Epigenetic association study uncovered H3K27 acetylation enhancers and dysregulated genes in high-fat-diet-induced nonalcoholic fatty liver disease in rats.

What is this summary about? Nonalcoholic fatty liver disease (NAFLD) is a typical metabolic disease, which is becoming the most common liver disease in the world. Despite its high prevalence and morbidity, there is currently no effective diagnostic or approved therapy, and the molecular mechanisms for NAFLD have not been fully clarified, especially for epigenetics. Herein, we focused on histone modification and investigated the impact of active enhancer to explore the epigenetic regulation of NAFLD, seeking new targets for the prevention and treatment of the disease. What were the results? We identified the alteration of H3K27 acetylation and differential gene expression, enriched potential transcription-factor binding motifs and highlighted the hub risk genes of CYP8B1, PLA2G12B, SLC27A5, CYP7A1 and APOC3 in a NAFLD rat model. What do the results mean? This work emphasized the vital roles of histone modification of H3K27ac in a high-fat-diet-induced NAFLD model, which could regulate the expression of key genes and transcription factor binding motifs, and H3K27ac induced the formation of NAFLD. Targeting the H3K27ac modification, dysregulated target genes and enriched pathways may be of great importance for NAFLD prediction and prevention, and serve as a valuable resource for genome-wide studies of epigenomic regulation in lipid metabolic disease.