65zinc metabolism is altered during diabetic pregnancy in rats.

To assess further diabetes-induced alterations in gestational Zn metabolism we examined the uptake/retention and distribution of 65Zn during pregnancy. Control and streptozotocin-induced diabetic rats, with and without insulin treatment, were gavaged with 65Zn on gestational d 12 or 18. Six hours post-intubation, untreated diabetic dams at d 12 of gestation had a lower percentage of retained 65Zn in bone, plasma, erythrocytes, pancreas and spleen than did controls. Retention of 65Zn in amniotic fluid and sacs and in embryos was similar among groups. Untreated diabetic dams at d 18 of gestation had a higher percentage of retained 65Zn in liver, intestine and urine, and most notably a lower percentage in amniotic fluid, placenta, fetus and fetal liver. Lower percentages of 65Zn were found in bone, muscle, plasma, erythrocytes, lung, spleen, heart, pancreas and uterus of diabetic dams compared with controls. HPLC fractionation of samples from maternal livers showed a higher percentage of Zn, Cu and 65Zn associated with the metallothionein peak in samples from untreated diabetic dams compared with other groups, whereas the percentages of Zn, Cu and 65Zn per fraction in fetal liver were similar. The marked decrease in retained 65Zn in products of conception at d 18 suggests either decreased placental transport or altered maternal and/or fetal Zn-binding ligands. Insulin treatment significantly reversed the streptozotocin diabetes-induced derangements in maternal and fetal Zn metabolism.