The Metabolism of Corticosterone in Man

Peterson, Ralph E.; Pierce, Charles E.

doi:10.1172/jci104091

Cited by 105 publications

(32 citation statements)

References 43 publications

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“…The minimal amount of aldosterone secreted in the presence of increased secretion of B and excretion of TH-18-OH compound A may also indicate a second biosynthetic defect either in the conversion of 18-OH-B to aldosterone because of lack of dehydrogenase activity or in the conversion of angular methyl group of B to an aldehyde. The secretory rates of B and DOC were far greater than rates observed after infusion of ACTH (10). Plasma levels of B were continually elevated and varied diurnally, and the pool size was much greater than normal.…”

Section: Miscellaneous Measurementsmentioning

confidence: 83%

“…Cortisol and corticosterone were measured by a double isotope dilution derivative technique (9). The half-life of corticosterone was determined after the intravenous administration of corticosterone-4-14C (10). Aldosterone was measured by the constant infusion (daldosterone-1-2-3H) technique of Tait, Tait, Little, and Laumas (11).…”

Section: Steroid Measurementsmentioning

confidence: 99%

“…Insulin sensitivity was assessed after intravenous administration of .05 kg crystalline insulin 16 hours after fasting by measuring blood sugar (27) and levels of free fatty acids and glycerol in plasma. 10 Results C-21 steroids derived from progesterone. The concentration of progesterone in plasma was 0.…”

Section: Miscellaneous Measurementsmentioning

confidence: 99%

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17-hydroxylation deficiency in man.

Biglieri¹,

Herron²,

Brust³

1966

J. Clin. Invest.

526

147

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The biosynthesis of steroid hormones 1 requires a number of hydroxylating enzymes. Deficiency of these enzymes is demonstrated by increased or decreased amounts of certain steroid metabolites in blood and urine and is best exemplified by the deficiency of 11,8-hydroxylase (1) and 21-hydroxylase (2) in patients with congenital adrenal hyperplasia. 17a-Hydroxylase activity is present in these disorders because of the increases in secretion of androgens and excretion of pregnanetriol. In addition, a lack of 3-hydroxysteroid dehydrogenase has also been described (3). 17-Hydroxylation is essential not only to the biosynthesis of cortisol but also to the formation of * Submitted for publication July 19, 1966; accepted September 7, 1966 androstenedione = 4-androsten-3,17-dione; compound S= li-deoxycortisol = 4-pregnen-17a,21-diol-3,20-dione; dehydroepiandrosterone = 5-androsten -3,8 -ol -17 -one; dexamethasone = 1,4-pregnandien-9-fluoro-16a-methyl-1 ll,17a, 21-triol-3,20-dione; etiocholanolone = 5,B-androstan-3a-ol-17-one; pregnanediol = 5,8-pregnan-3a,20a-diol; pregnanetriol = 5p6-pregnan-3a,11a,20a-triol; stilbestrol = diethylstilbestrol = aca'diethyl-4,4'stilbenediol; tetrahydroaldosterone = TH aldosterone = 5,8-pregnan-3a,11p,21-trihydroxy-20 keto-18-ol; tetrahydrocortisol = THF = 5fi-pregnan-3a,1llf,17a,21-tetrol-20-one; tetrahydrocortisone = THE = 5fi-pregnan-3a,17a,21-triol-11,20-dione; tetrahydrodeoxycorticosterone = THDOC = 5#-pregnan-3a, 21-diol-20-one; tetrahydro-ll-deoxycortisol = 5,0-pregnan3a,17a,21-triol-20-one; and tetrahydro-18-OH-dehydrocorticosterone = TH-18-OH compound A = 5#-pregnan3a,18,21-trihydroxy-11,20-dione.gonadal hormones (4, 5), the androgenic steroids, androstenedione, testosterone, and, eventually, estrogens (6). Deficiency of this enzyme system should be manifested clinically in both adrenal and gonadal abnormalities if the enzyme is similar in both glands. Furthermore, it is reasonable to assume that lack of 1 7-hydroxylated steroids would allow uninhibited release of adrenocorticotropin. In such a circumstance in which cortisol secretion is absent, prolonged survival would not be anticipated because mineralocorticoids would be the only adrenal steroids produced. We will describe and discuss a patient with deficiency in 17a-hydroxylase activity with possibly a second defect in production of aldosterone. MethodsCase report The female patient M. H. was the product of a full-term normal pregnancy and weighed 7 pounds at birth. Several severe episodes of bronchitis occurred before 5 years of age. The patient was hospitalized for an influenza-like syndrome when she was 5 years old; the mother (29 years) and one sibling (11 months) died from "influenza" at this time. From 5 to 10 years of age the patient was absent from school about one-third of the time because of infections of the upper respiratory tract. She was hospitalized at age 9 for severe upper respiratory infection, high fever, and unconsciousness. Intravenous glucose therapy promptly restored consciousness, and hypoglycemia was d...

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Section: Miscellaneous Measurementsmentioning

confidence: 83%

Section: Steroid Measurementsmentioning

confidence: 99%

See 1 more Smart Citation

17-hydroxylation deficiency in man.

Biglieri¹,

Herron²,

Brust³

1966

J. Clin. Invest.

526

147

View full text Add to dashboard Cite

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“…These values were similar to those of Lindner (1972) for the excretion of cortisol and its metabolites in sheep. Thus for both the natural hormone cortisol and its synthetic analogue the sheep can be placed between the rat on the one hand which shows a predominant faecal route of excretion (Rice et al 1974) and man on the other hand with mainly urinary excretion (Peterson and Pierce 1960).…”

Section: Discussionmentioning

confidence: 99%

Studies on Intravenously Infused Dexamethasone in Sheep

Leish¹,

Panaretto²

1978

Aust. Jnl. Of Bio. Sci.

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Aust. J. Bioi. Sci., 1978, 31, 373-83 The metabolism of [1,2(n)-3Hldexamethasone intravenously infused for periods of 4 and S days was examined in four Merino wethers.On average 85·6±2·8 (s.e.m.) % of the total dose was recovered, 56·2±5·1 and 29·4±3·3% being excreted in urine and faeces respectively. In total 12·4 % of the dose was associated with the unconjugated steroid fraction which represented 22% of the total urinary radioactivity.Thin layer chromatography of the urinary unconjugated fractlon revealed, apart from dexamethasone, five major and three minor radioactive components designated as I, III, IV, V, VIII and II, VII, IX respectively. Approximately 83 % of the radioactivity associated with the unconjugated fractions was found in constituents more polar than dexamethasone with the radioactivity mainly confined to the principal metabolite IV, Rc = 0·24 (dexamethasone, Rc = 0·45;'cbloroform: formarnide 50:1). The urinary constituent VI, Rc = 0·37, was detected only -during-the second half of the 8-day infusion with the peak of excretion on day 6.During the first 30 h of [3Hldexamethasone administration the plasma radioactivity reached the level which remained relatively constant throughout the infusions. The initial high level of radioactivity detected in the plasma unconjugated fraction as well as dexamethasone during the first 24 h infusion declined over the next 2 days; this was followed by a small increase during the final period of infusions.The radioactivity of the plasma unconjugated fraction was distributed, apart from dexamethasone, into six constituents (I, III, IV, V, VIII and IX) which when analysed by thin layer chromatography appeared to be qualitatively similar to those found in urine.These results led to the conclusion that one or more products of dexamethasone metabolism might be biologically active and thus potentially important in inhibiting wool fibre growth in sheep.

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“…Therefore, when the animal is fed on a low-protein diet, it may lead to insufficiency in the turnover of liver protein. Furthermore, the liver is the organ primarily responsible for the catabolism of the steroid hormone (19). It may be thought that changes in the liver function could either directly or indirectly influence the steroid hormone metabolism in the lens as reported previously (20), and finally it would bring about a reduction in the synthesis of cortisol-binding protein in the lens.…”

Section: Discussionmentioning

confidence: 80%