Levels of Chorionic Gonadotrophin in the Newborn Infant and Their Relationship to Adrenal Dehydroepiandrosterone

Lauritzen, C; Lehmann, W. D.

doi:10.1677/joe.0.0390173

Cited by 43 publications

(6 citation statements)

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“…In our culture system, h C 6 failed to enhance the sulfation of DHA. Because our cultured fetal adrenal cells more closely resemble the results obtained from fetal adrenals using in vivo experimental approaches (I), we have t o conclude that hCG is not a trophic factor stimulating DHAS formation and thereby stimulating estriol formation by the placenta as earlier proposed (25,26). In a s much as CAMP has been suggested as a possible mediator of ACTH action, in the two concentrations of dbcAMP used, the nucleotide did not have any apparent effect.…”

Section: Discussionsupporting

confidence: 66%

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Control of steroid synthesis in human fetal adrenals in monolayer culture

Baird¹,

Brisson²,

Kan³

et al. 1978

Can. J. Biochem.

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S. (1978) Control of steroid synthesis in human fetal adrenals in monol;myer culture. Can. 9. Bioclaern. 56,577-584The actions of adrenocorticotrophin 1-39 (ACTH), N6,02-dibutyryl adenosine-3',5'-cyclic phosphate (dbcAMP), and human chorionic gonadotrophin (hCG) on the sulfation of DHA and the synthesis of cortisol by human fetal adrenal cells in monolayer culture have been described. Electron microscopic studies indicate that the cells present in our cultures at the end of 5 days are intact and have many of the characteristics of secretory cells. Sulfation of DHA was strongly inhibited by 11-deoxycorticosterone, testosterone, androsterone, and dihydrotestosterone. Very small effects were observed with progesterone and corticosterone and insignificant effects with estrone, estradiol, and estriol. Androstenedione as well as 17a-hydroxylated corticosteroids showed no inhibition. When used as substrate, C,, A4-3-ketosteroids were good precursors of cortisol with 11-deoxycortisol being the best one followed by 17a-hydroxyprogesterone and progesterone. The conversion of progesterone (4pg12 ml) to cortisol was fivefold greater than under conditions where no substrate was present (endogenous production). ACTH in the concentration of 5 x Ulml added twice daily to the cell cultures for 8 days increased eightfold the sulfation of DHA and increased cortisol synthesis from progesterone 35-fold in 5 days. The addition of dbcAMP (5 x lW5 M ) or hCG used at 2.0 or 0.2 Ulml did not stimulate the sulfation of DHA. A lag period of at least 36 h is required before the stimulation of DHA sulfation or cortisol synthesis from progesterone can be observed. dbcAMP can stimulate the conversion of progesterone, 17a-hydroxyprogesterone, and I I-deoxycortisol to cortisol by the adrenal cells. These data suggest that 1 la-and 21-hydroxylation are stimulated by dbcAMP but 17a-hydroxylation is not altered.

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Section: Discussionsupporting

confidence: 66%

“…1) For personal use only. vated DHA excretion in the urine of the newborn infant (25,261. In our culture system, h C 6 failed to enhance the sulfation of DHA.…”

Section: Discussionmentioning

confidence: 99%

Control of steroid synthesis in human fetal adrenals in monolayer culture

Baird¹,

Brisson²,

Kan³

et al. 1978

Can. J. Biochem.

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“…1 An hCGresponsive, estrogen-secreting adrenal tumor has been reported (13). The adrenal cortex and the ovary have a mutual embryologic origin and the fetal and neonatal adrenal cortex are responsive to hCG (14). Our patient's adrenal adenoma may have been derived from adrenocortical cells that acquired, or failed to lose, their responsiveness to gonadotropin.…”

Section: Discussionmentioning

confidence: 77%

A Gonadotropin-Responsive Adrenocortical Adenoma

Givens¹,

Andersen²,

Wiser³

et al. 1974

The Journal of Clinical Endocrinology & Metabolism

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A 49-yr-old virilized woman had a peripheral plasma testosterone (T) concentration of 783-911 ng/100 ml with a normal plasma concentration of androstenedione (A) and normal urinary 17-ketosteroids (17-KS). Plasma LH was below normal and FSH was low normal. Plasma T was not changed by dexamethasone 2 mg/day and the 17-KS were not normally suppressible. The administration of 5,000 units of human chorionic gonadotropin (hCG) increased plasma T to 3,744 ng/100 ml and also increased A and the 17-KS. Based on these results an ovarian source of T was suspected and bilateral oophorectomy was performed. Bilateral ovarian cortical stromal hyperplasia was found. Removal of both ovaries did not correct the hypertestosteronemia.Because an adrenal lesion was suspected, an 8-hr ACTH infusion test was done. Plasma T was decreased 42% and LH 3 1 % at the sixth hour of the ACTH infusion. Plasma T was again increased by hCG to 2,379 ng/100 ml after the ovaries were removed. Both adrenals were explored and a 4 cm X 3 cm X 2 cm brown adrenocortical adenoma weighing 21 g was removed from the right adrenal. Plasma T was 17 ng/100 ml after the removal of the tumor and was now not increased by hCG. This gonadotropin-responsive adrenal adenoma further emphasizes that the results of hormonal manipulative procedures may be misleading in determining the source of excess androgen production. (/ Clin Endocrinol Metab 38: 126, 1974)

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“…Maximal testosterone levels in fetal serum are observed near the time of peak hCG secretion (16,17). Third, hCG stimulates fetal adrenal synthesis of dehydroepiandrosterone sulfate (18,19). Fourth, hCG promotes steroidogenesis in the placenta, enhancing the conversion of cholesterol to pregnenolone and progesterone (20), stimulating adenyl cyclase (21), and increasing estrogen formation (22,23).…”

Section: Discussionmentioning

confidence: 99%

Cellular Localization of Chorionic Gonadotropin in Human Fetal Kidney and Liver*

Goldsmith

Mcgregor

Raymoure

et al. 1983

The Journal of Clinical Endocrinology & Metabolism

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Earlier, we reported that second trimester human fetal kidney and, to a much lesser extent, human fetal liver were capable of synthesizing and secreting the beta-subunit of hCG. Recently, we also have shown that these tissues, likewise, synthesize and secrete the alpha-subunit of hCG. The hCG produced is biologically active. To determine the cellular localization of these peptides, immunocytochemical studies were performed on human fetal tissues using antibodies against beta hCG, alpha hCG, and the intact hormone. Placental syncytiotrophoblast served as an immunopositive control. In the human fetal kidney, the ascending (thick) limb of the loop of Henle, distal convoluted tubule, and occasional cells in the collecting ducts were distinctly immunopositive for both beta hCG and the alpha-subunit. Small amounts of light positive staining occurred in only a few hepatocytes. Placental syncytiotrophoblast was routinely positive for both subunits, but fetal lung and striated muscle were negative. These immunocytochemical results indicate that immunoreactive beta hCG as well as the alpha-subunit are present in placental syncytiotrophoblast, in the distal renal nephron, and in a limited population of hepatocytes. The qualitative number and intensity of immunopositive cells closely correlate with the quantitative amounts of their hCG subunit synthesis. Taken together with our previous biosynthetic data, the immunocytochemical localization reported here indicates the probable cellular sites of alpha- and beta hCG synthesis in these tissues. The presence of comparable alpha- and beta-subunit staining in identical cell populations suggests that both hCG subunits and, therefore, perhaps intact hCG are produced at these same cellular sites during fetal life.

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Levels of Chorionic Gonadotrophin in the Newborn Infant and Their Relationship to Adrenal Dehydroepiandrosterone

Cited by 43 publications

References 0 publications

Control of steroid synthesis in human fetal adrenals in monolayer culture

Control of steroid synthesis in human fetal adrenals in monolayer culture

A Gonadotropin-Responsive Adrenocortical Adenoma

Cellular Localization of Chorionic Gonadotropin in Human Fetal Kidney and Liver*

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