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Background  The growth hormone secretagogue receptor (GHSR) is mediating hunger sensation when stimulated by its natural ligand ghrelin. In the present study, we tested the hypothesis that common and rare variation in the  GHSR  locus are related to increased prevalence of obesity and overweight among Whites.    Methodology/Principal Findings  In a population-based study sample of 15,854 unrelated, middle-aged Danes, seven variants were genotyped to capture common variation in an 11 kbp region including  GHSR . These were investigated for their individual and haplotypic association with obesity. None of these analyses revealed consistent association with measures of obesity. A -151C/T promoter mutation in the  GHSR  was found in two unrelated obese patients. One family presented with complete co-segregation, but the other with incomplete co-segregation. The mutation resulted in an increased transcriptional activity (p<0.02) and introduction of a specific binding for Sp-1-like nuclear extracts relative to the wild type. The -151C/T mutation was genotyped in the 15,854 Danes with a minor allele frequency of 0.01%. No association with obesity in carriers (mean BMI: 27±4 kg/m 2 )  versus  non-carriers (mean BMI: 28±5 kg/m 2 ) (p>0.05) could be shown.    Conclusions/Significance  In a population-based study sample of 15,854 Danes no association between  GHSR  genotypes and measures of obesity and overweight was found. Also, analyses of  GHSR  haplotypes lack consistent associations with obesity related traits. A rare functional  GHSR  promoter mutation variant was identified, yet there was no consistent relationship with obesity in neither family- nor population-based studies.

Family and Population-Based Studies of Variation within the Ghrelin Receptor Locus in Relation to Measures of Obesity