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Background  Ghrelin may influence the development of obesity through its role in the control of energy balance, food intake, and regulation of body weight. The effects of ghrelin are mediated via the growth hormone secretagogue receptor (GHSR).    Methodology/Principal Findings  We genotyped 7 single nucleotide polymorphisms (SNPs) in the  GHSR  gene and assessed the association between those SNPs and obesity and type 2 diabetes-related phenotypes from 507 middle-aged overweight persons with impaired glucose tolerance participating in the Finnish Diabetes Prevention Study (DPS). Additionally, we performed  in silico  screening of the 5′-regulatory region of  GHSR  and evaluated SNPs disrupting putative transcription factor (TF) binding sites  in vitro  with gelshift assays to determine differences in protein binding between different alleles of SNPs. Rs9819506 in the promoter region of  GHSR  was associated with body weight (p = 0.036); persons with  rs9819506-AA  genotype having the lowest body weight. Individuals with  rs490683-CC  genotype displayed highest weight loss in the whole study population (p = 0.032). The false discovery rate for these results was <10%. Rs490683 and rs509035 were associated with several measures of glucose and insulin metabolism during the follow-up. Rs490683 may be a functional SNP, since gelshift experiments showed differential protein binding between the alleles, with higher binding to the G-allele.  Rs490683-C  may disrupt a putative binding site for the TF nuclear factor 1 (NF-1), thus  rs4906863-GG  genotype where the NF-1 site is intact may lead to a higher  GHSR  gene expression.    Conclusion/Significance  Polymorphisms in the  GHSR  promoter may modify changes in body weight during long-term lifestyle intervention and affect ghrelin receptor signalling through modulation of  GHSR  gene expression.

Variations in the Ghrelin Receptor Gene Associate with Obesity and Glucose Metabolism in Individuals with Impaired Glucose Tolerance