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Increasing association between a neuropeptide Y promoter polymorphism and body mass index during the course of development
Author(s) -
Hohmann S.,
Buchmann A. F.,
Witt S. H.,
Rietschel M.,
JennenSteinmetz C.,
Schmidt M. H.,
Esser G.,
Banaschewski T.,
Laucht M.
Publication year - 2012
Publication title -
pediatric obesity
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.226
H-Index - 69
eISSN - 2047-6310
pISSN - 2047-6302
DOI - 10.1111/j.2047-6310.2012.00069.x
Subject(s) - body mass index , neuropeptide y receptor , medicine , obesity , confounding , longitudinal study , orexigenic , genotype , allele , endocrinology , young adult , demography , physiology , neuropeptide , genetics , biology , gene , pathology , receptor , sociology
SummaryWhat is already known about this subject? NPY serves as a potent orexigenic signal and plays an important role in body weight regulation. Recently, evidence for the impact of NPY gene variation on body weight regulation and risk of obesity was provided. Research has indicated that genetic influences on some traits such as BMI change with age, with often showing a stronger effect as children mature.What this study adds? We show first evidence from a longitudinal study, demonstrating an association between NPY rs16147 genotype and BMI development from infancy into young adulthood. The NPY effect appears to increase with age, being more pronounced in older age groups than in younger ones.Objective To investigate the association of the neuropeptide Y ( NPY ) promoter polymorphism rs16147 with body mass index ( BMI ) during the course of development from infancy to adulthood. Design Longitudinal, prospective study of a G erman community sample. Subjects n = 306 young adults (139 males, 167 females). Measurements Participants’ body weight and height were assessed at the ages of 3 months and 2, 4.5, 8, 11, 15 and 19 years. NPY rs16147 was genotyped. Results Controlling for a number of possible confounders, homozygote carriers of the rs16147 C allele exhibited significantly lower BMI scores when compared with individuals carrying the T allele. In addition, a significant genotype by age interaction emerged, indicating that the genotype effect increased during the course of development. Conclusions This is the first longitudinal study to report an association between rs16147 and BMI during childhood and adolescence. The finding that this effect increased during the course of development may either be due to age‐dependent alterations in gene expression or to maturation processes within the weight regulation circuits of the central nervous system.