MATERNAL AND FOETAL CORTICOSTERONE LEVELS DURING LATE PREGNANCY IN RATS

1975 ◽  
Vol 65 (3) ◽  
pp. 347-352 ◽  
Author(s):  
J. P. DUPOUY ◽  
H. COFFIGNY ◽  
S. MAGRE

SUMMARY Adrenal and plasma corticosterone levels were determined in rat foetuses and in intact or adrenalectomized mothers during late pregnancy. Foetal adrenal and plasma corticosterone concentrations reached a peak on day 19 of pregnancy, while maternal plasma corticosterone increased on day 18 and remained high until parturition. From day 18, mothers adrenalectomized on day 14 had corticosterone levels similar to those of intact pregnant rats. At every stage of gestation (except day 21) plasma corticosterone levels were higher in the foetuses than in the mothers. The corticosterone concentration in the maternal plasma correlated with the number of live foetuses during the last 3 days of gestation. These results suggest that corticosterone can cross the placenta from foetus to mother as early as day 18 and that the foetus contributes to the maternal corticosterone pool after day 18.

1988 ◽  
Vol 116 (3) ◽  
pp. 381-385 ◽  
Author(s):  
T. M. Nguyen ◽  
A. Halhali ◽  
H. Guillozo ◽  
M. Garabedian ◽  
S. Balsan

ABSTRACT The effect of thyroparathyroidectomy (TPTX) on the plasma concentrations of the vitamin D metabolites (25-(OH)D, 24,25-(OH)2D and 1,25-(OH)2D) has been studied in pregnant rats and their fetuses during the last quarter of gestation. Maternal and fetal vitamin D metabolites were not significantly affected by TPTX. A significant increase in plasma 1,25-(OH)2D concentrations was observed in both TPTX and control mothers and fetuses from days 19 to 21. Fetal and maternal plasma 25-(OH)D were positively correlated in both control and TPTX groups. Such a correlation was also found for 24,25-(OH)2D in the two groups. In contrast, a positive correlation between maternal and fetal plasma concentrations of 1,25-(OH)2D was found in TPTX but not in control rats. These data suggest that major alterations in calcium metabolism, such as that produced by maternal TPTX, are insufficient to affect the changes in maternal and fetal plasma 1,25-(OH)2D during late pregnancy significantly. They also suggest that parathyroid hormone, thyroxine, and/or calcitonin may control a possible placental transfer of 1,25-(OH)2D in the rat. J. Endocr. (1988) 116, 381–385


1982 ◽  
Vol 95 (1) ◽  
pp. 49-58 ◽  
Author(s):  
S. Mulay ◽  
D. R. Varma ◽  
S. Solomon

The influence of dietary protein deficiency on maternal plasma corticosterone and progesterone levels as well as on maternal and fetal liver and lung cytoplasmic glucocorti-coid receptors has been studied in Sprague–Dawley rats during the last 3 days of gestation. Plasma corticosterone levels of control but not protein-deficient rats increased on days 20 and 21 of gestation; corticosterone levels of protein-deficient rats decreased on day 21 of gestation. Maternal adrenalectomy caused only a moderate decrease in corticosterone levels in both groups of pregnant rats. Fetal corticosterone levels of the two groups of rats were similar. Progesterone levels were consistently lower in protein-deficient than in control animals from day 20 of gestation until 2–12 h after parturition. There were no differences in the binding of [3H]dexamethasone to liver cytosol of non-pregnant control and protein-deficient rats. However, receptor levels were lower in pregnant controls than in pregnant protein-deficient rats. Maternal protein deficiency led to an increase in fetal liver glucocorticoid receptor levels but exerted no significant effect on receptor levels in fetal lung. It is suggested that lower levels of plasma corticosterone and progesterone and high levels of liver glucocorticoid receptors in protein-deficient rats might be related to some of the adverse consequences of maternal malnutrition on fetal development.


2015 ◽  
Vol 228 (3) ◽  
pp. 135-147 ◽  
Author(s):  
Michaela D Wharfe ◽  
Peter J Mark ◽  
Caitlin S Wyrwoll ◽  
Jeremy T Smith ◽  
Cassandra Yap ◽  
...  

Maternal physiological adaptations, such as changes to the hypothalamic–pituitary–adrenal (HPA) axis, are central to pregnancy success. Circadian variation of the HPA axis is dependent on clock gene rhythms in the hypothalamus, but it is not known whether pregnancy-induced changes in maternal glucocorticoid levels are mediated via this central clock. We hypothesized that hypothalamic expression of clock genes changes across mouse pregnancy and this is linked to altered HPA activity. The anterior hypothalamus and maternal plasma were collected from C57Bl/6J mice prior to pregnancy and on days 6, 10, 14 and 18 of gestation (term=d19), across a 24-h period (0800, 1200, 1600, 2000, 0000, 0400 h). Hypothalamic expression of clock genes and Crh was determined by qPCR, plasma ACTH concentration measured by Milliplex assay and plasma corticosterone concentration by LC-MS/MS. Expression of all clock genes varied markedly across gestation, most notably at mid-gestation when levels of each gene were elevated. The pregnancy-induced increase in maternal corticosterone levels (by up to 14-fold on day 14) was not accompanied by a parallel shift in plasma ACTH (28% lower on day 14 compared with non-pregnant levels). Moreover, while circadian rhythmicity in corticosterone was maintained up to day 14 of gestation, this was effectively lost by day 18. Overall, our data show that the central circadian clock undergoes marked adaptations throughout mouse pregnancy, changes that are likely to contribute to maternal physiological adaptations. Importantly, however, neither hypothalamic clock genes nor plasma ACTH levels appear to drive the marked increase in maternal corticosterone after mid-gestation.


1974 ◽  
Vol 61 (1) ◽  
pp. 21-28 ◽  
Author(s):  
KATUAKI ÔTA ◽  
TAKAO ÔTA ◽  
AKIRA YOKOYAMA

SUMMARY Levels of plasma corticosterone and of pituitary prolactin were studied in the mornings (10.00–10.30 h) and evenings (17.00–18.00 h) during the last week of pregnancy in the rat. Morning levels of plasma corticosterone started to rise on day 19 and reached a peak on day 21. The concentration of corticosterone in plasma on the morning of day 21 was about 2·3 times higher than that on day 15. Both content and concentration of prolactin in the pituitary began to fall on the morning of day 19 of pregnancy and the minimum values for both content and concentration were reached on the morning of day 21. Plasma corticosterone concentration and pituitary prolactin content measured in the evening, however, remained high throughout the period examined and there were no appreciable changes in the levels at the different stages of pregnancy. The results obtained on day 22 of pregnancy, the expected day of parturition, indicated that a surge of pituitary prolactin secretion and a temporary depression of corticosterone secretion occurred at about the time of parturition.


1986 ◽  
Vol 112 (3) ◽  
pp. 396-403 ◽  
Author(s):  
Jean Paul Dupouy ◽  
Alain Chatelain

Abstract. CBG and pituitary-adrenal activities were investigated in intact rat foetuses, in newborns spontaneously delivered by vaginal way and in postmature foetuses from mothers with delayed parturition caused by daily progesterone injection from day 20 of gestation. The postmature foetuses had lower body weights and higher adrenal weights on day 22, 23 and 24 of gestation than newborns of the same conceptional age. The corticosterone binding capacity of the plasma as well as the binding capacity of CBG for corticosterone decreased in intact foetuses for the last 3 days of gestation and stayed very low in pups from day 0 to day 8 postpartum. These parameters decreased more slowly in postmature foetuses; however, the differences between the latter and intact foetuses or newborns were not statistically significant. Similar evolution occurred in intact pregnant and suckling females as well as in females with prolonged gestation. The fall in CBG activity in normal rat pups and the subsequent rise in free steroids could explain a sharp decrease in plasma ACTH levels as well as the drop in adrenal and plasma corticosterone concentration. In foetuses with prolonged gestation, the same phenomenon did not occur. Stress conditions produced by maintaining growing foetuses in utero and the development of severe jaundice maintained high ACTH levels. In contrast, the fall in adrenal and plasma corticosterone concentrations in spite of the high level of circulating ACTH could be mainly due to the progesterone inhibition of the steroidogenic activity of the foetal adrenals.


1981 ◽  
Vol 241 (1) ◽  
pp. R21-R24 ◽  
Author(s):  
R. G. Doell ◽  
M. F. Dallman ◽  
R. B. Clayton ◽  
G. D. Gray ◽  
S. Levine

These experiments were undertaken to investigate the mechanism whereby a precipitous drop in plasma corticosterone concentration is brought about following drinking in rats on a restricted water schedule. No alteration in adrenocorticotrophic hormone (ACTH) output was found, nor was catabolism of corticosterone sufficient to account for the drop. It is concluded that corticosterone level is controlled under these conditions by a mechanism independent of ACTH concentration.


2005 ◽  
Vol 389 (3) ◽  
pp. 913-918 ◽  
Author(s):  
Julio Sevillano ◽  
Inmaculada C. López-Pérez ◽  
Emilio Herrera ◽  
María del Pilar Ramos ◽  
Carlos Bocos

The level of maternal circulating triacylglycerols during late pregnancy has been correlated with the mass of newborns. PPARγ (peroxisome-proliferator-activated receptor γ) ligands, such as TZDs (thiazolidinediones), have been shown to reduce triacylglycerolaemia and have also been implicated in the inhibition of tissue growth and the promotion of cell differentiation. Therefore TZDs might control cell proliferation during late fetal development and, by extension, body mass of pups. To investigate the response to EZ (englitazone), a TZD, on perinatal development, 0 or 50 mg of englitazone/kg of body mass was given as an oral dose to pregnant rats daily from day 16 of gestation until either day 20 for the study of their fetuses, or until day 21 of gestation for the study of neonates. EZ decreased maternal triacylglycerol levels at day 20 of gestation and neonatal mass, but not fetal mass. Fetuses and neonates from EZ-treated mothers exhibited high levels of insulin and were found to be hyperglycaemic. The apparent insulin-resistant state in neonates from EZ-treated pregnant rats was corroborated, since they showed higher plasma NEFA [non-esterified (‘free’) fatty acid] levels, ketonaemia and liver LPL (lipoprotein lipase) activity and lower plasma IGF-I (type 1 insulin-like growth factor) levels, in comparison with those from control mothers. Moreover, at the molecular level, an increase in Akt phosphorylation was found in the liver of neonates from EZ-treated mothers, which confirms that the insulin pathway was negatively affected. Thus the response of fetuses and neonates to maternal antidiabetic drug treatment is the opposite of what would be expected, and can be justified by the scarce amount of adipose tissue impeding a normal response to PPARγ ligands and by hyperinsulinaemia as being responsible for a major insulin-resistant condition.


2013 ◽  
Vol 98 (1) ◽  
pp. 299-307 ◽  
Author(s):  
R. J. Moon ◽  
N. C. Harvey ◽  
S. M. Robinson ◽  
G. Ntani ◽  
J. H. Davies ◽  
...  

1974 ◽  
Vol 63 (1) ◽  
pp. 213-222 ◽  
Author(s):  
JULIA C. BUCKINGHAM ◽  
J. R. HODGES

SUMMARY Changes in pituitary and plasma corticotrophin (ACTH), estimated by redox bioassay, were correlated with changes in plasma corticosterone in adrenalectomized rats, with and without corticosterone treatment, before and after exposure to stress. After adrenalectomy, the plasma ACTH concentration was persistently increased. The pituitary ACTH content declined and then increased markedly. These changes were prevented by physiological doses of corticosteroids. Stress caused only a small rise in the plasma ACTH concentration in intact and sham-operated rats but a marked increase in adrenalectomized animals. This exaggerated response was reduced to normal by physiological doses of corticosterone. Prolonged treatment with higher doses of corticosterone was necessary to abolish completely the adrenocorticotrophic response to stress. However, one injection of the steroid, in a dose sufficient to raise the plasma corticosterone concentration to a similar level, did not impair the stress-induced release of ACTH. The results suggest that the synthesis and the basal release of ACTH are directly controlled by the concentration of corticosteroid in the blood, but the corticosteroids exert only a delayed effect in modulating the stress-induced release of the hormone.


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