Localization and quantification of glucose transporters in liver of growth-retarded fetal and neonatal rats

To determine whether altered transport of glucose into the hepatocyte may b e an important factor contributing to abnormal hepatic glucose metabolism i n the intrauterine growth-retarded (IUGR) fetus and newborn, we measured gl ucose transport (glucose uptake, GLUT protein, and mRNA) and localization o f GLUT protein in liver of control (sham operated) and IUGR fetal (day 20) and postnatal (1, 4, 14, and 21 days) rats. GLUT-1 and -2 proteins were loc alized to the hepatocyte. Glucose uptake and GLUT-I protein and mRNA levels were increased in IUGR fetal and neonatal liver. GLUT-2 protein and mRNA l evels were low in IUGR and control fetal liver. After birth, GLUT-2 abundan ce did not differ from controls. Run-on experiments showed that the rate of transcription of GLUT-1 and -2 did not differ between IUGR and control rat s. However, the transcription rate of GLUT-1 decreased with age, and the GL UT-2 transcription rate increased with age. These studies indicate that the metabolic and physiological factors that cause IUGR also alter glucose tra nsporter expression in fetal liver.