Placental-fetal glucose exchange and fetal glucose metabolism.

摘要: Fetal glucose metabolism depends on additive effects of fetal plasma and insulin. Glucose-stimulated insulin secretion increases over gestation, is down-regulated by constant hyperglycemia, but enhanced pulsatile hyperglycemia. Insulin production diminished in fetuses with intrauterine growth restriction (IUGR) inhibition pancreatic β-cell replication, not mechanisms that regulate or secretion, while the opposite occurs hypoglycemia alone, despite its common occurrence IUGR. Chronic hyperglycemia down-regulates tolerance sensitivity decreased expression skeletal muscle hepatic Glut 1 4 transporters, chronic up-regulates these transporters. The for signal transduction proteins amino acid synthesis into protein. These results demonstrate mixed phenotype IUGR fetus utilization capacity, protein growth. Such adaptations might underlie childhood adult metabolic disorders resistance, obesity, diabetes mellitus.