Hypoglycemia in the fetal alcohol syndrome in rat.

As a treatable cause of central nervous system dysfunctions in the fetal alcohol syndrome, ethanol-induced hypoglycemia was studied in experimental rat models. Female Wistar rats were divided into ethanol and control groups. Before mating and during pregnancy, the ethanol group received 30% ethanol (E), or E with 20% sucrose (S) or 20% glucose (G), and the control group received water (W), or W with S or G. Pregnancies were terminated on gestational day (gd) 15, 18, and 21 by cesarean section or by spontaneous delivery. Dams and offspring were weighed and examined for several biochemical factors. Maternal blood glucose levels were higher on gd 15, but significantly lower on gd 18 and 21 in the ethanol group than in the control group. The fetal blood glucose levels were correlated with maternal blood glucose levels on gd 21. Maternal serum insulin levels were lower on gd 15 and 18 in the ethanol group than in the control group. The body and cerebral weights were significantly lower on gd 15, 18, 21 and postnatal day 1 in the ethanol offspring than in the controls. Administration of S or G with E during pregnancy resulted in no better effects on fetal biochemical development and blood glucose levels than administration of E alone. In this work we demonstrated hypoglycemia only in the late gestational and perinatal periods in experimental rat models, which may cause the high perinatal mortality and growth retardation in the fetal alcohol syndrome.