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1 School of Women's and Infants' Health, Univ of Western Australia, perth, Western Australia, Australia; Women and Infants Research Foundation, 6008, Western Australia, Australia
2 School of Women's and Infants' Health, University of Western Australia, Nedlands, Western Australia, Australia; Women and Infants Research Foundation, Perth, Western Australia, Australia
3 School of Women's and Infants' Health, University of Western Australia, Nedlands, Western Australia, Australia
4 Physiology, University of Toronto, toronto, Canada; Obstetrics and Gynecology, University of Toronto, toronto, Canada
5 School of Women's and Infants' Health, University of Western Australia, Perth, Western Australia, Australia; Women and Infants Research Foundation, Perth, Western Australia, Australia
* To whom correspondence should be addressed. E-mail: dsloboda{at}obsgyn.uwa.edu.au.
Fetal exposure to synthetic glucocorticoids in sheep results in increased fetal hypothalamic-pituitary-adrenal (HPA) activity persisting to one year of age. Aim: to determine effects of single or repeated maternal or fetal betamethasone injection on offspring HPA activity at 2 and 3 years of age and whether changes in adrenal mediators of steroidogenesis contribute to changes in pituitary-adrenal function. Pregnant ewes or their fetuses received either repeated intramuscular saline (MS, FS) or betamethasone injections (0.5mg/kg; M4, F4) at 104, 111, 118 and 124 days of gestation (dG), or a single betamethasone injection at 104, followed by saline at 111, 118 and 124 dG (M1, F1). Offspring were catheterised at 2 and 3 years of age and given corticotrophin-releasing hormone + arginine vasopressin challenges. Adrenal tissue was collected for quantitative RT-PCR mRNA determination at 3.5 years of age. In 2-year-old offspring, maternal betamethasone injections did not alter basal ACTH or cortisol levels but repeated injections elevated ACTH responses. At 3 years of age, basal ACTH was elevated and both basal and stimulated cortisol levels were suppressed by repeated maternal injections. Basal and stimulated cortisol to ACTH ratios and basal cortisol to P450c17 mRNA ratios were suppressed by repeated injections. Repeated fetal betamethasone injections attenuated basal ACTH and cortisol levels in offspring at 2 but not 3 years of age. Plasma changes were not associated with altered adrenal P450c17, ACTH receptor, 11
HSD2 or glucocorticoid receptor mRNA levels. These data suggest that maternal, but not fetal, betamethasone administration results in adrenal suppression in adulthood.
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 D. M Sloboda, T. J M Moss, S. Li, S. G Matthews, J. R G Challis, and J. P Newnham Expression of glucocorticoid receptor, mineralocorticoid receptor, and 11{beta}-hydroxysteroid dehydrogenase 1 and 2 in the fetal and postnatal ovine hippocampus: ontogeny and effects of prenatal glucocorticoid exposure J. Endocrinol., May 1, 2008; 197(2): 213 - 220. [Abstract] [Full Text] [PDF]
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T. Braun, S. Li, T. J M Moss, J. P Newnham, J. R G Challis, P. D Gluckman, and D. M Sloboda Maternal betamethasone administration reduces binucleate cell number and placental lactogen in sheep J. Endocrinol., August 1, 2007; 194(2): 337 - 347. [Abstract] [Full Text] [PDF]
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