Regulation of placental metabolism by glucose supply.
Glucose is supplied to the placenta and fetus from the maternal plasma according to concentration-dependent mechanisms exhibiting saturation kinetics that are mediated by facilitative transporter proteins on both the maternal-facing microvillus and fetal-facing basal trophoblast membranes. Placental glucose transport to the fetus requires a net maternal-to-fetal plasma glucose concentration gradient that is determined by placental as well as fetal glucose consumption. Fetal plasma glucose concentration, independent of maternal glucose concentration, regulates the partition of placental glucose uptake into transfer to the fetus and consumption by the placenta. Placental transport capacity increases with advancing gestation, probably by an increased number of transporter proteins as surface area increases. Placental glucose consumption contributes to most or all of placental lactate and fructose production and other less well defined non-oxidative pathways of carbon metabolism. Placental glucose consumption accounts for at least 50% of placental oxygen consumption which remains independent of short-term or long-term changes in placental glucose supply, thus requiring varying amounts of other carbon substrates. Placental glucose supply, therefore, plays a key role in regulating placental glucose metabolism and placental carbon balance, and interacts reciprocally with other carbon substrates to maintain placental oxidative metabolism.
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Department of Pediatrics, University of Colorado School of Medicine, Denver 80262, USA.
D000818:Animals; D001692:Biological Transport; D001786:Blood Glucose / Q000378:metabolism; D050260:Carbohydrate Metabolism; D005260:Female; D005312:Fetal Blood / Q000378:metabolism; D005947:Glucose / Q000378:metabolism*; D006801:Humans; D010920:Placenta / Q000378:metabolism*; D011247:Pregnancy
D001786:Blood Glucose; D005947:Glucose