Abstract
BackgroundResults from genome-wide association studies (GWAS) identified many loci and biological pathways that influence adult body mass index (BMI). We aimed to identify if biological pathways related to adult BMI also affect infant growth and childhood adiposity measures.MethodsWe used data from a population-based prospective cohort study among 3,975 children with a mean age of 6 years. Genetic risk scores were constructed based on the 97 SNPs associated with adult BMI previously identified with GWAS and on 28 BMI related biological pathways based on subsets of these 97 SNPs. Outcomes were infant peak weight velocity, BMI at adiposity peak and age at adiposity peak, and childhood BMI, total fat mass percentage, android/gynoid fat ratio, and preperitoneal fat area. Analyses were performed using linear regression models.ResultsA higher overall adult BMI risk score was associated with infant BMI at adiposity peak and childhood BMI, total fat mass, android/gynoid fat ratio, and preperitoneal fat area (all p-values < 0.05). Analyses focused on specific biological pathways showed that the membrane proteins genetic risk score was associated with infant peak weight velocity, and the genetic risk scores related to neuronal developmental processes, hypothalamic processes, cyclicAMP, WNT-signaling, membrane proteins, monogenic obesity and/or energy homeostasis, glucose homeostasis, cell cycle, and muscle biology pathways were associated with childhood adiposity measures (all p-values <0.05). None of the pathways were associated with childhood preperitoneal fat area.ConclusionsA genetic risk score based on 97 SNPs related to adult BMI was associated with peak weight velocity during infancy and general and abdominal fat measurements at the age of 6 years. Risk scores based on genetic variants linked to specific biological pathways, including central nervous system and hypothalamic processes, influence body fat development from early life onwards.Electronic supplementary materialThe online version of this article (doi:10.1186/s12863-016-0425-y) contains supplementary material, which is available to authorized users.
Highlights
Results from genome-wide association studies (GWAS) identified many loci and biological pathways that influence adult body mass index (BMI)
Of the 28 adult BMI genetic risk scores based on biological pathways, only the membrane proteins pathway genetic risk score was associated with peak weight velocity (PWV) (p-value
The overall adult WHR genetic risk score was not associated with any infant growth measure (Table 2; Additional file 6: Figure S2a-c), whereas the childhood BMI genetic risk score was associated with PWV and BMI at adiposity peak (BMIAP) (0.048 Standard deviation scores (SDS) and 0.051 SDS (0.017, 0.084), respectively, per Standard deviation (SD) increase in the genetic risk score) (Table 2; Additional file 7: Figure S3a-c)
Summary
Results from genome-wide association studies (GWAS) identified many loci and biological pathways that influence adult body mass index (BMI). We aimed to identify if biological pathways related to adult BMI affect infant growth and childhood adiposity measures. Large genome-wide association studies (GWAS) have identified many single nucleotide polymorphisms (SNPs) associated with body mass index (BMI) in adults [7, 8]. We previously reported that a genetic risk score based on 29 SNPs related to adult BMI was associated with infant growth and childhood adiposity measures [12]. In adults especially central nervous system processes seem to play a role [8] The role of these pathways in body fat development during early life is not known yet. Knowledge on the biological pathways influencing BMI from early life onwards may help to better understand the development of overweight and obesity in children
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