Department of Medical & Surgical Therapeutics Division of Pharmacology Medical School University of Extremadura Badajoz Spain.
Service of Clinical Analyses General University Hospital Valencia Spain.
Brain Behav. 2017 Jul 27;7(9):e00784. doi: 10.1002/brb3.784. eCollection 2017 Sep.
and are obesity-related genes that interact to regulate feeding behavior. We hypothesize that variability in these loci, isolated or in combination, could also be related to the risk of eating disorders (ED) and/or associated psychological traits.
We screened 425 participants (169 ED patients, 75 obese subjects, and 181 controls) for 10 clinically relevant and tag single-nucleotide polymorphisms (SNPs) in and by the Sequenom MassARRAY platform and direct sequencing. Psychometric evaluation was performed with EDI-2 and SCL-90R inventories.
The rs287103 T variant allele was associated with increased risk of bulimia nervosa (BN) (OR = 4.34 [1.47-29.52]; = .003) and with scores of psychopathological scales of these patients. Haplotype in was more frequent in controls (OR = 0.40 [0.20-0.80], = .009 for anorexia nervosa), while haplotype in affected all three scales of the SCL-90R inventory in BN patients ( ≤ .01). Epistasis analyses revealed relevant interactions with body mass index of BN patients ( < .001). Genetic profiles in obese patients did not significantly differ from those found in ED patients.
This is the first study that evaluates the combined role of and genes in ED. Our preliminary findings suggest that the interaction of genetic variability in these loci could influence the risk for ED and/or anthropometric and psychological parameters.
和 是与肥胖相关的基因,它们相互作用调节进食行为。我们假设这些基因座的变异性,无论是单独还是组合,也可能与饮食失调(ED)的风险和/或相关的心理特征有关。
我们通过 Sequenom MassARRAY 平台和直接测序筛选了 425 名参与者(169 名 ED 患者、75 名肥胖患者和 181 名对照),以检测 10 个临床相关和标签单核苷酸多态性(SNP)。使用 EDI-2 和 SCL-90R 量表进行心理计量评估。
中的 rs287103 T 变体等位基因与神经性贪食症(BN)的风险增加相关(OR=4.34[1.47-29.52];=0.003),并与这些患者的心理病理量表评分相关。 中的单倍型 在对照组中更为常见(OR=0.40[0.20-0.80],=0.009 用于神经性厌食症),而 中的单倍型 则影响 BN 患者 SCL-90R 量表的所有三个维度( ≤ 0.01)。上位性分析显示与 BN 患者的体重指数有显著的相互作用( < 0.001)。肥胖患者的遗传特征与 ED 患者的遗传特征没有显著差异。
这是首次评估 和 基因在 ED 中的联合作用的研究。我们的初步研究结果表明,这些基因座遗传变异性的相互作用可能影响 ED 和/或人体测量和心理参数的风险。