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Optimized Analysis of In Vivo and In Vitro Hepatic Steatosis
Published on: March 11, 2017
Hepatic lipid metabolic pathways modified by resveratrol in rats fed an obesogenic diet
Goiuri Alberdi1, Víctor M Rodríguez, M Teresa Macarulla
1Nutrition and Obesity Group, Department of Nutrition and Food Science, Faculty of Pharmacy, University of the Basque Country-UPV/EHU, Vitoria, Spain.
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.
Insights
Resveratrol helps prevent fatty liver by boosting fat burning and reducing fat creation, primarily through activating the AMPK/SIRT1 pathway. This natural compound offers a potential strategy for managing obesity-related liver issues.
Area of Science:
- Metabolic research
- Nutritional science
- Biochemistry
Background:
- Obesity and fatty liver disease are significant health concerns.
- Identifying safe biomolecules for prevention is a priority.
- Resveratrol is a natural polyphenol with potential health benefits.
Purpose of the Study:
- To investigate the effects of resveratrol on hepatic triacylglycerol metabolism.
- To determine resveratrol's impact on key enzymes involved in lipid metabolism.
- To explore the molecular mechanisms underlying resveratrol's action in preventing fatty liver.
Main Methods:
- Male Sprague-Dawley rats were fed an obesogenic diet for 6 weeks.
- Resveratrol (30 mg/kg/day) was administered to the treatment group.
- Key enzymes, protein levels, and mRNA expressions related to lipid metabolism were analyzed.
- Serum insulin was quantified.
Main Results:
- Resveratrol reduced liver fat accumulation.
- It increased fatty acid oxidation enzymes (CPT-Ia, ACO) and decreased lipogenic enzyme (ACC) activity.
- Resveratrol activated AMPK and PGC-1α.
- No significant changes were observed in other lipogenic enzymes, specific gene expressions, or serum insulin levels.
Conclusions:
- Resveratrol partially prevents high-fat, high-sucrose diet-induced fatty liver.
- This prevention is achieved by enhancing fatty acid oxidation and reducing lipogenesis.
- The effects are mediated by the activation of the AMPK/SIRT1 signaling pathway.
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