myo-Inositol homeostasis in the human fetus.

The concentration of myo-inositol in the serum of pregnant women (21.4 microM) remained unchanged throughout pregnancy and was not significantly different from that in the serum of nonpregnant women (24.5 microM). myo-Inositol concentrations in mixed cord serum averaged 125 microM at midgestation. At term, the concentration of myo-inositol was 60.2 microM in the umbilical artery and 45.4 microM in the umbilical vein. In every umbilical cord examined, the ratio of myo-inositol concentration in umbilical artery to that in umbilical vein exceeded 1.0. Activity of a putative regulatory enzyme in the biosynthesis of myo-inositol from glucose, ie, glucose 6-P:inositol 1-P cyclase (cyclase), was measured in placenta, fetal lung, and fetal liver. In placenta at midgestation and at term, cyclase activity was 87.8 and 90.7 nmol X g-1 tissue X h-1, respectively. Cyclase activity in fetal lung and liver at midgestation was 54.6 and 54.4 nmol X g-1 tissue X h-1, respectively. The gestational decline in the concentration of myo-inositol in fetal serum may represent a decreasing availability of myo-inositol to the fetal lungs and could be important in the mechanism whereby the amounts of phosphatidylglycerol and phosphatidylinositol in lung surfactant are regulated during fetal lung development.