Enhanced placental GLUT1 and GLUT3 expression in dexamethasone-induced fetal growth retardation

• Published in: Molecular and cellular endocrinology 2001-12, Vol.185 (1), p.109-117
• Main Authors: Langdown, Maria L., Sugden, Mary C.
• Format: Article
• Language: English
• Subjects: Animals; Dexamethasone - administration & dosage; Dexamethasone - adverse effects; Dose-Response Relationship, Drug; Female; Fetal Growth Retardation - chemically induced; Fetal Growth Retardation - metabolism; Fetus; Gene Expression Regulation - drug effects; Glucocorticoid; Glucocorticoids - administration & dosage; Glucocorticoids - adverse effects; Glucose transporter; Glucose Transporter Type 1; Glucose Transporter Type 3; Heart - embryology; Intrauterine growth retardation; Monosaccharide Transport Proteins - drug effects; Monosaccharide Transport Proteins - metabolism; Nerve Tissue Proteins; Placenta; Placenta - chemistry; Placenta - drug effects; PPAR-γ; Pregnancy; Rats; Rats, Wistar; Receptors, Cytoplasmic and Nuclear - metabolism; Transcription Factors - metabolism
• ISSN: 0303-7207; 1872-8057
• DOI: 10.1016/S0303-7207(01)00629-3

Intrauterine growth retardation (IUGR) increases the risk of developing glucose intolerance and cardiovascular disease in adulthood. Fetal exposure to excess glucocorticoids may contribute to IUGR. Despite the importance of glucose supply for fetal growth, studies on glucose transporter expression in IUGR are few. Two glucose transporters, GLUT1 and GLUT3, are expressed in placenta. In rodent placenta, GLUT1 is replaced by GLUT3 during late gestation. We examined placental GLUT protein expression in 21-day pregnant rats administered dexamethasone (DEX) from day 15 of gestation via osmotic minipump (at doses of 100 or 200 μg/kg body wt. per day). A dose-dependent decline in placental and fetal weight occurred in the DEX groups at day 21. Placental GLUT3 protein expression increased dose-dependently in the DEX groups (by 1.3-fold (n.s) and 2.3-fold ( P