Project 1A) To Determine Whether the Transplacental Gradients for 6 Polyols and Mannose Are Altered in IUGR Pregnancies Compared to Normal Pregnancies. Project 1B) To Determine the Relative Contributions of Transplacental Transport vs. Production by the Conceptus of Both Myoinositol (Major Polyol) and Mannose in IUGR and Normal Pregnancies Using Stable Isotopic Methodology.

The purposes of this study fall in 2 categories: 1) information important to an understanding of normal pregnancies and the roles of polyols and trace carbohydrates in human fetal nutrition and metabolism and 2) determination of the impact of the small IUGR placenta upon the delivery of polyols and trace carbohydrates to the fetus. Stable isotopes of D-mannose, D-glucose and myoinositol are used to determine the contributions of placental transport of these carbohydrates from the maternal circulation to the fetus vs their synthesis in the fetus and placental tissues. The IUGR pregnancies compare the transport and synthesis of these compounds vs a classification of clinical severity based upon Doppler velocimetry data.

The investigators anticipate that, (just as the investigators have shown for glucose) the fetal enrichment of mannose m+6 will be ~ equal to the maternal enrichment. Thus, without any appreciable dilution of fetal mannose m+6 there is no evidence of fetal production of mannose. This will be further confirmed by the infusion of D-[1-13C]glucose into the maternal circulation. Our previous studies have shown that the fetal enrichment will equal the maternal enrichment. Thus, confirmation will be obtained by comparing the enrichment of fetal mannose m+1 with the fetal enrichment of glucose m+1. The mannose enrichment should be 10% or less of the glucose enrichment. These findings would establish unequivocally that fetal requirements for mannose are met primarily by transplacental transport, not fetal production from glucose.

Conversely, the investigators anticipate demonstrating that the fetal enrichment of myoinositol m+6 is significantly less than the maternal enrichment demonstrating minimal transplacental flux of myoinositol with very little dilution of fetal enrichment by myoinositol production from glucose. This will receive further confirmation by comparing the fetal enrichment of myoinositol m+1 with the fetal enrichment of glucose m+1. For example if the fetal enrichment of myoinositol m+1 is 70% of the fetal enrichment of glucose m+1, then 70% of fetal plasma myoinositol is derived from fetal plasma glucose. This would establish that fetal myoinositol requirements are met by fetal production from glucose rather than by transplacental transport.