OBJECTIVES: The pathophysiological mechanisms underlying binge eating disorder are poorly understood. Evidence exists for the fact that abnormalities in peptides involved in the regulation of appetite, including ghrelin, may play a role in binge eating behavior. Genes involved in the ghrelin physiology may therefore contribute to the biological vulnerability to binge eating disorder. METHODS: We examined whether two polymorphisms of the ghrelin gene, the G152A (Arg51Gln) and C214A (Leu72Met), were associated with binge eating disorder. Ninety obese or nonobese women with binge eating disorder and 119 normal weight women were genotyped at the ghrelin gene. RESULTS: Statistical analyses showed that the Leu72Met ghrelin gene variant was significantly more frequent in binge eating disorder patients (chi2=5.940; d.f.=1, P=0.01) and was associated with a moderate, but significant risk to develop binge eating disorder (odds ratio=2.725, 95% confidence interval: 1.168-6.350). CONCLUSIONS: Although these data should be regarded as preliminary because of the small sample size, they suggest that the Leu72Met ghrelin gene variant may contribute to the genetic susceptibility to binge eating disorder.
OBJECTIVES: The pathophysiological mechanisms underlying binge eating disorder are poorly understood. Evidence exists for the fact that abnormalities in peptides involved in the regulation of appetite, including ghrelin, may play a role in binge eating behavior. Genes involved in the ghrelin physiology may therefore contribute to the biological vulnerability to binge eating disorder. METHODS: We examined whether two polymorphisms of the ghrelin gene, the G152A (Arg51Gln) and C214A (Leu72Met), were associated with binge eating disorder. Ninety obese or nonobese women with binge eating disorder and 119 normal weight women were genotyped at the ghrelin gene. RESULTS: Statistical analyses showed that the Leu72Met ghrelin gene variant was significantly more frequent in binge eating disorderpatients (chi2=5.940; d.f.=1, P=0.01) and was associated with a moderate, but significant risk to develop binge eating disorder (odds ratio=2.725, 95% confidence interval: 1.168-6.350). CONCLUSIONS: Although these data should be regarded as preliminary because of the small sample size, they suggest that the Leu72Met ghrelin gene variant may contribute to the genetic susceptibility to binge eating disorder.
Authors: Sebastian Cardona Cano; Myrte Merkestein; Karolina P Skibicka; Suzanne L Dickson; Roger A H Adan Journal: CNS Drugs Date: 2012-04-01 Impact factor: 5.749
Authors: Lorenzo Leggio; Anna Ferrulli; Silvia Cardone; Antonio Nesci; Antonio Miceli; Noemi Malandrino; Esmeralda Capristo; Benedetta Canestrelli; Palmiero Monteleone; George A Kenna; Robert M Swift; Giovanni Addolorato Journal: Addict Biol Date: 2011-03-11 Impact factor: 4.280
Authors: Zeynep Yilmaz; Allan S Kaplan; Arun K Tiwari; Robert D Levitan; Sara Piran; Andrew W Bergen; Walter H Kaye; Hakon Hakonarson; Kai Wang; Wade H Berrettini; Harry A Brandt; Cynthia M Bulik; Steven Crawford; Scott Crow; Manfred M Fichter; Katherine A Halmi; Craig L Johnson; Pamela K Keel; Kelly L Klump; Pierre Magistretti; James E Mitchell; Michael Strober; Laura M Thornton; Janet Treasure; D Blake Woodside; Joanne Knight; James L Kennedy Journal: J Psychiatr Res Date: 2014-04-16 Impact factor: 4.791