PC1163: Longitudinal Trajectory and Early Life Determinants of Childhood Plasma Adipokines Levels: Findings from an Urban Racially Diverse Birth Cohort

Background: Leptin and adiponectin are adipocyte-derived hormones that play an important role in systemic metabolic homeostasis, beginning in utero. There is limited data on the levels and trajectories of these two hormones at birth and in childhood and their early life biological and social determinants. Such data may provide valuable insights into the developmental origins of metabolic alterations and modifiable early life factors.
Our objective was to examine the longitudinal trajectories of leptin and adiponectin from birth to early childhood and to identify influential prenatal and infancy factors; and whether the trajectories and risk factors differ by preterm birth status.

Methods: We included mother-infant pairs in the Boston Birth Cohort enrolled 2-3 days after birth. We measured infant plasma leptin and adiponectin levels at birth (in cord blood) and in early childhood. Unit of measurements are in pg/ml for leptin and ng/ml for adiponectin. We used student t-tests to compare cord hormonal levels by infant gestational age (GA). We used multivariable linear regression models to examine how prenatal maternal and infancy factors are associated with early childhood hormonal levels in total sample and by preterm status.

Results: We analyzed 716 infants (158 preterm) who had leptin and adiponectin levels measured at birth and in early childhood. Cord leptin was higher in infants born at term vs. preterm (40230 vs. 20481 , p < 0.0001) but wasn’t significantly different when measured in early childhood (4123 vs. 4181, p = 0.9). Adiponectin at birth was higher in infants born term vs preterm (18416 vs. 11223, p < 0.0001) and continued to stay elevated in early childhood (12108 vs. 10532 , p = 0.046). We found independent positive associations between childhood leptin and female sex, maternal DM, higher maternal age and Black race. Significant negative associations were found between childhood leptin and LGA status at birth. We found significant positive associations between childhood adiponectin with cord adiponectin levels and male sex while a significant negative association with childhood leptin and Black race, higher maternal age and maternal smoking was found in our study (Tables too large to upload). For the preterm subpopulation childhood leptin was positively associated with female sex and negatively with chronic lung disease. Childhood adiponectin was positively associated with maternal index pregnancy stress and negatively with maternal smoking history in preterm subgroup. (preterm data not shown)

Conclusion: Our findings underscore fetal programing of adiponectin and leptin levels that likely persists into childhood with implications for future metabolic health. Our results may help identify children at risk of future adverse cardio metabolic outcomes, beyond prematurity, who could benefit from interventions during a potential therapeutic window that could possibly reverse developmental metabolic programming .