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J Physiol Volume 554, Number 2, 529-541, January 15, 2004 DOI: 10.1113/jphysiol.2003.054577
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Ovine feto-placental metabolism

J. W. Ward, F. B. P. Wooding and A. L. Fowden

Department of Physiology, University of Cambridge, Downing Street, Cambridge CB2 3EG, UK

Fetal growth depends on the transplacental nutrient supply, which, in turn, is determined partially by the consumption and production of nutrients by the uteroplacental tissues. In fetal sheep, the rates of growth and umbilical glucose uptake decline coincidently towards term in parallel with the normal prepartum rise in plasma cortisol. While cortisol is known to reduce growth in fetal sheep, its effects on the uteroplacental handling and delivery of nutrients remain unknown. Hence, this study, quantified the rates of umbilical uptake and uteroplacental consumption of nutrients in preterm fetuses infused with cortisol for 5 days to mimic the prepartum cortisol surge. Umbilical uptakes of glucose and lactate, but not oxygen, were significantly lower in cortisol- than saline-infused fetuses, irrespective of whether values were expressed as absolute or weight-specific rates. The rate of uteroplacental consumption of glucose, but not oxygen, was significantly higher in cortisol- than saline-infused animals. Absolute rates of uteroplacental lactate production were lower in cortisol-infused animals. When all data were combined, fetal plasma cortisol levels were positively correlated to uteroplacental glucose consumption and inversely related to umbilical glucose uptake. Cortisol treatment had no apparent effect on placental mRNA expression for the glucose transporters, GLUT-1 and GLUT-3. The results demonstrate that cortisol is physiological regulator of uteroplacental metabolism and nutrient delivery to the sheep fetus. These observations have important implications for fetal growth both in late gestation and during adverse intrauterine conditions, which raise fetal cortisol levels earlier in gestation.

(Received 5 September 2003; accepted after revision 30 October 2003; first published online 31 October 2003)
Corresponding author A. L. Fowden: Department of Physiology, University of Cambridge, Downing Street, Cambridge CB2 3EG, UK.  Email: alf1000{at}cam.ac.uk




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