Comment on: Nyirenda MJ, Dean S, Lyons V, Chapman KE, Seckl JR (2006) Prenatal programming of hepatocyte nuclear factor 4a in the rat: a key mechanism in the ‘foetal origins of hyperglycaemia’? Diabetologia 49: 1412–1420, and on: McCurdy CE, Friedman JE (2006) Early foetal programming of hepatic gluconeogenesis: glucocorticoids strike back. Diabetologia 49:1138–1141

Background/Aims: Nutrition during fetal and early postnatal development can have permanent effects on physiology resulting in an increased risk for disease in later life. The aim of this study was to explore changes in gene expression related to maternal energy restriction during pregnancy in rat fetuses and in neonatal rat offspring. Methods: From day 4 of gestation until parturition, energy-restricted dams received either 75 or 50% of ad libitum food intake. Microarray analyses were performed on whole 13- and 17-day fetuses and 1-day-old pups. Protein and fat contents of the dams’ milk were analyzed in the different feeding groups. Results: A surprisingly small number of genes were differentially expressed between the groups, probably due to the strict control of fetal development. Interestingly, the expressions of many pancreatic digestion enzymes were reduced in the 1-day-old pups of the energy-restricted dams. A statistically significant difference in milk protein content was observed on day 1 post-partum between the gestationally food-restricted groups. Conclusions: The expressions of several genes that may have an important role in the normal development of organs were affected by undernutrition during fetal development. In addition, undernutrition may have affected the function of the exocrine pancreas.

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Differential effects of prenatal stress and glucocorticoid administration on postnatal growth and glucose metabolism in rats

Franko

Forhead²,

Fowden

2009

Journal of Endocrinology

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Glucocorticoid administration during pregnancy programmes cardiovascular and metabolic functions in the adult offspring. Often, the control procedures are stressful per se and raise maternal glucocorticoid concentrations. This study compared the effects of maternal injection with dexamethasone (dex, 200 mg/kg) or saline with no treatment from 15 to 20 days of rat pregnancy on offspring growth and glucose metabolism. Near term, maternal corticosterone concentrations were higher in the saline-treated dams and lower in the dex-treated dams relative to untreated animals. In both male and female offspring, growth rate was measured for 14 weeks, and glucose tolerance was assessed between 12 and 13 weeks together with body fat content and plasma concentrations of insulin, leptin, and corticosterone between 14 and 15 weeks. Offspring liver was collected at different ages and was analyzed for glycogen content and gluconeogenic enzyme activity. Compared with untreated animals, both dex and saline treatments altered postnatal growth although adult body weight was unaffected. The two treatments had different effects on adult insulin concentrations and on hepatic glycogen content and gluconeogenic enzyme activities both pre-and postnatally. Relative to untreated animals, adult glucose tolerance was improved by maternal saline injection in males but not in females, while it was impaired in female offspring but not in male offspring of the dex-treated dams. Adult glucose tolerance was related to male body fat content but not to female body fat content. Dex and saline treatments of pregnant rats have differential sex-linked effects on the growth and glucose metabolism of their offspring, which indicates that the programming actions of natural and synthetic glucocorticoids may differ.

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Abstract: 3. Burns SP, Desai M, Cohen RD et al (1997) Gluconeogenesis, glucose handling, and structural changes in livers of the adult offspring of rats partially deprived of protein during pregnancy and lactation.

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Gene Expression Profiles in Fetal and Neonatal Rat Offspring of Energy-Restricted Dams

Differential effects of prenatal stress and glucocorticoid administration on postnatal growth and glucose metabolism in rats

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