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Medical AI Inquiry: You was designed to assist in medical decision-making based on the provided user questions. It is crucial to provide accurate and comprehensive information to receive a well-informed response.  Labels: METHODS, METHODS, RESULTS. Meshes: Acetylation, Animals, Apolipoprotein A-V, Biflavonoids, Catechin, Dose-Response Relationship, Drug, Fibroblast Growth Factors, Grape Seed Extract, Histone Deacetylase 2, Histone Deacetylase Inhibitors, Histone Deacetylases, Histones, Lipid Metabolism, Liver, Male, Mice, Inbred C57BL, PPAR alpha, Phosphorylation, Proanthocyanidins, Triglycerides.
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Does a grape seed procyanidin extract inhibit HDAC activity leading to increased Pparα phosphorylation and target-gene expression? Context: Histone deacetylases (HDACs) have emerged as epigenetic regulators of risk factors associated with the metabolic syndrome (MetS), and certain botanical extracts have proven to be potent HDAC inhibitors. Understanding the role of dietary procyanidins in HDAC inhibition is important in exploring the therapeutic potential of natural products. C57BL/6 mice were gavaged with vehicle (water) or grape seed procyanidin extract (GSPE, 250 mg/kg) and terminated 14 h later. Liver and serum were harvested to assess the effect of GSPE on HDAC activity, histone acetylation, Pparα activity and target-gene expression, and serum lipid levels. GSPE increased histone acetylation and decreased Class I HDAC activity in vivo, and dose-dependently inhibited recombinant HDAC2 and 3 activities in vitro. Accordingly, Pparα gene and phosphorylated protein expression were increased, as were target genes involved in fatty acid catabolism, suggesting increased Pparα activity. Serum fibroblast growth factor 21 (Fgf21) was elevated, and triglyceride levels were reduced by 28%.
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GSPE regulates HDAC and Pparα activities to modulate lipid catabolism and reduce serum triglycerides in vivo. Final Decision: yes