Department of Psychosomatic Medicine and Psychotherapy, Medical University Hospital Tübingen, Osianderstr. 5, 72076, Tübingen, Germany.
Centre of Excellence for Eating Disorders (KOMET), Osianderstr. 5, 72076, Tübingen, Germany.
Clin Epigenetics. 2022 Aug 30;14(1):108. doi: 10.1186/s13148-022-01318-3.
The neuropeptide oxytocin (OXT) plays a role in the regulation of eating behavior and metabolism. OXT functioning is altered in patients with eating and weight disorders, and a variant of the oxytocin receptor gene (OXTR) has been associated with impulsive eating behavior as it is seen in patients with binge eating disorder (BED). Gene × environment interactions could play a role in BED. One mechanism mediating this interaction is the epigenetic alteration of gene expression. We therefore investigated if DNA methylation of the OXTR differs between individuals with obesity depending on a comorbid BED. We analyzed DNA methylation of the OXTR in peripheral blood of 227 individuals on the obesity spectrum (mean age: 40.3 ± 13.1 yrs; mean BMI: 38.6 ± 7.3 kg/m), 130 of which were diagnosed with BED.
There were no overall differences in OXTR methylation between participants with and those without BED (p > 0.05), while both subgroups were comparable regarding age and body mass index (BMI), but significantly differed in sex distribution (p = 0.035). We found no relationship between mean DNA methylation and BMI or self-reported eating disorder (ED) pathology. Analyzing potential sex differences revealed a significantly lower OXTR DNA methylation in male participants with BED as compared to those without BED (p = 0.017). No such difference was found in the female subsample (p > 0.05).
Clinically significant binge eating pathology might be associated with lower OXTR DNA methylation exclusively in males. The differential DNA methylation of OXTR in males with BED supports the view that BED represents a phenotype within the obesity spectrum that is characterized by specific vulnerability factors. A better understanding of the epigenetic underpinnings of the OXT system might contribute to the refinement of OXT administration approaches as potential interventions in eating and weight disorders.
神经肽催产素（OXT）在调节进食行为和代谢方面发挥作用。患有饮食和体重障碍的患者的 OXT 功能发生改变，并且催产素受体基因（OXTR）的变体与冲动性进食行为有关，因为它见于暴食障碍（BED）患者。基因与环境的相互作用可能在 BED 中起作用。一种介导这种相互作用的机制是基因表达的表观遗传改变。因此，我们研究了肥胖个体中 OXTR 的 DNA 甲基化是否因并发 BED 而不同。我们分析了 227 名肥胖患者（平均年龄：40.3±13.1 岁；平均 BMI：38.6±7.3 kg/m）和 130 名患有 BED 的个体外周血中的 OXTR DNA 甲基化。
患有 BED 和不患有 BED 的参与者之间的 OXTR 甲基化没有总体差异（p>0.05），而这两个亚组在年龄和体重指数（BMI）方面具有可比性，但在性别分布方面存在显著差异（p=0.035）。我们没有发现平均 DNA 甲基化与 BMI 或自我报告的饮食障碍（ED）病理之间的关系。分析潜在的性别差异表明，患有 BED 的男性参与者的 OXTR DNA 甲基化明显低于不患有 BED 的男性参与者（p=0.017）。在女性亚组中没有发现这种差异（p>0.05）。
临床上显著的暴食病理可能与男性 OXTR DNA 甲基化水平降低有关。患有 BED 的男性中 OXTR 的差异 DNA 甲基化支持这样一种观点，即 BED 是肥胖谱系中的一种表型，其特征是存在特定的脆弱性因素。对 OXT 系统的表观遗传基础有更深入的了解可能有助于完善 OXT 给药方法，作为饮食和体重障碍的潜在干预措施。
