Prenatal exposure to ethanol has been reported to cause developmental defects in the brain. During brain development, a sufficient energy source is deemed essential and glucose is regarded as the primary energy source for neurons. In this study, the impact of ethanol on embryonic malformation and cerebral glucose metabolism in developing embryo was investigated. Different doses of ethanol (0, 10, 20, 40 mg/egg) were administrated to chicken embryos after 36 h incubation. Embryonic brain weight was found significantly decreased. Moreover, we observed an obvious reduction of neurofilament expression in the central nervous system (CNS) by immunostaining assay. All the above indicated that ethanol exposure caused obvious CNS damages and resulted malformations in the developing brain. Mechanism research showed that cerebral glucose and lactic acid contents, activities of hexokinase, pyruvate kinase and lactic dehydrogenase were decreased dose dependently. Meanwhile, mRNA levels of glucose transporter 1, glucose transporter 3 and insulin-like growth factor I in the brain demonstrated a significant decrease in gene expression after ethanol exposure. These results suggested that glucose metabolism disorder is an important risk factor in ethanol exposure induced malformation in embryonic brain.
Keywords: Chicken embryo; Ethanol toxicity; GLUT1; Glucose metabolism; IGF-1.
Crown Copyright © 2013. Published by Elsevier Ltd. All rights reserved.