyphenol activated AMPK and PGC-1 alpha. The expression of SRBP-1c, PPAR-alpha, SIRT1, PGC-1 alpha, HNF-4 alpha, TFAM, and COXII was not modified. No changes in serum insulin levels were observed. Conclusion: Resveratrol partly prevents the increase in liver fat accumulation induced by high-fat high-sucrose feeding by increasing fatty acid oxidation and decreasing lipogenesis. These effects are mediated by the activation of the AMPK/SIRT1 axis. (C) 2013 Elsevier Inc. All rights reserved.