title: Association of ghrelin receptor gene polymorphism with bulimia nervosa in a Japanese population.
abstract: Eating disorders (EDs) have a highly heterogeneous etiology and multiple genetic factors might contribute to their pathogenesis. Ghrelin, a novel growth hormone-releasing peptide, enhances appetite and increases food intake, and human ghrelin plasma levels are inversely correlated with body mass index. In the present study, we examined the 171T/C polymorphism of the ghrelin receptor (growth hormone secretagogue receptor, GHSR) gene in patients diagnosed with EDs, because the subjects having ghrelin gene polymorphism (Leu72Met) was not detected in a Japanese population, previously. In addition, beta3 adrenergic receptor gene polymorphism (Try64Arg) and cholecystokinin (CCK)-A receptor (R) gene polymorphism (-81A/G, -128G/T), which are both associated with obesity, were investigated. The subjects consisted of 228 Japanese patients with EDs [96 anorexia nervosa (AN), 116 bulimia nervosa (BN) and 16 not otherwise specified (NOS)]. The age- and gender-matched control group consisted of 284 unrelated Japanese subjects. The frequency of the CC type of the GHSR gene was significantly higher in BN subjects than in control subjects (chi(2) = 4.47, p = 0.035, odds ratio = 2.05, Bonferroni correction: p = 0.070), while the frequency in AN subjects was not different from that in controls. The distribution of neither beta3 adrenergic receptor gene nor CCK-AR polymorphism differed between EDs and control subjects. Therefore, the CC type of GHSR gene polymorphism (171T/C) is a risk factor for BN, but not for AN.
authors.affiliation: Department of Clinical Physiology, Tokyo Metropolitan Institute of Gerontology, Tokyo, Japan. miyasaka@tmig.or.jp
authors.forename: K
authors.initials: K
authors.lastname: Miyasaka
authors.forename: H
authors.initials: H
authors.lastname: Hosoya
authors.forename: A
authors.initials: A
authors.lastname: Sekime
authors.forename: M
authors.initials: M
authors.lastname: Ohta
authors.forename: H
authors.initials: H
authors.lastname: Amono
authors.forename: S
authors.initials: S
authors.lastname: Matsushita
authors.forename: K
authors.initials: K
authors.lastname: Suzuki
authors.forename: S
authors.initials: S
authors.lastname: Higuchi
authors.forename: A
authors.initials: A
authors.lastname: Funakoshi
mesh_terms: D000328:Adult; D000368:Aged; D015992:Body Mass Index; D052018:Bulimia Nervosa / Q000453:epidemiology / Q000235:genetics* / Q000523:psychology; D002766:Cholecystokinin / Q000235:genetics / Q000502:physiology; D004247:DNA / Q000235:genetics; D001068:Feeding and Eating Disorders / Q000235:genetics; D005260:Female; D005838:Genotype; D006801:Humans; D007564:Japan / Q000453:epidemiology; D008297:Male; D008875:Middle Aged; D016584:Panic Disorder / Q000235:genetics; D020641:Polymorphism, Single Nucleotide / Q000235:genetics*; D022702:Receptors, Adrenergic, beta-3 / Q000187:drug effects / Q000235:genetics; D011949:Receptors, Cholecystokinin / Q000235:genetics / Q000502:physiology; D043562:Receptors, G-Protein-Coupled / Q000235:genetics*; D054440:Receptors, Ghrelin; D020133:Reverse Transcriptase Polymerase Chain Reaction; D012307:Risk Factors
chemical_list: D022702:Receptors, Adrenergic, beta-3; D011949:Receptors, Cholecystokinin; D043562:Receptors, G-Protein-Coupled; D054440:Receptors, Ghrelin; D004247:DNA; D002766:Cholecystokinin