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• W38389750 abstract "Fetal glucose metabolism depends on additive effects of fetal plasma glucose and insulin. Glucose-stimulated insulin secretion increases over gestation, is down-regulated by constant hyperglycemia, but enhanced by pulsatile hyperglycemia. Insulin production is diminished in fetuses with intrauterine growth restriction (IUGR) by inhibition of pancreatic beta-cell replication, but not by mechanisms that regulate insulin production or secretion, while the opposite occurs with hypoglycemia alone, despite its common occurrence in IUGR. Chronic hyperglycemia down-regulates glucose tolerance and insulin sensitivity with decreased expression of skeletal muscle and hepatic Glut 1 and 4 glucose transporters, while chronic hypoglycemia up-regulates these transporters. The opposite occurs for signal transduction proteins that regulate amino acid synthesis into protein. These results demonstrate the mixed phenotype of the IUGR fetus with enhanced glucose utilization capacity, but diminished protein synthesis and growth. Such adaptations might underlie childhood and adult metabolic disorders of insulin resistance, obesity, and diabetes mellitus." @default.
• W38389750 created "2016-06-24" @default.
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• W38389750 date "2006-01-01" @default.
• W38389750 modified "2023-10-17" @default.
• W38389750 title "Placental-fetal glucose exchange and fetal glucose metabolism." @default.
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• W38389750 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/1500912" @default.
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