Influence of Corticosteroids on Glycogen Content and Steroid 11-Reductase Activity in Lung and Liver of the Fetal and Newborn Rat

Bt, Smith; Tanswell, A. Keith; Minshall, D.; Wn, Bogues; Vreeken, E

doi:10.1159/000241600

Cited by 19 publications

(9 citation statements)

References 15 publications

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“…The rate of choline incorporation into phosphatidylcholine more than tripled between 19-20 days gestation and 1 day after birth. These profiles are similar to those previously reported for glycogen content (28,(30)(31)(32) and phosphatidylcholine synthesis (28,(33)(34)(35)(36) in the rat. Similar developmental profiles have been reported in other species (1,14).…”

Section: Resultssupporting

confidence: 90%

Thyroid Hormone Opposes Some Glucocorticoid Effects on Glycogen Content and Lipid Synthesis in Developing Fetal Rat Lung

1986

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ABSTRACT. Because of current interest in use of a com-used prophylactically to accelerate fetal lung maturation and bination of glucocorticoid and thyroid hormones for pre-prevent RDS in human newborns (2, 3) and in at least one vention of respiratory distress syndrome we examined the clinical study (4) thyroxine was also reported to be effective in effects of dexamethasone and triiodothyronine (T3), alone this regard. However, the findings in a recent multicenter study and in combination, on glycogen content and rates of fatty that glucocorticoids are not as efficacious in preventing RDS as acid and phosphatidylcholine synthesis in fetal rat lung. earlier believed and that its effects may be largely confined to The hormones were administered to the mothers on the 2 female infants (5) has led to interest in use of a combination of days before delivery on days 17-22 of gestation. Both glucocorticoids and thyroid hormone for prevention of RDS (6).hormones increased the rate of choline incorporation into Prior to such clinical use, however, it is desirable to have inforphosphatidylcholine, an index of surfactant synthesis, on mation on the interaction of these hormones in the acceleration day 20 just prior to the normal developmental surge but of lung maturation in animals. had no effect on this parameter on days 19, 21, or 22.Previous studies in animals have shown that a combination of There is a developmental increase in lung glycogen on days glucocorticoid and thyroid hormones is more effective than either 17-20 with a decrease thereafter and a developmental hormone alone in accelerating fetal lung maturation and stimuincrease in the rate of fatty acid synthesis between days 20 lating surfactant production. In a morphological study in the and 21. The increases in glycogen content and fatty acid fetal rat, Hitchcock (7) reported maximal acceleration of lung synthesis were accelerated by dexamethasone and pre-maturation when glucocorticoids and thyroxine were both presvented by T3 and when the hormones were administered ent. Similarly, a synergistic interaction between glucocorticoids together T3 antagonized the stimulatory effects of dexa-and thyroid hormone in stimulating synthesis of phosphatidylmethasone on these parameters. Both dexamethasone and choline and disaturated phosphatidylcholine, the major compo-T3 accelerated the normal developmental decrease in lung nent of pulmonary surfactant (I), was demonstrated in fetal rat glycogen later in gestation and the effects of the two lung in vivo (8,9) and in fetal rat (10, 1 I), rabbit (12), and hormones on this parameter were additive. The combina-human (1 3) lung in culture. tion of dexamethasone and T3 led to significantly smaller In addition to morphology and synthesis of surfactant phosfetuses and increased mortality late in gestation. These pholipids, lung maturation may also be assessed by other criteria. data show that glucocorticoid and thyroid hormones have An increase followed by a decrease in glycogen content is a opposite as well as common effects on...

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Section: Resultssupporting

confidence: 90%

Thyroid Hormone Opposes Some Glucocorticoid Effects on Glycogen Content and Lipid Synthesis in Developing Fetal Rat Lung

1986

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“…Although glucocorticoids have been shown to increase llß-HSD enzyme activity in the fetal rat lung (Smith et al 1982), adult mouse thymus (Dougherty et al 1960) and cultured human skin fibroblasts (Hammami & Siiteri 1991), under the conditions of the present study we found no effects of short-term glucocorticoid treatment on fetal pituitary llß-HSDl mRNA. However, we cannot rule out the possibility that long-term glucocorti¬ coid treatment may be effective in this regard.…”

Section: Resultscontrasting

confidence: 82%

Developmental and glucocorticoid regulation of pituitary 11 β-hydroxysteroid dehydrogenase 1 gene expression in the ovine fetus and lamb

Yang

Matthews²,

Challis³

1995

Journal of Molecular Endocrinology

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To examine the role of 11 beta-hydroxysteroid dehydrogenase 1 (11 beta-HSD1) in the control of glucocorticoid actions in the ovine pituitary during development, we have sought developmental changes in the distribution and the level of 11 beta-HSD1 mRNA by in situ hybridization. In the pars distalis, 11 beta-HSD1 mRNA was present by day 60; its amount did not change significantly until term (days 145-147) when it increased dramatically. The level of 11 beta-HSD1 mRNA increased further during the postnatal period. In contrast, 11 beta-HSD1 mRNA in the pars intermedia was not detectable until day 135; it increased in amount at days 140-143, but did not change significantly thereafter through to adulthood. We have also measured levels of both dehydrogenase and reductase activities of 11 beta-HSD1 in the pars distalis of fetal sheep at day 140 and term, and of postnatal sheep at 1-2 months of age, to determine whether changes in 11 beta-HSD1 mRNA are reflected in the levels of enzyme activities. There were progressive increases in both dehydrogenase and reductase activities from day 140 to 1-2 months postnatally, although dehydrogenase activity was consistently higher than reductase activity. Finally, we have determined the effect of short-term intrafetal cortisol infusion (5 micrograms/min for 12 h) on levels of pituitary 11 beta-HSD1 mRNA by in situ hybridization. There was no effect of cortisol infusion on 11 beta-HSD1 mRNA expression.(ABSTRACT TRUNCATED AT 250 WORDS)

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“…Recent studies by Smith and Sabry [28] on 20-day-old fetal lung cul tures indicate that cortisol induced the syn thesis of a mesenchymal fibroblast-pneumonocyte factor which interacts with recep tors on the cell surface of alveolar type-11 cells to elevate intracellular level of cyclic AMP. An elevation in cyclic AMP presum ably initiates a cascade of enzyme reactions resulting in enhanced glycogen breakdown to glycolytic intermediates such as the aglyceraldehyde phosphate, dihydroxyacetone phosphate or acetate, all of which are utilized for the synthesis of phospholipids [22,29], Although we could not demon strate in vivo any effect of dexamethasone administration to pregnant rats on the fetal lung factor(s) potentiating adenylate cyclase activity to produce more cyclic AMP, the results of the present study and those of Smith and Sabry [28] support the earlier observations of Barrett et al [2,3] that cor ticosteroids enhance fetal lung maturation via cyclic AMP. The mechanism(s) by which corticosteroids elevate cyclic AMP in fetal lungs is not clearly understood.…”

Section: Discussionmentioning

confidence: 99%

Effects of Dexamethasone Administration to Pregnant Rats on Adenylate Cyclase and Cyclic AMP Phosphodiesterase Activities in the Maternal and Fetal Lungs

Chaudhary¹,

Nijjar²

1984

Neonatology

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Adenylate cyclase and cyclic AMP phosphodiesterase activities were examined in the maternal and fetal lungs before and after delivery from the saline- and dexamethasone-treated pregnant rats. Basal adenylate cyclase activity in the maternal lungs of control animals did not change after parturition whereas the enzyme activity in fetal lungs increased 2.5-fold after birth. Dexamethasone treatment reduced adenylate cyclase activity in the maternal lungs before and after parturition while the enzyme activity in fetal lungs was increased. The ability of the cytoplasmic factors to activate adenylate cyclase in maternal lungs decreased after parturition. Dexamethasone treatment of the pregnant rat lowered the cytoplasmic activation of the maternal enzyme before and after parturition, but the percent activation of the enzyme in both the maternal and fetal lungs was not affected. The decrease in activator activity of the maternal lungs after parturition was not apparently due to the reduced sensitivity of adenylate cyclase to the same level of the activator protein. However, it would appear that both adenylate cyclase and its activator protein have undergone some maturational changes during lung development. Adrenalectomy of rats did not alter the basal adenylate cyclase activity in lung membranes but reduced the cytoplasmic activation of the enzyme. Unlike pregnant rats, dexamethasone treatment of adrenalectomized rats restored the cytoplasmic activation of adenylate cyclase not only to the control value, but potentiated it even higher than the control without affecting the basal adenylate cyclase activity. Cyclic AMP phosphodiesterase activity in both the maternal and fetal lungs was not influenced by parturition. However, dexamethasone treatment lowered cyclic AMP phosphodiesterase activity in both the maternal and fetal lungs at both ages. Dexamethasone treatment of pregnant rats elevated phospholipids and lowered DNA levels in the maternal as well as fetal lungs. These data are consistent with the view that dexamethasone treatment of pregnant rats during late gestation may elevate cyclic AMP levels to induce fetal lung maturation with a concomitant decrease in cellular proliferation.

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Influence of Corticosteroids on Glycogen Content and Steroid 11-Reductase Activity in Lung and Liver of the Fetal and Newborn Rat

Cited by 19 publications

References 15 publications

Thyroid Hormone Opposes Some Glucocorticoid Effects on Glycogen Content and Lipid Synthesis in Developing Fetal Rat Lung

Thyroid Hormone Opposes Some Glucocorticoid Effects on Glycogen Content and Lipid Synthesis in Developing Fetal Rat Lung

Developmental and glucocorticoid regulation of pituitary 11 β-hydroxysteroid dehydrogenase 1 gene expression in the ovine fetus and lamb

Effects of Dexamethasone Administration to Pregnant Rats on Adenylate Cyclase and Cyclic AMP Phosphodiesterase Activities in the Maternal and Fetal Lungs

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