The Anabolic Effects of Chorionic Gonadotropin in Normal Young Men 123

Landau, Richard L.; Knowlton, Kathryn; Lugibihl, Kathleen; Brandt, Matthias; Kenyon, Allan T.

doi:10.1172/jci102299

Cited by 12 publications

(10 citation statements)

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“…The explanation for this disparity in the effectiveness of the two forms of the androgen is unknown, particularly since blood levels of the steroid were not obtained, but the difference in response between the free and esterified steroid is similar to that encountered in early experimental work with testosterone and its esters (25). The effect on nitrogen excretion is comparable to that achieved on the same dose of testosterone propionate, known to be a maximal stimulus, and to that induced by endogenous testosterone resulting from testicular stimulation by human chorionic gonadotropin administration (26). Case 1 (complete syndrome) (Fig.…”

Section: Plasma Steroids and Steroid Bindingsupporting

confidence: 54%

“…5). Previous studies with much lower doses of HCG have indicated near-maximal nitrogen retention by this time (26,29). The basis of the fall in nitrogen excretion that began on the second to third day of the recovery period is unclear.…”

Section: Plasma Steroids and Steroid Bindingmentioning

confidence: 57%

“…While these indexes do not represent the actual dialyzable fraction of testosterone and other androgens in circulating plasma, there is substantial evidence that they do reliably reflect the physiologically available fraction of circulating androgen. Urinary 17-ketosteroids (19), 17-hydroxycorticoids (20), gonadotropins (21), nitrogen, inorganic phosphorus and creatine (22) were measured by standard methods.…”

Section: Methodsmentioning

confidence: 99%

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Androgens and Androgen Responsiveness in the Feminizing Testis Syndrome. Comparison of Complete and “Incomplete” Forms¹

Rosenfield

Lawrence

Liao

et al. 1971

The Journal of Clinical Endocrinology & Metabolism

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The metabolic response to androgens was studied in a patient with the complete syndrome of testicular feminization in whom the conversion of testosterone to dihydrotestosterone by skin homogenates was below normal. The subject not only failed to manifest an anabolic response to chorionic gonadotropin and testosterone propionate, but also failed to respond to dihydrotestosterone and dihydrotestosterone acetate. Steroid dosages were those sufficient to induce maximal anabolism in normal men or women. The anticipated anabolic effect of estradiol benzoate was readily demonstrated. It is accordingly proposed that the resistance to androgen resulted from an abnormality of specific androgen retention by target cell nuclei or in the subsequent chain of intracellular events initiated by androgen. It is suggested that the remarkable degree of breast development in the complete syndrome is the result of the unopposed action of estrogen of testicular origin, acting upon mammary primordia not subjected to antenatal inhibition by androgen. The diagnosis of "incomplete testicular feminization" was presumed in a pubertal male pseudohermaphrodite on the basis of absent miillerian derivatives, early breast development, and evidence compatible with androgen insensitivity. Two experimental observations supported the concept of end organ resistance to the effects of androgen. The degree of development of secondary sex characteristics was seemingly poor considering the nearly adult male level of plasma testosterone. Delayed, if any, anabolic response resulted from chorionic gonadotropin stimulation in spite of a rise in plasma testosterone from 233 to 770 ng/100 ml. That no more than partial androgen resistance existed was indicated by the observation that an anabolic response was induced by both dihydrotestosterone acetate and testosterone propionate at plasma levels of unconjugated steroid over 1000-2000 ng/100 ml. Intracellular formation of dihydrotestosterone from testosterone was normal. No abnormality in the plasma concentration of androgenic intermediary metabolites was demonstrated in either patient. The comparative studies suggest that complete and incomplete forms of the feminizing testes syndrome exist which may differ in the degree or nature of androgen resistance. (J Clin Endocr 32: 625, 1971) T HE COMPLETE syndrome of testicular feminization is clinically characterized by a female phenotype with normal feminization, absent miillerian derivatives, and sparse or absent sexual hair in association with an XY karyotype and cryptorchid testes. Resistance to the effects of androgen has been demonstrated in such subjects by failure of testosterone admin-

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Section: Plasma Steroids and Steroid Bindingsupporting

confidence: 54%

Section: Plasma Steroids and Steroid Bindingmentioning

confidence: 57%

Section: Methodsmentioning

confidence: 99%

See 1 more Smart Citation

Androgens and Androgen Responsiveness in the Feminizing Testis Syndrome. Comparison of Complete and “Incomplete” Forms¹

Rosenfield

Lawrence

Liao

et al. 1971

The Journal of Clinical Endocrinology & Metabolism

Self Cite

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show abstract

“…Such persistence has been observed by others (Landau, Knowlton, Lugibihl, Brandt & Kenyon, 1950;Jayle, Scholler, Garrone & Morel, 1957;Huis in't Veld, Louwerens & van der Spek, 1961). These differences in the individual's response in terms of androstenol excretion to HCG and to ACTH do, moreover, indicate that the effects of the gonadotrophin preparation were not due to impurities directly affecting adrenocortical secretion, but that the parallel rises in urinary androstenol and 17-oxosteroids were probably due to stimulation of the gonads.…”

Section: Discussionsupporting

confidence: 62%

“…9. On the other hand, an alternative precursor of androstenol should be borne in mind, namely androstane-3a, 17 jS-diol, also formed from testosterone by human liver and rat testis homogenates (Stylianou et al 1961 , b) and reported briefly by Lieberman, Praetz, Humphries & Dobriner (1953) to be a constituent of human urine. It remains to be determined whether the introduc¬ tion of the C16-C17 double bond is effected principally before or after reduction of ring A.…”

Section: Discussionmentioning

confidence: 99%

URINARY EXCRETION OF ANDROST-16-EN-3α-OL LEVELS IN NORMAL SUBJECTS, AND EFFECTS OF TREATMENT WITH TROPHIC HORMONES

Wl¹

1962

Journal of Endocrinology

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Data are presented on the urinary excretion of androst-16-en-3\g=a\-olby normal human subjects over the age span 4-86 years. The figures range from < 100 to 2630 \g=m\g./24 hr. in males, and < 100 to 1100 \g=m\g./24 hr. in females, the mean for men of 16-45 years being nearly three times that for women of the same age.The effect on urinary androstenol and 17-oxosteroids of human chorionic gonadotrophin (HCG) and of corticotrophin (ACTH) have been compared in three normal young men and two women. Marked elevation of androstenol excretion occurred after ACTH in both sexes, while HCG administration resulted in an increased urinary output of androstenol and 17-oxosteroids only in two of the men and not in the women tested in either phase of the menstrual cycle. Intramuscular injection of androstenol itself (20 mg.) resulted in increased levels of androstenol in the urine equivalent only to a very small proportion of the injected dose.The metabolic origin of androstenol is discussed in the light of the results presented and of those of other investigators. It seems likely that androstenol arises not primarily from testosterone but mainly from an adrenal precursor.

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The Metabolic Effects of Anabolic Steroids in Man

Landau¹

1976

Anabolic-Androgenic Steroids

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The Anabolic Effects of Chorionic Gonadotropin in Normal Young Men 123

Cited by 12 publications

References 11 publications

Androgens and Androgen Responsiveness in the Feminizing Testis Syndrome. Comparison of Complete and “Incomplete” Forms¹

Androgens and Androgen Responsiveness in the Feminizing Testis Syndrome. Comparison of Complete and “Incomplete” Forms¹

URINARY EXCRETION OF ANDROST-16-EN-3α-OL LEVELS IN NORMAL SUBJECTS, AND EFFECTS OF TREATMENT WITH TROPHIC HORMONES

The Metabolic Effects of Anabolic Steroids in Man

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The Anabolic Effects of Chorionic Gonadotropin in Normal Young Men 123

Cited by 12 publications

References 11 publications

Androgens and Androgen Responsiveness in the Feminizing Testis Syndrome. Comparison of Complete and “Incomplete” Forms1

Androgens and Androgen Responsiveness in the Feminizing Testis Syndrome. Comparison of Complete and “Incomplete” Forms1

URINARY EXCRETION OF ANDROST-16-EN-3α-OL LEVELS IN NORMAL SUBJECTS, AND EFFECTS OF TREATMENT WITH TROPHIC HORMONES

The Metabolic Effects of Anabolic Steroids in Man

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Androgens and Androgen Responsiveness in the Feminizing Testis Syndrome. Comparison of Complete and “Incomplete” Forms¹

Androgens and Androgen Responsiveness in the Feminizing Testis Syndrome. Comparison of Complete and “Incomplete” Forms¹