offspring (p = 0.076). Taken together, these results suggest an association of the G-allele of rs1800437 with obesity. If a dysfunctional GIPR receptor leads to a lower fat mass we have to assume that obesity would be associated with gain of function mutations. Hence, we assume a gain of function for the G-allele of non-synonymous SNP rs1800437 and the respective risk alleles of the SNPs in the putatively regulatory region (rs2302382 and rs8111428) which might alter transcription binding sites causing an increased gene expression. Investigations with independent and large samples are necessary to validate our observed associations. Samples from the extremes of the phenotype would be the best choice. Once an even more robust signal is obtained, re-sequencing as well as functional studies will be necessary to elucidate the functional role of the GIPR variants.
