Fetal Metabolism of Cortisol

Murphy, Beverley E. Pearson; Branchaud, Charlotte L.

doi:10.1016/b978-0-12-153205-5.50014-2

Cited by 15 publications

(10 citation statements)

References 157 publications

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“…Thomas et al (25) showed in prematurely delivered sheep that infusion of cortisol simulating the prepartum plasma corticosteroid surge was accompanied by an increase in fetal plasma T3 concentration, which was ascribed to an increase in the T3-generating capacity of the fetal liver (26). In this respect, the present findings that minimum and optimum hydrocortisone concentrations to induce iodothyronine-5'-deiodinating activity are on the order of 0.01 and 0.4 gg/ml, respectively, are physiologically very feasible, since these corticosteroid levels are those attainable in the perinatal period of humans and rodents (27,28). A supraphysiological concentration of glucocorticoid, however, inhibits the enzyme activity in accordance with clinical observations in human subjects (18) (Fig.…”

Section: Discussionmentioning

confidence: 66%

Ontogenesis of iodothyronine-5'-deiodinase. Induction of 5'-deiodinating activity by insulin, glucocorticoid, and thyroxine in cultured fetal mouse liver.

Sato¹,

Mimura²,

Han³

et al. 1984

J. Clin. Invest.

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Abstract. To elucidate the regulatory mechanism of ontogenetic development of iodothyronine-5'-deiodinase in the fetal and neonatal period, fetal mouse liver of the 19th day of gestation, in which no iodothyronine-5'-deiodinating activity was detectable, was cultured in Dulbecco-Vogt medium supplemented with 10% thyroid hormone-depleted fetal calf serum, insulin, hydrocortisone, and thyroid hormones. Iodothyronine-5'-deiodinating activity of the homogenate was assessed by the amount of iodide released from outer-ring-labeled reverse T3 and expressed as picomoles of 1271-per milligram of protein per minute. The enzyme activity was induced in a dose-dependent manner; optimal concentrations for insulin, hydrocortisone, and thyroxine were 1 ;ig/ml, 0.4 jg/ml, and 10-6 M, respectively.Without supplementation of either hydrocortisone or thyroxine, no 5'-deiodination was detected. The enzyme activity was observed after 3 d of culture, peaked at days 14-20, and then gradually decreased. Lineweaver-Burk analysis revealed that the increase in activity was primarily due to an increase in Vmax (day 3, 0.2 pmol/mg protein per min; day 20, 2.5 pmol/mg protein per min). Half maximal thyroxine (T4) and triiodothyronine (T3) concentrations were 1 X l0-7 M (free T4: 4 X 10-10 M), and 2 X 10-9 M (free T3: 5.0 X 10-" M), respectively, whereas reverse T3 did not elicit any activity at 10-8_ 10-6 M.These results suggest that ontogenetic development of iodothyronine-5'-deiodinase in the liver of the fetal and neonatal mouse is induced by physiological concentrations of glucocorticoid and thyroid hormones, and that insulin plays a permissive role in enhancing T3 formation from T4 in the liver. IntroductionRecently, the ontogenesis of thyroid hormone metabolism in peripheral tissues was extensively studied in man, sheep, chick, and especially rodents (1-5). In contrast to newborn of humans and sheep, in which hypothalamic-pituitary-thyroid function is already mature and the sera contain adult thyroxine (T4)' levels, the rat (and probably mouse) is delivered in the hypothyroid state. The serum T4 concentration of newborn of rats is very low (1.6 ,ug/dl) and triiodothyronine (T3) is hardly detectable (-5 ng/dl) (1-3). Active thyroid hormone (T3) then increases in parallel with serum T4. In fetal liver of mice (6) and rats (3), iodothyronine-5'-deiodinating activity is hardly detectable. However, in the neonatal period, there occurs a progressive increase in the enzyme activity, which peaks at 2-

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Section: Discussionmentioning

confidence: 66%

Ontogenesis of iodothyronine-5'-deiodinase. Induction of 5'-deiodinating activity by insulin, glucocorticoid, and thyroxine in cultured fetal mouse liver.

Sato¹,

Mimura²,

Han³

et al. 1984

J. Clin. Invest.

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“…A role for cortisol in the fetus earlier in gestation has not been established. The placenta is permeable to steroid hormones but contains an isomerase that converts most of the cortisol to inactive cortisone (4,15). Additionally, although many adult tissues are capable ofconverting cortisone to cortisol, fetal tissues seem devoid of this capacity during most of fetal life (4,15).…”

Section: Neutralization Ofhormone Action In Thefetusmentioning

confidence: 99%

“…In humans, anencephaly or fetal adrenal hypoplasia also prolong gestation (13). There is an increase in cord plasma cortisol during the last 3-5 wk in human neonates (13)(14)(15), and this increase is more marked in infants delivered vaginally or by cesarean section of women in labor (14,15). Whether these changes represent a cause or effect of labor remains to be determined (13).…”

mentioning

confidence: 99%

“…Cortisol serves as an important maturational stimulus to prepare the fetus for extrauterine survival. The fetal cortisol surge serves to (a) augment surfactant synthesis in lung tissue (14)(15)(16)(17), (b) increase insulin, fl-adrenergic, and EGF receptors in fetal lung tissue (18)(19)(20), (c) increase adrenal medullary phenylethanolamine N-methyl transferase activity (to augment epinephrine biosynthesis from norepinephrine) (5,16) In addition, the fetal testes produce an inhibitor of mullerian duct differentiation, mullerian-inhibiting factor or MWF (28)(29)(30). This substance, the existence of which was first proposed by Jost, appears to be a glycoprotein with a monomer molecular weight of 72,000 and multimer molecular weights ranging from 145,00 to 235,000 (27)(28)(29)(30).…”

mentioning

confidence: 99%

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The unique endocrine milieu of the fetus.

Fisher¹

1986

J. Clin. Invest.

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“…Glucocorticoid levels are low in the rat fetus and neonate, with surges during late gestation (17) and parturition (18). Cytosolic glucocorticoid receptors have been identified in the hearts of 8-d chick embryos (2) at a stage of cardiac development equivalent to that of an E-14 rat fetus (19).…”

Section: Glucocorticoids and Growth Of Intraocular Cardiac Graftsmentioning

confidence: 99%

Glucocorticoid Stimulation Interacts with Sympathetic Innervation to Affect Cardiac Development in Oculo

Torres

Tucker

1995

Pediatr Res

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The effects of chronic glucocorticoid stimulation and sympathetic innervation on myocardium developing in the absence of hemodynamic load were tested by grafting embryonic rat hearts into the anterior eye chamber (in oculo) of adult host rats. Myocardial grafts in control rats with normal hormonal milieu were compared with grafts in rats with chronic glucocorticoid stimulation (dexamethasone 40 pg/d) or glucocorticoid receptor type I1 blockade (RU 38486, 330 pg/d). Unilateral superior cervical ganglionectomy of one eye chamber prevented sympathetic innervation to one graft in each host. Two indices of growth, graft size (projected area) and terminal graft weight, were obtained. Dexamethasone treatment increased both size and weight of sympathetically innervated grafts, whereas RU486 treatment significantly decreased graft weight. Conversely, dexamethasone treatment decreased graft size in denervated eye chambers, whereas RU486 treatment had no effect. No differences in graft beating rate were observed among conditions. Sympathetic innervation modulated the effect of glucocorticoids on developing myocardium, suggesting that growth of sympathetically innervated myocardium is enhanced with glucocorticoid exposure, but growth of noninnervated myocardium (e.g. fetal heart) may be compromised by excessive glucocorticoid exposure. (Pediatr Res 38: 479-484, 1995) Abbreviations CON, control DEX, dexamethasone E-0, -12, and 14, embryonic d 0, 12, and 14 SCGin, superior cervical ganglion intact SCGx, superior cervical ganglion removed RU38486, Mefipristone TGF-P, transforming growth factor-/3The literature provides evidence that glucocorticoid stimulation can either facilitate or impede cardiac growth. Excess glucocorticoid exposure in adult rats reduced body weight without a concomitant reduction in heart weight (I), a phenomenon known as cardiac sparing. In embryonic chick heart, a single high dose of cortisol increased cardiac mass measured 48 h later (2). However, DEX treatment of rats on d 17-19 of gestation decreased cardiac DNA content, possibly reflecting deficits in cell proliferation (3). DEX treatment of neonatal rats decreased left ventricular mass at maturity (i.e. 60 d) (4). The present study examined the effects of glucocorticoids on cardiac development using the anterior eye chamber culture system (i.e. in oculo) which allows one to manipulate the neurohumoral environment of myocardium developing in the absence of hemodynamic load.

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Fetal Metabolism of Cortisol

Cited by 15 publications

References 157 publications

Ontogenesis of iodothyronine-5'-deiodinase. Induction of 5'-deiodinating activity by insulin, glucocorticoid, and thyroxine in cultured fetal mouse liver.

Ontogenesis of iodothyronine-5'-deiodinase. Induction of 5'-deiodinating activity by insulin, glucocorticoid, and thyroxine in cultured fetal mouse liver.

The unique endocrine milieu of the fetus.

Glucocorticoid Stimulation Interacts with Sympathetic Innervation to Affect Cardiac Development in Oculo

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