Beschreibung:
<jats:title>Abstract</jats:title><jats:sec>
<jats:title>Background</jats:title>
<jats:p>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 <jats:italic>OXTR</jats:italic> differs between individuals with obesity depending on a comorbid BED. We analyzed DNA methylation of the <jats:italic>OXTR</jats:italic> 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<jats:sup>2</jats:sup>), 130 of which were diagnosed with BED.
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<jats:title>Results</jats:title>
<jats:p>There were no overall differences in <jats:italic>OXTR</jats:italic> methylation between participants with and those without BED (<jats:italic>p</jats:italic> > 0.05), while both subgroups were comparable regarding age and body mass index (BMI), but significantly differed in sex distribution (<jats:italic>p</jats:italic> = 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 <jats:italic>OXTR</jats:italic> DNA methylation in male participants with BED as compared to those without BED (<jats:italic>p</jats:italic> = 0.017). No such difference was found in the female subsample (<jats:italic>p</jats:italic> > 0.05).
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<jats:title>Conclusions</jats:title>
<jats:p>Clinically significant binge eating pathology might be associated with lower <jats:italic>OXTR</jats:italic> DNA methylation exclusively in males. The differential DNA methylation of <jats:italic>OXTR</jats:italic> 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.</jats:p>
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