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University Research Centre for Neuroendocrinology (L.A.N., E.J.H., R.J.W., S.A.W., C.D.I., A.L.), University of Bristol, Bristol Royal Infirmary, Bristol BS2 8HW, United Kingdom; and Department of Physiology (X.W.H., A.J.L.), Cardiovascular Research Laboratories, University of Bristol, Bristol BS8 1TD, United Kingdom
Address all correspondence and requests for reprints to: Dr. A. Levy, University Research Centre for Neuroendocrinology, University of Bristol, Bristol Royal Infirmary, Lower Maudlin Street, Bristol BS2 8HW, United Kingdom. E-mail: a.levy{at}bris.ac.uk
To further define the neuroendocrine consequences of intrauterine growth retardation (IUGR), we have used a rat model of maternal protein restriction throughout pregnancy to examine the pattern of corticosterone and GH secretion under basal conditions and in response to psychological stress in male offspring at 4, 9, and 18 months of age. The findings were correlated with studies of behavioral activity. Despite a consistent reduction in birth weight and failure of catch-up growth, there were no significant differences in GH secretory profiles between IUGR and control rats at any age. We were unable to demonstrate a difference in the number, amplitude, length, or area of corticosterone secretory pulses between control and IUGR animals; although again, there was a significant decrease with age. The mean peak plasma concentration of corticosterone in response to a noise stress also declined with age but was unaffected by IUGR. There were no consistent, statistically significant differences in behavioral responses between normal control and IUGR animals or between groups of animals at different ages. These results do not, therefore, support the presence of major functional abnormalities in either GH or corticosterone secretory responses in adult male rats subjected to IUGR.
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