1045-P: Relative Cord Hyperleptinaemia Is Associated with Higher Cord C Peptide and Lower Birthweight in Male but Not Female Neonates Born to Overweight/Obese Women

Abstract

Aim: Umbilical cord leptin is higher than expected in some babies (relative cord hyperleptinaemia) . We test the hypothesis that a higher cord leptin:fat mass ratio, putatively reflecting “leptin resistance” might be associated with adverse pregnancy outcomes. Methods: Secondary analyses from Vitamin D And Lifestyle Intervention for gestational diabetes prevention (DALI) trial a pan European study among women with a BMI ≥29 kg/m2 between 2012-14. Cord sampling and skin caliper measurements followed standardized methods. Serum cord leptin (µg/l) to fat mass ratio (kg) was classified into low, middle, and high tertiles across (where stated) and within sexes. Large/small for gestational age (SGA) used GROW. Pregnancy outcomes were compared between low and high tertiles adjusted for potential confounders using binomial logistic regression. Results: Among the 349 eligible babies (mean gestational age 39.7 ± 1.4 weeks, female 49%) the median (interquartile range) leptin-fat mass ratio (both sexes combined) was 20.2 (11.4-30.8) , top tertile (TT) was >25.3 and low tertile (LT) was <14.9 . Compared with babies in the LT group, those in the TT group had higher cord erythropoietin (30.2 (16.7-59.2) vs. 20.3 (12.4-35.6) µg/l p = 0.002, respectively, both sexes) with higher cord serum C peptide (0.7 (0.5­-1.0) vs. 0.5 (0.3-0.8) µg/l p = 0.005) , lower birthweight (3435 ± 5vs. 37± 412 gm, p = 0.002) in boys but not in girls. Cord glucose was similar. Among males, those in the TT had higher risk of SGA (25.0% vs. 8.5%; OR 3.61 (95%CI 1.21-10.76)) but lower risk of cesarean section (0.39 (0.17-0.88)) . Among females, mothers in the TT had higher rate of pregnancy induced hypertension (3.93 (1.21-12.71)) . Conclusions: Relative cord hyperleptinaemia is associated with reduced fetal growth (boys only) , and possible relative fetal hypoxia (both sexes) . Further studies are required to evaluate the implications of these findings on future metabolism. Disclosure J.Immanuel: None. D.M.Jensen: None. E.R.Mathiesen: Consultant; Novo Nordisk A/S, Speaker's Bureau; Novo Nordisk A/S. D.J.Hill: None. P.Damm: Advisory Panel; Novo Nordisk A/S. F.J.Snoek: Advisory Panel; Abbott Diabetes, Lilly Diabetes, Roche Diabetes Care, Research Support; Novo Nordisk A/S, Sanofi, Speaker's Bureau; Insulet Corporation. J.Adelantado: None. E.Wender-ozegowska: None. D.Simmons: Other Relationship; Elsevier, Research Support; Abbott, Hitachi, Ltd., Novo Nordisk, Speaker's Bureau; Sanofi. G.Desoye: None. M.Vanpoppel: None. A.Kautzky-willer: None. R.Corcoy: None. A.Bertolotto: Research Support; AstraZeneca, Novo Nordisk, Speaker's Bureau; Abbott Diagnostics, Lilly Diabetes. F.P.Dunne: None. J.Harreiter: None. L.Andersen: None. Funding EU FP7 (242187)