CONTEXT: Mature ghrelin has been shown to stimulate eating and to participate in the regulation of insulin signaling and glucose homeostasis. Its gene, GHRL, is located on chromosome 3 in a region where we have shown linkage to eating behavior, percentage body fat, and total and low-density lipoprotein cholesterol levels in subjects of the Amish Family Diabetes Study. OBJECTIVE: Our objective was to determine whether mutations in GHRL might influence eating behavior and risk for metabolic syndrome, obesity, diabetes, and related traits. DESIGN: We genotyped 856 Amish samples for three missense polymorphisms in GHRL, Arg51Gln, Leu72Met (rs696217), and Gln90Leu (rs4684677) and performed association analyses with eating behavior traits and metabolic syndrome as defined by the National Cholesterol Education Program Adult Treatment Panel III guidelines. SUBJECTS: Our subjects were adult participants in the Amish Family Diabetes Study. RESULTS: The allele frequencies of these variants were 0.03, 0.04, and 0.03, respectively. The prevalence of metabolic syndrome was lower among those carrying the 51Gln allele (3.8 vs. 15.8%; age- and sex-adjusted odds ratio = 0.22; P = 0.031). Hunger scores tended to be lower among 51Gln allele carriers but did not reach statistical significance (P = 0.07). The Leu72Met variant was also associated with increased prevalence of metabolic syndrome (23.2 vs. 13.4%; age- and sex-adjusted odds ratio = 2.57; P = 0.02) as well as higher fasting glucose, lower high-density lipoprotein, and higher triglyceride levels (P = 0.02, P = 0.007, and P = 0.04, respectively). The two variants were not in linkage disequilibrium with each other, suggesting independent effects. We conclude that mutations in GHRL may confer risk for the metabolic syndrome.
CONTEXT: Mature ghrelin has been shown to stimulate eating and to participate in the regulation of insulin signaling and glucose homeostasis. Its gene, GHRL, is located on chromosome 3 in a region where we have shown linkage to eating behavior, percentage body fat, and total and low-density lipoprotein cholesterol levels in subjects of the Amish Family Diabetes Study. OBJECTIVE: Our objective was to determine whether mutations in GHRL might influence eating behavior and risk for metabolic syndrome, obesity, diabetes, and related traits. DESIGN: We genotyped 856 Amish samples for three missense polymorphisms in GHRL, Arg51Gln, Leu72Met (rs696217), and Gln90Leu (rs4684677) and performed association analyses with eating behavior traits and metabolic syndrome as defined by the National Cholesterol Education Program Adult Treatment Panel III guidelines. SUBJECTS: Our subjects were adult participants in the Amish Family Diabetes Study. RESULTS: The allele frequencies of these variants were 0.03, 0.04, and 0.03, respectively. The prevalence of metabolic syndrome was lower among those carrying the 51Gln allele (3.8 vs. 15.8%; age- and sex-adjusted odds ratio = 0.22; P = 0.031). Hunger scores tended to be lower among 51Gln allele carriers but did not reach statistical significance (P = 0.07). The Leu72Met variant was also associated with increased prevalence of metabolic syndrome (23.2 vs. 13.4%; age- and sex-adjusted odds ratio = 2.57; P = 0.02) as well as higher fasting glucose, lower high-density lipoprotein, and higher triglyceride levels (P = 0.02, P = 0.007, and P = 0.04, respectively). The two variants were not in linkage disequilibrium with each other, suggesting independent effects. We conclude that mutations in GHRL may confer risk for the metabolic syndrome.
Authors: Esteban L Ortega-Vega; Sandra J Guzmán-Castañeda; Omer Campo; Eliana P Velásquez-Mejía; Jacobo de la Cuesta-Zuluaga; Gabriel Bedoya; Juan S Escobar Journal: Gut Microbes Date: 2019-06-03
Authors: Wendy K Chung; Amit Patki; Naoki Matsuoka; Bert B Boyer; Nianjun Liu; Solomon K Musani; Anna V Goropashnaya; Perciliz L Tan; Nicholas Katsanis; Stephen B Johnson; Peter K Gregersen; David B Allison; Rudolph L Leibel; Hemant K Tiwari Journal: Hum Hered Date: 2008-12-15 Impact factor: 0.444
Authors: Mireia Mora; Victoria Adam; Elisabet Palomera; Sebastian Blesa; Gonzalo Díaz; Xavier Buquet; Mateu Serra-Prat; Juan Carlos Martín-Escudero; Ana Palanca; Javier Felipe Chaves; Manuel Puig-Domingo Journal: PLoS One Date: 2015-09-16 Impact factor: 3.240
Authors: Rim Hassouna; Philippe Zizzari; Odile Viltart; Seung-Kwon Yang; Robert Gardette; Catherine Videau; Emilio Badoer; Jacques Epelbaum; Virginie Tolle Journal: PLoS One Date: 2012-12-10 Impact factor: 3.240