Genomics of Psychiatric and Neurodegenerative Diseases Laboratory, National Institute of Genomic Medicine (INMEGEN), Mexico City 01090, Mexico.
Biomedical Postgraduate Program, Academic Division of Health Sciences, Juárez Autonomous University of Tabasco, Villahermosa 86000, Mexico.
Nutrients. 2021 Apr 22;13(5):1413. doi: 10.3390/nu13051413.
Binge-eating disorder, recently accepted as a diagnostic category, is differentiated from bulimia nervosa in that the former shows the presence of binge-eating episodes and the absence of compensatory behavior. Epigenetics is a conjunct of mechanisms (like DNA methylation) that regulate gene expression, which are dependent on environmental changes. Analysis of DNA methylation in eating disorders shows that it is reduced. The present study aimed to analyze the genome-wide DNA methylation differences between individuals diagnosed with BED and BN. A total of 46 individuals were analyzed using the Infinium Methylation EPIC array. We found 11 differentially methylated sites between BED- and BN-diagnosed individuals, with genome-wide significance. Most of the associations were found in genes related to metabolic processes ( and ), which are hypomethylated genes in BED. Cg04781532, located in the body of the gene (protein kinase AMP-activated non-catalytic subunit gamma 2), was hypomethylated in individuals with BED. Agonists of PRKAG2, which is the subunit of AMPK (AMP-activated protein kinase), are proposed to treat obesity, BED, and BN. The present study contributes important insights into the effect that BED could have on activation.
暴食障碍,最近被接受为一种诊断类别,与神经性贪食症不同,前者表现为暴食发作和没有补偿行为。表观遗传学是一种调节基因表达的机制(如 DNA 甲基化)的结合体,这些机制依赖于环境变化。对饮食失调症的 DNA 甲基化分析表明,其甲基化减少。本研究旨在分析诊断为 BED 和 BN 的个体之间全基因组 DNA 甲基化差异。使用 Infinium Methylation EPIC 阵列分析了总共 46 名个体。我们发现了 11 个在 BED 和 BN 诊断个体之间差异甲基化的位点,具有全基因组意义。大多数关联发生在与代谢过程相关的基因(和)中,这些基因在 BED 中是低甲基化的基因。位于基因(蛋白激酶 AMP 激活非催化亚基 γ2)主体内的 Cg04781532 在 BED 个体中呈低甲基化。PRKAG2 的激动剂,即 AMPK(AMP 激活蛋白激酶)的亚基,被提议用于治疗肥胖症、BED 和 BN。本研究为 BED 对 AMP 激活的影响提供了重要的见解。