GLUCOSE-TRANSPORTER GENE-EXPRESSION IN RAT CONCEPTUS DURING HIGH GLUCOSE CULTURE

Citation
Y. Takao et al., GLUCOSE-TRANSPORTER GENE-EXPRESSION IN RAT CONCEPTUS DURING HIGH GLUCOSE CULTURE, Diabetologia, 36(8), 1993, pp. 696-706
Citations number
52
Categorie Soggetti
Endocrynology & Metabolism","Medicine, General & Internal
Journal title
ISSN journal
0012186X
Volume
36
Issue
8
Year of publication
1993
Pages
696 - 706
Database
ISI
SICI code
0012-186X(1993)36:8<696:GGIRCD>2.0.ZU;2-7
Abstract
We investigated the expression of glucose transporter genes and protei n in embryo and yolk sac during organogenesis and the regulation of gl ucose transporters during culture in hyperglycaemic media. Erythrocyte -type glucose transporter (GLUT 1) and brain-type glucose transporter (GLUT 3) mRNA were expressed in embryo and yolk sac. The expression of GLUT-1 and GLUT-3 mRNA was abundant on day 9-11 and day 9-10 in the e mbryo, respectively, and day 9-14 and day 10-11 in the yolk sac, respe ctively. The levels of GLUT-1 protein in the embryo increased in paral lel with the expression of GLUT-1 mRNA during the corresponding period . Immunohistochemical staining of GLUT-1 protein was found principally in the neuroepithelial cells surrounding the neural tube in the embry o on day 10 and appeared in the microvessels surrounding the neural tu be after day 12. To test whether the expression of glucose transporter genes and protein was suppressed during hyperglycaemia, conceptuses w ere cultured in high glucose medium. The abundant expression of GLUT-1 protein was not decreased during culture in high glucose media for 24 h (day 9-10) and was only down-regulated by prolonged exposure to thi s media for 48 h (day 9-11). We have demonstrated the predominant expr ession of the high affinity glucose transporter (GLUT 1 and GLUT 3) ge nes and (GLUT 1) protein in embryo during the early period of organoge nesis. The persistently abundant expression of glucose transporter dur ing the critical period of neural tube formation (day 9-10) even in th e presence of hyperglycaemia may explain one of the mechanisms of incr eased glucose flux into the neuroepithelium, which may lead to neural tube defects.