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Fetal and Maternal Lipoprotein Metabolism in Human Pregnancy Complicated by Type I Diabetes Mellitus¹

Department of Fetal Medicine, Birmingham Womens Hospital, University of Birmingham (M.D.K), Birmingham B15 2TG; Department of Medicine, Manchester Royal Infirmary (M.I.M, P.N.D), Manchester, M13 9WL; and Department of Chemical Pathology, North Staffordshire Hospital (R.H.N), Stoke-on-Trent, ST4 6SD, United Kingdom

Address all correspondence and requests for reprints to: R. Neary, Consultant Clinical Biochemist, Clinical Pathology Block, North Staffordshire Hospitals, Keele University, Stoke-on-Trent, ST4 6SD, United Kingdom.

Serum lipid, apolipoprotein concentration, and lipoprotein composition were determined in maternal and umbilical venous cord blood at delivery by elective Cesarean section (CS) in 10 singleton, full-term pregnancies with maternal insulin-dependent diabetes mellitus (type I DM), which predated pregnancy, and in 22 nondiabetic pregnancies. The objectives of the study were to determine the influence of maternal type I DM, and hence potential fetal overnutrition on fetal lipid metabolism. There were no significant differences in gestational age, fetal weight, or fetal serum insulin concentration between the type I DM group and those with nondiabetic pregnancies, although fetal venous cord blood glucose was 3.4 mmol/L (3.0–4.5 mmol/L) (median and 25th–75th percentiles) and 2.9 mmol/L (2.0–3.4 mmol/L), respectively, and maternal Hemoglobin A1c [9.6% (8.2–10.7%) and 6.8% (6.3–7.8%), respectively], was significantly greater in the type I DM subjects (P < 0.02 and 0.002 respectively). Plasma nonesterified fatty acid (NEFA) concentrations were lower in the type I DM mothers [0.85 mmol/L (0.56–2.31 mmol/L) compared with 1.14 mmol/L (0.88–1.24 mmol/L] in nondiabetic pregnancies; P < 0.0001). Serum high-density lipoprotein phospholipids (HDL-PL) were increased in type I DM mothers because of elevated HDL₂ phospholipid [0.39 mmol/L (0.27–0.48 mmol/L) compared with 0.12 mmol/L (0.06–0.21 mmol/L), respectively, P < 0.01). The maternal HDL cholesterol (C) concentration was not significantly different in the uncomplicated and type I DM pregnancies. However, in the umbilical venous cord blood, serum levels of NEFA [0.49 mmol/L (0.33–1.29 mmol/L) in type I DM compared with 0.13 mmol/L (0.06–0.33 mmol/L) in nondiabetics;P < 0.02)], total cholesterol (TC) [2.87 mmol/L (1.65–4.86 mmol/L) in type I DM compared with 1.65 mmol/L (1.46–1.87 mmol/L) in nondiabetics; P < 0.02], free cholesterol (FC) [0.97 mmol/L (0.60–1.26 mmol/L) in type I DM compared with 0.62 mmol/L (0.37–0.75 mmol/L) in nondiabetics; P < 0.05), and cholesteryl ester (CE) [1.90 mmol/L (1.44–3.33 mmol/L) in type I DM compared with 1.01 mmol/L (0.83–1.24 mmol/L) in nondiabetics; P < 0.02), triglyceride (TG) (1.06 [0.50–1.91) mmol/L in type I DM compared with 0.29 [0.25–0.36] mmol/l in nondiabetics; P < 0.001), phospholipid (PL) (2.52 [1.73–3.03) mmol/L in type I DM compared with 1.34 [1.27–1.48] mmol/L in nondiabetics; P < 0.01], and the apolipoproteins A-I and B had significantly higher concentrations in type I DM. In umbilical venous cord blood, ratios of HDL-TC and HDL-PL to apo AI, reflecting the lipid content of HDL, were reduced when the mother had type I DM during pregnancy (P < 0.02 and P < 0.0001, respectively).

These results indicate that maternal type I DM may lead to a fetal serum lipoprotein composition more closely resembling that seen in the adult. In type I DM, maternal TG and PL and fetal TC, TG, PL CE, and FC were correlated to NEFA levels (P < 0.05), but not to glucose, insulin secretion, or maternal control of type I DM. These data suggest that the enhanced supply of NEFA to the fetus in type I DM pregnancies may drive the synthesis of cholesterol as well as TGs and PLs.

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