Introduction and Objective: Maternal fasting triglycerides (FTG), mainly hepatic VLDL TG, are higher in obese pregnancies and rise substantially over gestation under the influence of a 100-fold increase in placental estradiol (EST). Historically this rise was thought to occur in a dose-dependent pattern to support maternal metabolism as glucose is spared for fetal growth. Data are sparse examining the effect of EST on the rise in FTG in obesity, where TG may be a strong driver for fetal fat accretion. We examined the FTG increase in relation to rising EST with changes in insulin resistance (HOMA-IR) and gestational weight gain (GWG) in obesity between 16 and 34 wks’ gestation to discern response patterns.Methods: In a prospective cohort, 32 women (BMI 31±4) had FTG, glucose, insulin, and EST drawn at 16 and 34 wks’ in addition to collecting point-of-care FTG for 4 days both weeks (~320 FTG). The change in mean FTG and EST (ΔFTG, ΔEST 34-16) and % increases (+%) were calculated. Women were divided into tertiles (T1-T3) according to the ΔFTG/ΔEST [1-way ANOVA].Results: At 16 wks’, T1 (n=11; FTG 120mg/dL) was least responsive to EST, with the smallest ΔFTG (53±30 mg/dL; +52%) for the largest ΔEST (23,954±8817 pg/mL). Conversely, T3 (n=10; FTG 145mg/dL) was most responsive, showing the largest ΔFTG (132±63 mg/dL; +100%) but smallest ΔEST (12,827±3998 pg/mL; p<0.05, all). The range was wide for the rise in FTG (~0-290 mg/dL) and estradiol (6834-37440 pg/mL). GWG or HOMA-IR did not explain differences (T1 vs. T3). ΔHOMA-IR was highest in T2 (1.61; p=0.05).Conclusion: Counter to historic data, obese pregnancies had variable FTG responses to EST, largely unexplained by changes in HOMA-IR and GWG. T3 had the highest response (107mg/dL FTG rise per 10,000 pg/mL EST) but T1 a blunted response (27 mg/dL/10,000 pg/mL EST). These data underscore variability in the rise in FTG and EST, which may have clinical implications in TG lowering treatments to prevent fetal overgrowth or hypertriglyceridemia since EST is a strong driver to increase FTG in some, but not all, women.
T.L. Hernandez: None. E.G. Dunn: None. B. Fosdick: None. J. Hinojosa: None. C. Ingram: None. S. Hagen-Lillevik: None. R. Baldermann: None. L. Barbour: None.
R01HD102726
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