Hormones and the lung. I. Thyroid hormones and glucocorticoids in lung development

Hitchcock, Karen R.

doi:10.1002/ar.1091940103

Cited by 87 publications

(33 citation statements)

References 44 publications

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“…Such a regimen might improve/normalize intracellular T 3 concentrations in all tissues (32). It is known that lung maturation is T 3 -dependent (33). A combined T 4 /T 3 treatment could stimulate maturation in both central nervous tissue and peripheral organs such as the lungs.…”

Section: European Journal Of Endocrinology (1998) 139mentioning

confidence: 99%

“…In addition, T 3 enhances expression of the type I deiodinase gene (27), and T 3 treatment thus could increase endogenous T 3 production. It may, however, be difficult to find an appropriate T 4 /T 3 regimen, because a middle course must be found between a T 3 dose by which maturation is enhanced and morbidity is decreased (33,34), and a T 3 dose that does not increase protein catabolism (35). Treatment with T 3 alone is not advisable, as it will result in lower plasma T 4 concentrations by negative feedback (19), and thus will increase the risk of depletion of cerebral thyroid hormone supply.…”

Section: European Journal Of Endocrinology (1998) 139mentioning

confidence: 99%

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Thyroxine administration to infants of less than 30 weeks gestational age decreases plasma tri-iodothyronine concentrations

Wassenaer¹,

Kok²,

Dekker³

et al. 1998

European Journal of Endocrinology

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Objective: To investigate the effect on thyroid hormone metabolism of the administration of thyroxine to very preterm infants. Design and methods: Two hundred infants of less than 30 weeks gestation were enrolled into a randomized, double-blind, placebo-controlled trial. Thyroxine (T 4 ) (at a fixed daily dose of 8 mg/kg birthweight) or placebo was started 12-24 h after birth and discontinued 6 weeks later. Plasma concentrations of T 4 , tri-idothyronine (T 3 ), reverse T 3 (rT 3 ), TSH, and thyroxine-binding globulin were measured weekly during trial medication and 2 weeks thereafter. Results: The T 4 and the placebo group each comprised 100 infants. Antenatal, perinatal, and postnatal clinical characteristics were comparable in both groups. T 4 and rT 3 were significantly increased in the T 4 group. TSH concentrations were depressed in the T 4 group and T 3 was significantly decreased, probably as a result of TSH depression. The T 4 /T 3 and T 4 /rT 3 ratios differed significantly between the two study groups. Conclusions: Daily T 4 administration during the first 6 weeks after birth to infants of less than 30 weeks gestation prevents hypothyroxinemia, but decreases plasma T 3 concentrations. Our finding possibly implies that very preterm infants should receive supplements of both T 4 and T 3 .

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Section: European Journal Of Endocrinology (1998) 139mentioning

confidence: 99%

Section: European Journal Of Endocrinology (1998) 139mentioning

confidence: 99%

Thyroxine administration to infants of less than 30 weeks gestational age decreases plasma tri-iodothyronine concentrations

Wassenaer¹,

Kok²,

Dekker³

et al. 1998

European Journal of Endocrinology

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“…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.…”

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confidence: 96%

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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“…Although the physiologic importance of this T3 neogenesis remains unclear, it is quite possible that T3 exerts the biologic effects of thyroid hormone and, therefore, is responsible for the morphologic changes in fetal and adult type I1 cells which have been described by a number of investigators (for review, see [20][21][22]. It is also possible that T4, rather than acting as a prohormone, has effects of its own, and that in the course of its activity it is metabolized peripherally to other thyronines such as T3 and rT3 These compounds might then simply represent by-products of thyroid hormone action.…”

Section: Discussionmentioning

confidence: 99%

“…More recently, Hitchcock and collaborators (20)(21)(22) demonstrated that thyroxine (T4) can accelerate rat lung development and that this acceleration is maximal in the presence of glucocorticoids. Similar findings were noted by Ballard and associates (1, 2) during transplacental stimulation of fetal rabbit lung by an analog of T4 known as DIMIT.…”

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confidence: 99%

Thyroxine Metabolism in Cultured Cells Derived from Fetal Rat Lung

et al. 1983

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SummaryThe role of thyroxine (T4) in fetal lung development has been demonstrated previously. Because triiodothyronine (T3), not T4, is thought to be the active hormone, and because T3 nuclear recep tors appear to be present in fetal lung, the following studies were performed to examine peripheral metabolism of [12'I] [1311JT3 and [1251]T3; the ratio of these provided an index of intracellular conversion of [12'I]T4 to [l2'IjT3. The mean of five such experiments demonstrated that of the total ['2'IJT3 attached to the nuclear fraction at the end of the incubation, 32% was newly generated and 68% was derived by influx from the medium. These results indicate that organotypic cultures derived from day 19 fetal rat lung are capable of deiodinating T4 and that both rT3 and T3 are generated. The generated T3 appears to be retained by the lung cells and is bound to the nuclear fraction. On the other hand, rT3 is distributed more evenly throughout the cell and in the medium and presumably is not bound. Abbreviations DIMIT, 3,5-dimethyl-3'-isopropyl-L-thyronine FBS, fetal bovine serum PC, phosphatidylcholme T3, triiodothyronine rT3, reverse T3 T4, thyroxine TAA, hexane-tertiary amyl alcohol3 N ammoniaThe role of thyroid hormone in fetal lung development is well recognized, but its mechanism of action is not clear (20-22, 27, 38). The hormonal milieu of the mammalian fetus is characterized by low triiodothyronine (T3) levels and high concentrations of reverse T3 (rT3) (16, 38); and yet, certain target organs, including the lung, appear to depend on the active form of thyroid hormone (i.e., T3) during certain developmental stages.Early studies by Redding et al. (27) showed that thyroidectomy and subsequent thyroid hormone replacement profoundly influenced the morphologic characteristics of type I1 pneumonocytes and their lamellar bodies, and that there was a correlation between the demonstrated ultrastructural changes and lung surfactant secretion. More recently, Hitchcock and collaborators (20-22) demonstrated that thyroxine (T4) can accelerate rat lung development and that this acceleration is maximal in the presence of glucocorticoids. Similar findings were noted by Ballard and associates (1, 2) during transplacental stimulation of fetal rabbit lung by an analog of T4 known as DIMIT. The effects of hormones on fetal lung metabolism have also been studied using fetal lung cells under conditions of short term monolayer culture. smith and Torday (33), using monolayer cultures of fetal rabbit lung cells, found that T4 produced a significant increase in incorporation of [14C]-choline into PC. In a similar tissue culture system, Farrell et al. (14) have shown an increase in activity of cholinekinase, and both T4 and cortisol exposure led to an increase in choline phosphotransferase.With the increasing evidence that most, if not all, actions of thyroid hormone are expressed by T3, there have been additional investigations of the effect of T3 on lung development. Using organotypic cultures of fetal rat lung alveolar type I1 ...

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Hormones and the lung. I. Thyroid hormones and glucocorticoids in lung development

Cited by 87 publications

References 44 publications

Thyroxine administration to infants of less than 30 weeks gestational age decreases plasma tri-iodothyronine concentrations

Thyroxine administration to infants of less than 30 weeks gestational age decreases plasma tri-iodothyronine concentrations

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

Thyroxine Metabolism in Cultured Cells Derived from Fetal Rat Lung

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