Methylation of the glucocorticoid receptor gene promoter in bulimic women: associations with borderline personality disorder, suicidality, and exposure to childhood abuse.
Methylation of the glucocorticoid receptor gene promoter in bulimic women: associations with borderline personality disorder, suicidality, and exposure to childhood abuse.
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DOI：
10.1002/eat.22113
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发表时间：
2013-04
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影响因子：
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通讯作者：
H. Steiger;B. Labonté;P. Groleau;G. Turecki;Mimi Israel
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文献类型：
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作者：
H. Steiger;B. Labonté;P. Groleau;G. Turecki;Mimi Israel
目的比较神经性贪食症（BN）女性和无进食障碍（ED）女性的糖皮质激素受体（GR）基因（NR3C1）启动子甲基化水平，并探讨BN女性中GR基因启动子甲基化在多大程度上与儿童虐待、自杀或边缘性人格障碍（BPD）相关。方法：我们使用从64名BN女性（32名有严重儿童期虐待史，32名没有儿童期虐待史）和32名没有ED或儿童期虐待史的女性的淋巴细胞中获得的DNA，测量了选定的NR3C1启动子区域的甲基化水平。结果：与无饮食失调的女性相比，患有BN和合并BPD（或有自杀史的BN）的女性特异性外显子1C位点的甲基化显著增加。还有一个（不显著的）结果表明，与没有ED的女性相比，BN女性的一些1C位点的甲基化程度更高。没有观察到童年虐待造成的类似影响。我们的研究结果将BN（当伴有BPD或自杀倾向时）与某些GR外显子1C启动子位点的超甲基化联系起来。我们讨论了我们的发现的理论和临床意义。
OBJECTIVE To compare levels of methylation of the glucocorticoid receptor (GR) gene (NR3C1) promoter between women with bulimia nervosa (BN) and women with no eating disorder (ED), and also to explore, in women with BN, the extent to which methylation of the GR gene promoter corresponds to childhood abuse, suicidality, or borderline personality disorder (BPD). METHOD We measured methylation levels in selected NR3C1 promoter regions using DNA obtained from lymphocytes in 64 women with BN (32 selected as having a history of severe childhood abuse and 32 selected as having no such history) and 32 comparison women with no ED or history of childhood abuse. RESULTS Compared to noneating disordered women, women with BN and comorbid BPD (or BN with a history of suicidality) showed significantly more methylation of specific exon 1C sites. There was also a (nonsignificant) result indicative of greater methylation in some 1C sites among women with BN, when compared (as a group) to women with no ED. No parallel effects owing to childhood abuse were observed. DISCUSSION Our findings associate BN (when accompanied by BPD or suicidality) with hypermethylation of certain GR exon 1C promoter sites. We discuss theoretical and clinical implications of our findings.