48-OR: Maternal Triglycerides in Diet-Controlled GDM Correlate with Newborn Triglycerides and Infant Fat Mass at Four Months of Life

The early hours of newborn (NB) life are critical for metabolic transition from the prenatal to postnatal period and possibly subsequent metabolic development. Although the relationship between maternal glucose and neonatal hypoglycemia in gestational diabetes (GDM) is strongly supported, little is known about the relationship between maternal and NB triglycerides (TG). We tested the hypothesis that maternal TG in GDM would correlate positively with NB pre-feed TG (NBpfTG) at 24hrs, and that NBpfTG would correlate with infant adiposity (Inf%fat). After GDM diagnosis (~28-30 wks), 16 diet-controlled GDM women (mean±SD; BMI 32±1) were randomized to eucaloric diets differing in carbohydrate and fat percentages (all food provided). Fasting (F) and 1-hr/2-hr postprandial (PP) glucose, insulin, and TG were measured during breakfast test meals at 31 and 36 wks. Newborn “fasting” blood (NBpfTG, NBpfGluc) was collected at 24 hrs. Inf%fat was measured at 24 hrs and 4 mos (PeaPod). All women met conventional glucose targets with diet alone; no neonates had hypoglycemia. At 31 but not 36 wks, maternal FTG and PPTG were correlated with NBpfTG (92±7mg/dL)(r=0.52-0.53, p=0.03 both) and NBpfTG correlated with 24 hr Inf%fat (r=0.50, p=0.06). Maternal fasting insulin, HOMA-IR, glucose and PP glucose at 31 and 36 wks correlated with Inf%fat at 24 hrs (r=0.47-0.68, p<0.05 all). Strikingly, NBpfTG were uniquely and highly correlated with Inf%fat at 4 mos (r=0.81, p<0.0001); NBpfGluc was not. Inf%fat was similar between maternal diet groups (p>0.05). These data show that maternal TG soon after GDM diagnosis correlated with NBpfTG, which in turn correlated with Inf%fat at 24 hrs, but had a sustained, stronger correlation with Inf%fat at 4 mos. This connection between 32 wk maternal TG and NBpfTG, and their association with Inf%fat from 24 hrs to 4 mos support future studies to address whether maternal TG might be therapeutically targeted to normalize fetal growth in well-controlled GDM.