Ando Tetsuya, Komaki Gen, Nishimura Hiroki, Naruo Tetsuro, Okabe Kenjiro, Kawai Keisuke, Takii Masato, Oka Takakazu, Kodama Naoki, Nakamoto Chiemi, Ishikawa Toshio, Suzuki-Hotta Mari, Minatozaki Kazunori, Yamaguchi Chikara, Nishizono-Maher Aya, Kono Masaki, Kajiwara Sohei, Suematsu Hiroyuki, Tomita Yuichiro, Ebana Shoichi, Okamoto Yuri, Nagata Katsutaro, Nakai Yoshikatsu, Koide Masanori, Kobayashi Nobuyuki, Kurokawa Nobuo, Nagata Toshihiko, Kiriike Nobuo, Takenaka Yoshito, Nagamine Kiyohide, Ookuma Kazuyoshi, Murata Shiho
Department of Psychosomatic Research, National Institute of Mental Health, National Center of Neurology and Psychiatry, Kodaira, Tokyo, Japan.
Psychiatr Genet. 2010 Aug;20(4):153-9. doi: 10.1097/YPG.0b013e32833a1f0e.
Patients with anorexia nervosa restricting type (AN-R) often develop bulimic symptoms and crossover to AN-binge eating/purging type (AN-BP), or to bulimia nervosa (BN). We have reported earlier that genetic variants of an orexigenic peptide ghrelin are associated with BN. Here, the relationship between a ghrelin gene variant and the rate of change from AN-R to other phenotypes of eating disorders (EDs) was investigated.
Participants were 165 patients with ED, initially diagnosed as AN-R. The dates of their AN-R onset and changes in diagnosis to other subtypes of ED were investigated retrospectively. Ghrelin gene 3056 T-->C SNP (single nucleotide polymorphism) was genotyped. Probability and hazard ratios were analyzed using life table analysis and Cox's proportional hazard regression model, in which the starting point was the time of AN-R onset and the outcome events were the time of (i) onset of binge eating, that is, when patients changed to binge eating AN and BN and (ii) recovery of normal weight, that is, when patients changed to BN or remission.
Patients with the TT genotype at 3056 T-->C had a higher probability and hazard ratio for recovery of normal weight. The ghrelin SNP was not related with the onset of binge eating.
The 3056 T-->C SNP of the ghrelin gene is related to the probability and the rate of recovery of normal body weight from restricting-type AN.
神经性厌食症限制型(AN-R)患者常出现贪食症状,并转变为神经性厌食症暴饮暴食/清除型(AN-BP)或神经性贪食症(BN)。我们之前报道过,促食欲肽胃饥饿素的基因变异与BN有关。在此,我们研究了胃饥饿素基因变异与从AN-R转变为其他饮食失调(ED)表型的变化率之间的关系。
研究对象为165例最初被诊断为AN-R的ED患者。回顾性调查他们AN-R发病日期以及诊断转变为其他ED亚型的情况。对胃饥饿素基因3056 T→C单核苷酸多态性(SNP)进行基因分型。使用生命表分析和Cox比例风险回归模型分析概率和风险比,其中起点为AN-R发病时间,结局事件为(i)暴饮暴食发作时间,即患者转变为暴饮暴食型AN和BN的时间,以及(ii)体重恢复正常时间,即患者转变为BN或缓解的时间。
3056 T→C位点为TT基因型的患者体重恢复正常的概率和风险比更高。胃饥饿素SNP与暴饮暴食发作无关。
胃饥饿素基因的3056 T→C SNP与限制型AN患者体重恢复正常的概率和速率有关。