GLUCOSE REGULATES GLUT-1 FUNCTION AND EXPRESSION IN FETAL-RAT LUNG AND MUSCLE INVITRO

The mechanisms that regulate cellular glucose transport (glucose uptak e, Glut 1 protein, and mRNA) in the fetus are not known. We attempted to define the effects of glucose availability alone in vitro on glucos e transport in fetal rat lung and muscle. On day 20 of gestation (term = 21.5 days), lung and muscle tissues were harvested from normal feta l rats, minced into explants, and cultured for 24 h in standard cultur e medium (lung, 28 mm; muscle, 5.5 mM glucose). Explant cultures were washed and cultured for an additional 1 or 24 h in medium containing o ne of four concentrations of glucose: 1) glucose free, 2) low glucose, 3) high glucose, and 4) standard. Twenty-four-hour, but not 1-h, trea tment of fetal lung and muscle in vitro with low concentrations of glu cose increased 2-deoxyglucose uptake and Glut 1 protein and mRNA level s (P < 0.05). Culture in high glucose medium for 24 h, but not 1 h, de creased 2-deoxyglucose uptake and Glut 1 protein and mRNA levels (P < 0.05). Culture in glucose-free medium for 24 h up-regulated glucose tr ansport in lung and down-regulated glucose transport in muscle, indica ting that regulation of fetal glucose transport may be tissue specific . These findings differ from our studies of in vivo models of altered fetal growth and abnormal glucose availability. Maternal bilateral ute rine artery ligation limits glucose availability to the fetus, and glu cose transport is down-regulated. Low glucose in vitro has the opposit e effect. Maternal diabetes increases glucose availability to the fetu s, and glucose transport is up-regulated. High glucose in vitro does t he opposite. We conclude that while glucose alone in vitro affects its uptake by the cell, other factors that are altered in these in vivo c onditions act in concert with glucose to regulate glucose transport in the fetus.