Maternal undernutrition during early to mid gestation (28-77 days (d)) followed by adequate feeding up to term determines fetal tissue development in the absence of any effect on fetal body or tissue weight. GCR mRNA abundance is nutritionally upregulated in the adrenal, kidney, liver, lung, and perirenal adipose tissue of resultant neonatal offspring (Whorwood et al. 2001). However the extent to which hepatic GCR gene expression is programmed by nutrient availability to the fetus before birth remains to be determined.

Eighteen singleton-bearing ewes of similar body weight and parity were randomly allocated to one of two feeding groups from 28 d gestation (Dandrea, 2001). Nine nutrient restricted (NR) ewes consumed 60 % of their total metabolisable energy (ME) requirements from 28 to 80 d gestation, whilst control (C) ewes consumed 150 % of ME requirements. At 80 d gestation, four NR and five C ewes were fed 150 % of ME requirements until term (term = 147 d). Ewes were humanely euthanased (100 mg kg ^-1 pentobarbital sodium: Euthatal, I.V.) at either 80 d or 140 d gestation, to enable fetal and liver tissue sampling. The relative abundance of hepatic GCR to 18S rRNA was analysed by RT-PCR. Results are given as means and standard errors in arbitrary units (a.u.) as a percentage of a reference sample present on all gels. Statistical differences between nutritional groups were analysed using an unpaired student t test (P < 0.05).

Maternal nutrient restriction between 28-80 d gestation had no effect upon fetal body or liver weights. GCR mRNA abundance was comparable in 80 d NR fetuses (C 50.3 ± 14.3; NR 47.0 ± 2.5 a.u.). However, following 60 d of nutritional rehabilitation to 150 % of ME requirement GCR mRNA abundance in 140 d late gestation fetal livers was significantly decreased (C 98.3 ± 12.9; NR 40.1 ± 6.3 a.u. (P = 0.01). This result differs to that seen by Whorwood et al. 2001 where NR offspring when re-fed to 100 % ME requirements and had increased hepatic GCR levels.

In conclusion, GCR mRNA abundance in late-gestation fetuses is more susceptible to levels of refeeding following maternal undernutrition than by nutrient availability in early gestation. That is NR fetuses failed to undergo the normal gestational rise in hepatic GCR mRNA.

M.A. Hyatt was supported by a University of Nottingham Postgraduate Scholarship and by the University of Nottingham, Children’s Brain Tumour Research Centre.