title: Effect of reduced inspired oxygen on fetal growth and maternal glucose metabolism in rat pregnancy.
abstract: The effect of prolonged exposure to a reduced fraction of inspired oxygen ([FiO2] 0.17 for 3 days) on maternal glucose kinetics, placental glucose transporters GLUT1 and GLUT3, and fetal growth was examined in rat pregnancy. Arterial and venous catheters were placed 3 days before the study. [3-(3)H]glucose tracer and deuterium labeling of water were used to measure the rates of glucose turnover and gluconeogenesis (GNG), respectively. Glucose uptake by maternal tissues was measured using [14C]2-deoxyglucose. Exposure to a reduced FiO2 resulted in a significant decrease (mean +/- SE) in fetal weight (room air, 4.02 +/- 0.04 g; 0.17 FiO2, 3.27 +/- 0.6 g, P < .02). There was a significant increase in the maternal-fetal glucose gradient (maternal-fetal glucose ratio: room air, 1.48 +/- 0.11; 0.17 FiO2, 2.26 +/- 0.24, P < .05), but there was no change in the maternal or fetal blood lactate concentration. No significant change in maternal blood pH was observed; however, a significant decrease in the blood partial pressure of O2 (PO2) occurred (room air, 97 +/- 0.5 torr; 0.17 FiO2, 81 +/- 1.8) on day 3. There was no change in the rate of turnover of glucose or GNG in the maternal compartment, nor was there any effect on glucose uptake by the maternal tissues. Placental GLUT1 and GLUT3 mRNA were not different in the control or experimental animals. We conclude that a mild reduction in the FiO2 for 3 days in rat pregnancy results in a significant fetal growth restriction that is not related to any observed alteration in maternal glucose metabolism. The lower glucose concentration in the fetal blood may be the consequence of an increase in fetal glucose metabolism, thereby resulting in an increased maternal-fetal gradient of glucose.
authors.affiliation: Department of Pediatrics and Medicine, Metrohealth Medical Center, Case Western Reserve University School of Medicine, Cleveland, OH 44109-1998, USA.
authors.forename: F
authors.initials: F
authors.lastname: Saker
authors.forename: D M
authors.initials: DM
authors.lastname: Voora
authors.forename: S D
authors.initials: SD
authors.lastname: Mahajan
authors.forename: I
authors.initials: I
authors.lastname: Kiliç
authors.forename: F
authors.initials: F
authors.lastname: Ismail-Beigi
authors.forename: S C
authors.initials: SC
authors.lastname: Kalhan
mesh_terms: D000818:Animals; D001786:Blood Glucose / Q000378:metabolism*; D005314:Embryonic and Fetal Development; D005260:Female; D005333:Fetus / Q000378:metabolism*; D051272:Glucose Transporter Type 1; D051274:Glucose Transporter Type 3; D000860:Hypoxia / Q000097:blood; D007700:Kinetics; D019344:Lactic Acid / Q000097:blood; D009004:Monosaccharide Transport Proteins / Q000378:metabolism; D009419:Nerve Tissue Proteins; D010100:Oxygen / Q000097:blood*; D011247:Pregnancy; D011270:Pregnancy, Animal / Q000097:blood*; D051381:Rats; D017207:Rats, Sprague-Dawley
chemical_list: D001786:Blood Glucose; D051272:Glucose Transporter Type 1; D051274:Glucose Transporter Type 3; D009004:Monosaccharide Transport Proteins; D009419:Nerve Tissue Proteins; C495679:Slc2a1 protein, rat; C495690:Slc2a3 protein, rat; D019344:Lactic Acid; D010100:Oxygen