Maternal glucocorticoids can also influence birth weight of the offspring. Under normal conditions, fetal exposure to glucocorticoids is relatively low due to the presence of placental 11/3-hydroxysteroid dehydrogenase 2 (11^HSD2), an enzyme that acts as a placental barrier by inactivating maternal glu-cocorticoids before they cross into the fetal environment. Maternal glucocorticoid treatment during pregnancy or inhibition of the placental 11/3HSD2 can therefore increase the amount of active gluco-corticoid crossing the placenta. Excess glucocorti-coid exposure has also been implicated in disturbing the normal growth and development of the fetus with consequential effects on the overall health of the adult offspring. There does, however, appear to be a critical window of sensitivity where the developing fetus is particularly sensitive to glu-cocorticoids. Glucocorticoid overexposure in the 3rd trimester is known to cause reductions in birth weight. Studies in rats have established that glucocorticoid-exposed offspring undergo rapid postnatal catch-up growth, which proves deleterious to their adult health. These studies have demonstrated that excess exposure to glucocorti-coids during fetal life is linked to low birth weight, altered functioning of the hypothalamic-pituitary-adrenal (HPA) axis, and the subsequent development of hypertension and impaired glucose tolerance in adulthood.
Increased HPA activity has been demonstrated in low-birth-weight human adult populations. Enhanced responsiveness of plasma cortisol to ACTH and increased urinary cortisol metabolite excretion has been reported in low-birth-weight adult males. Prenatal alteration of the HPA axis may therefore be involved in the subsequent development of cardiovascular disease in low-birth-weight adults.
Cord plasma leptin levels have been shown to correlate positively with birth weight and neonatal adiposity. It has been suggested that leptin has a regulatory role in growth and development. Low levels of cord blood leptin have been reported in growth-restricted offspring. These low leptin levels may also predict significant weight gain and catchup growth, both of which are evident in these growth-restricted offspring. Ong and colleagues hypothesized that there may be a link between in utero programing of leptin levels and the predisposition to the development of metabolic diseases.
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