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Cord blood leptin level and a common variant of its receptor as determinants of the BMI trajectory: The EDEN mother–child cohort
Author(s) -
Cissé Aminata H.,
Taine Marion,
Tafflet Muriel,
de LauzonGuillain Blandine,
Clément Karine,
Khalfallah Olfa,
Davidovic Laetitia,
Lioret Sandrine,
Charles Marie A.,
Heude Barbara
Publication year - 2022
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/ijpo.12955
Subject(s) - leptin , medicine , cord blood , body mass index , leptin receptor , endocrinology , obesity , cohort , adipokine , confounding
Summary Background Cord blood leptin is an indicator of neonatal fat mass and could shape postnatal adiposity trajectories. Investigating genetic polymorphisms of the leptin receptor gene ( LEPR ) could help understand the mechanisms involved. Objectives We aimed to investigate the association of cord blood leptin level and the LEPR rs9436303 polymorphism, with body mass index (BMI) at adiposity peak (AP) and age at adiposity rebound (AR). Methods In the EDEN cohort, BMI at AP and age at AR were estimated with polynomial mixed models, for 1713 and 1415 children, respectively. Multivariable linear regression models allowed for examining the associations of cord blood leptin level and LEPR rs9436303 genotype with BMI at AP and age at AR adjusted for potential confounders including birth size groups. We also tested interactions between cord blood leptin level and rs9436303 genotype. Results Increased leptin level was associated with reduced BMI at AP and early age at AR (comparing the highest quintile of leptin level to the others). Rs9436303 G‐allele carriage was associated with increased BMI at AP and later age at AR but did not modulate the association with leptin level. Conclusion These results illustrate the role of early life body composition and the intrauterine environment in the programming of adiposity in childhood.