CHANGES IN BRAIN GLUCOSE-LEVELS AND GLUCOSE-TRANSPORTER PROTEIN ISOFORMS IN ALCOHOL-TREATED OR NICOTINE-TREATED CHICK-EMBRYOS

Suppression of fetal brain growth during pregnancy as the result of ma ternal smoking or alcohol consumption leads to significant problems fo r the offspring as well as for the society who must care for these ind ividuals. Chronic maternal intake of cigarette smoke is frequently obs erved in humans and studies using animal models suggest that in utero nicotine exposure is an important component of the growth suppression that results. Similarly, maternal consumption of alcohol (ethanol) has a profound, negative effect on fetal growth. The developing fetal cen tral nervous system (CNS) is sensitive to the growth inhibitory effect of nicotine or alcohol and morphological as well as functional CNS de ficits may result from fetal exposure. Using an embryonic chick model which minimizes drug-induced changes in maternal nutrition and behavio r, the studies presented here indicate that nicotine or alcohol exposu re during early embryonic development inhibits brain growth to a degre e comparable to that seen in the rest of the organism, i.e., there was no 'brain sparing' in this model. Glucose content per milligram tissu e was markedly decreased in brains of the nicotine-treated embryos but was not significantly different in the alcohol-exposed embryos. Weste rn blots of fetal brain glucose transporter protein isoforms showed no change in the Glut 3 transporter content in the growth suppressed bra ins compared to vehicle-treated brains. The Glut 1 55 kilodalton (kd) isoform protein content was significantly decreased in the nicotine-tr eated brains but unchanged in the ethanol-treated brains, while the re verse was true for the Glut 1 45 kd isoform. Thus, the changes in the 55 kd isoform protein content were correlated with tissue glucose leve ls in the ethanol-and nicotine-treated embryos. (C) 1997 Elsevier Scie nce B.V.