Lw. Eckstein et al., CHANGES IN BRAIN GLUCOSE-LEVELS AND GLUCOSE-TRANSPORTER PROTEIN ISOFORMS IN ALCOHOL-TREATED OR NICOTINE-TREATED CHICK-EMBRYOS, Developmental brain research, 103(1), 1997, pp. 59-65
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.