GLUCOSE TRANSPORTER GENE EXPRESSION IN RAT EMBRYO AND ITS REGULATION IN THE DIABETIC STATE

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We have shown that hyperglycemia-induced embryopathy could be mediated by myo-inositol depletion of embryo as a result of increased accumulation of glucose (Diabetologia 33 : 597, 1990). The present study was performed to investigate glucose transporter (GLUT) expression during early organogenesis and its regulation in the diabetic conditions. Both GLUT-1 mRNA and protein, by Northern and Western blot analysis, were highly expressed in embryo during early organogenesis, reaching peak levels on day 10 of gestation (the main period of neural tube formation). Immunohistochemical staining showed that GLUT-1 protein was predominantly distributed in the tissue of neural tube and noted to be localized at the plasma membrane of the neuroepithelial cell. High expression of GLUT-1 mRNA and protein levels persisted in the embryo on day 10 even in the diabetic conditions in streptozotocin-induced diabetic rats. To test whether the expression of glucose transporter gene and protein was suppressed during extreme hyperglycemia, embryos were cultured in high glucose medium (720 and 1320 mg/dl) for 24 h (Day 9-10). The expression of GLUT-1 mRNA and protein were not down-regulated in culture of hyperglycemia (39.9mM or 73.3mM) for 24 h (Day 9-10). Furthermore, the diabetic states did not change also the staining intensity and cellular distribution of the GLUT-1 in the neural tube during the period of neurulation. High expression of the glucose transporter despite the diabetic environment may play a role in hyperglycemia-induced neural tube defects, by permitting increased entry of glucose into neuroepithelial cells, leading to myo-inositol depletion of embryo.