Helen Budge, Terence Stephenson and Michael E. Symonds Pages 888 - 893 ( 6 )
An increase in fetal glucocorticoid exposure has long been considered to be a primary mechanism by which maternal nutritional manipulation may result in long term adaptations in the fetus such that it is at increased risk of a range of adult diseases including hypertension, diabetes and obesity. Animal studies in which high doses of synthetic glucocorticoids have been administered to the mother shown some long term programming effects, but these are nearly always accompanied by a reduction in maternal food intake. In this review, we will, therefore, consider the extent to which maternal food restriction and elevated maternal glucocorticoid concentrations can result in the same or different adaptations within the fetus such that they exhibit developmental changes in blood pressure control and/or metabolic homeostasis. One factor that appears to be critical in determining the mothers response is the stage of gestation at which her nutrient intake is manipulated. This may be explained in part by the placentas ability to inactivate glucocorticoids. Irrespective of the mechanisms involved, it is clear that long term tissue specific adaptations within a range of organs, including adipose tissue and the kidney, can be greatly altered following changes in maternal glucocorticoid secretion.
Nutrition, blood pressure, cortisol, growth
Academic Division of Child Health, School of Human Development, Queen's edical Centre, University Hospital, Nottingham, NG7 2UH, United Kingdom.