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-Ia (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-γ coactivator-1α (PGC-1α) 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-α (PPAR-α), sirtuin-1 (SIRT1), hepatocyte nuclear factor receptor-4α (HNF-4α), and PGC-1α mRNA levels were also analyzed. Serum insulin was quantified.
Results: Resveratrol decreased liver fat accumulation, increased CPT-Ia and ACO, and decreased ACC activities. Other lipogenic enzymes, FAS, ME, and G6PDH were not modified. The polyphenol activated AMPK and PGC-1α. The expression of SRBP-1c, PPAR-α, SIRT1, PGC-1α, HNF-4α, 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.
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