SNP analyses of postprandial responses in (an)orexigenic hormones and feelings of hunger reveal long-term physiological adaptations to facilitate homeostasis

Abstract

Background: The postprandial responses in (an)orexigenic hormones and feelings of hunger are characterized by large interindividual differences. Food intake regulation was shown earlier to be partly under genetic control. Objective: This study aimed to determine whether the postprandial responses in (an)orexigenic hormones and parameters of food intake regulation are associated with single nucleotide polymorphisms (SNPs) in genes encoding for satiety hormones and their receptors. Design: Peptide YY (PYY), glucagon-like peptide 1 and ghrelin levels, as well as feelings of hunger and satiety, were determined pre-and postprandially in 62 women and 41 men (age 31±14 years; body mass index 25.0±3.1 kg/m 2 ). Dietary restraint, disinhibition and perceived hunger were determined using the three-factor eating questionnaire. SNPs were determined in the GHRL, GHSR, LEP, LEPR, PYY, NPY, NPY2R and CART genes. Results: The postprandial response in plasma ghrelin levels was associated with SNPs in PYY (215G4C, Po0.01) and LEPR (326A4G and 688A4G, Po0.01), and in plasma PYY levels with SNPs in GHRL (À501A4C, Po0.05) and GHSR (477G4A, Po0.05). The postprandial response in feelings of hunger was characterized by an SNP-SNP interaction involving SNPs in LEPR and NPY2R (668A4G and 585T4C, Po0.05). Dietary restraint and disinhibition were associated with an SNP in GHSR (477G4A, Po0.05), and perceived hunger with SNPs in GHSR and NPY (477G4A and 204T4C, Po0.05). Conclusions: Part of the inter-individual variability in postprandial responses in (an)orexigenic hormones can be explained by genetic variation. These postprandial responses represent either long-term physiological adaptations to facilitate homeostasis or reinforce direct genetic effects.

The impact of obesity-related SNP on appetite and energy intake

“…Ratings of fullness and prospective food consumption were found to be different between the genotype groups for LEP with a significant increase in feelings of fullness and suppressed prospective food consumption in AA homozygotes relative to G carriers. This is in contrast with the two studies by den Hoed et al ( 26 , 32 ) , in which LEP was not associated with hunger and satiety ( 26 ) and where GG homozygotes felt more hungry compared with GA, but not AA individuals ( 32 ) . Additionally, den Hoed et al ( 26 ) showed that AA individuals had lower hunger ratings compared with carriers of the risk allele in LEPR , while in the present study, there was no effect of LEPR on appetite.…”