Repositori URV

Identificador: imarina:9002835

Handle: https://hdl.handle.net/20.500.11797/imarina9002835

Autores:
Vogelezang SBradfield JPAhluwalia TSCurtin JALakka TAGrarup NScholz Mvan der Most PJMonnereau CStergiakouli EHeiskala AHorikoshi MFedko IOVilor-Tejedor NCousminer DLStandl MWang CAViikari JGeller FÍñiguez CPitkänen NChesi ABacelis JYengo LTorrent MNtalla IHelgeland ØSelzam SVonk JMZafarmand MHHeude BFarooqi ISAlyass ABeaumont RNHave CTRzehak PBilbao JRSchnurr TMBarroso IBønnelykke K

Resumen:
© 2020 Public Library of Science. All rights reserved. The genetic background of childhood body mass index (BMI), and the extent to which the well-known associations of childhood BMI with adult diseases are explained by shared genetic factors, are largely unknown. We performed a genome-wide association study meta-analysis of BMI in 61,111 children aged between 2 and 10 years. Twenty-five independent loci reached genome-wide significance in the combined discovery and replication analyses. Two of these, located near NEDD4L and SLC45A3, have not previously been reported in relation to either childhood or adult BMI. Positive genetic correlations of childhood BMI with birth weight and adult BMI, waist-to-hip ratio, diastolic blood pressure and type 2 diabetes were detected (Rg ranging from 0.11 to 0.76, P-values <0.002). A negative genetic correlation of childhood BMI with age at menarche was observed. Our results suggest that the biological processes underlying childhood BMI largely, but not completely, overlap with those underlying adult BMI. The well-known observational associations of BMI in childhood with cardio-metabolic diseases in adulthood may reflect partial genetic overlap, but in light of previous evidence, it is also likely that they are explained through phenotypic continuity of BMI from childhood into adulthood.