Laboratorio de Genómica de Enfermedades Psiquiátricas y Neurodegenerativas, Instituto Nacional de Medicina Genómica, CDMX, México; Hospital Psiquiátrico Infantil "Juan N. Navarro" Servicios de Administración Psiquiátrica, CDMX, México; División Académica de Ciencias de la Salud, Universidad Juárez Autónoma de Tabasco, Villahermosa, Tabasco, México.
Laboratorio de Genómica de Enfermedades Psiquiátricas y Neurodegenerativas, Instituto Nacional de Medicina Genómica, CDMX, México; División Académica Multidisciplinaria de Jalpa de Méndez, Universidad Juárez Autónoma de Tabasco, Jalpa de Méndez, Tabasco, México; División Académica de Ciencias de la Salud, Universidad Juárez Autónoma de Tabasco, Villahermosa, Tabasco, México.
Psychiatry Res. 2020 Sep;291:113270. doi: 10.1016/j.psychres.2020.113270. Epub 2020 Jul 2.
Eating disorders (ED) are characterized by disruption of eating behaviour and alteration of food intake. Leptin, is one of the main hormones that modulate food intake and are altered in individuals diagnosed with ED. Genetic risk variants for obesity, like those reported inFTO and ABCA1, have also been associated to ED disorders. The present study aimed to analysed leptin circulating levels and the interaction between obesity-risk variants in FTO and ABCA1, in adolescents diagnosed with ED. A total of 99 individuals diagnosed with ED were genotype using Taqman probes for FTO (rs9939609) and ABCA1 (p.Arg230Cys, rs9282541). Commercial enzyme-linked immunosorbent assays were utilized to determined circulating leptin. Differences in leptin concentration were analysed by t-Student or ANOVA test. Gene-gene interaction were analysed using general estimation equations. Circulating leptin levels differed between the three diagnostic groups, lead by individuals diagnosed with binge eating-disorder. In individuals with more than 3 of episodes of binge-eating per week having the highest leptin levels. Also, we found that carriers of both risk alleles had the highest leptin levels. Our observations found an interaction between FTO rs9969609 and the native American-origin ABCA1 p.Arg230Cys to modulate circulating leptin levels in Mexican adolescents diagnosed with eating-disorders.
饮食失调(ED)的特征是饮食行为紊乱和食物摄入改变。瘦素是调节食物摄入的主要激素之一,在被诊断患有 ED 的个体中发生改变。肥胖的遗传风险变体,如在 FTO 和 ABCA1 中报告的那些,也与 ED 障碍有关。本研究旨在分析患有 ED 的青少年的循环瘦素水平和 FTO 与 ABCA1 中肥胖风险变体之间的相互作用。共有 99 名被诊断患有 ED 的个体使用 Taqman 探针对 FTO(rs9939609)和 ABCA1(p.Arg230Cys, rs9282541)进行了基因分型。商业酶联免疫吸附试验用于测定循环瘦素。使用 t-Student 或 ANOVA 检验分析瘦素浓度的差异。使用一般估计方程分析基因-基因相互作用。循环瘦素水平在三种诊断组之间存在差异,以暴食障碍患者为最高。此外,我们发现每周暴食发作次数超过 3 次的个体具有最高的瘦素水平。我们还发现,FTO rs9969609 和美洲原住民起源的 ABCA1 p.Arg230Cys 之间存在相互作用,可调节墨西哥被诊断患有饮食障碍的青少年的循环瘦素水平。