P4.062: Maternal Adipose and Metabolic Health Biomarkers During Pregnancy and Child Growth and Adiposity from Birth to 5 years

Background: Maternal adipose and metabolic health biomarkers during pregnancy have been closely linked to fetal growth. However, their long-term influence on the developmental programming of growth and obesity risk later in life is largely unknown. The objective of our study was to examine the association between Adiponectin, Leptin, and Plasminogen Activator Inhibitor-1 (PAI-1) levels during pregnancy and child growth measures from birth to 5 years.

Methods: In the NYU Children’s Health and Environment Study (2016-2021, n=850), we measured Adiponectin (µg/mL), Leptin (ng/mL), and PAI-1 (ng/mL) levels in serum samples of pregnant participants during early and mid-pregnancy (up to 25 weeks). We used Adiponectin-to-Leptin (A/L) and PAI-1-to-Adiponectin (P/A) ratios as indicators of adipose and metabolic dysfunction. Birth measures were obtained from electronic health records and children’s anthropometrics (weight, length/height, BMI, and triceps (TR) and subscapular (SS) skinfold thicknesses) were measured at 1, 2, and 3-5-years. Subscapular-to-triceps (SS/TR) ratio was used as an indicator of central adiposity. We used linear mixed models to assess associations between the natural log-transformed biomarkers and repeated child outcome z-scores, with an interaction term for child visit age (1,2, 3-5). We employed simple linear and logistic regressions for birth outcomes, small- and large-for-gestational age (SGA, LGA), and overweight/obesity at 3-5 years. The models were adjusted for maternal BMI and other health and socioeconomic factors.

Results: In repeated measures analysis, the associations between biomarkers and child outcomes were null. However, in age-specific analyses, maternal Leptin was associated with higher weight (ß=0.20, 95%:0.02, 0.38) and BMI (ß=0.21, 95%:0.01, 0.42) z-scores at 3-5 years. At age 2, Leptin (ß=0.39, 95%:0.12, 0.65) and PAI-1 (ß=0.40, 95%:0.05, 0.76) were associated with increased SS thickness. PAI-1 was also linked to greater central adiposity at 3-5 years, as indicated by SS/TR (ß=0.07, 95%:0.01, 0.12). Additionally, higher maternal Leptin was associated with increased odds for obesity at 3-5 years (OR=1.83, 95%:1.11, 3.07), and P/A was associated with higher odds for LGA (OR=1.47, 95%:1.06, 2.05).

Conclusion: In this large and diverse NYC cohort, maternal adipose and metabolic biomarkers, particularly PAI-1 and Leptin, were associated with early-life adiposity and obesity risk, even after adjusting for maternal BMI and other health and sociodemographic factors. These findings suggest a potential role of maternal metabolic health in the developmental programming of childhood adiposity, regardless of maternal obesity status.