A radioimmunoassay for the estimation of serum dehydroepiandrosterone sulphate in normal and pathological sera

Smith, Margaret; Rudd, B. T.; Shirley, Anne; Rayner, P H; Williams, John W; Duignan, N. M.; Bertrand, P.

doi:10.1016/0009-8981(75)90328-9

Cited by 73 publications

(31 citation statements)

References 11 publications

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“…Circulating DHEA-S concentrations continue to rise and peak during the second decade of life, with levels being higher in males than in females ( Fig. 1) [3,5]. While circulating concentrations of DHEA and DHEA-S rise progressively in adrenarche, cortisol and ACTH concentrations do not change significantly in this period, indicating that adrenarche is not simply a global activation of the pituitary-adrenal axis.…”

Section: Background and Significancementioning

confidence: 96%

“…Hence, DHEA-S production declines precipitously during the first months of life and remains low until adrenarche commences at about age 6-8 [2]. This rise in the circulating concentrations of DHEA and DHEA-S is the biochemical hallmark of adrenarche [3]. Importantly, the rise in DHEA-S occurs prior to the increase of either estrogens or androgens associated with puberty [4].…”

Section: Background and Significancementioning

confidence: 99%

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Regulation of the adrenal androgen biosynthesis

Rainey

Nakamura

2008

The Journal of Steroid Biochemistry and Molecular Biology

144

107

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The human adrenal reticularis produces the so-called adrenal androgens, dehydroepiandrosterone (DHEA) and DHEA-sulfate (DHEA-S). As opposed to the cortisol and aldosterone little is known regarding the mechanisms that regulate the production of the adrenal androgens. Several recent studies have shown that type II 3β-hydroxysteroid dehydrogenase (HSD3B2), cytochrome b5 (CYB5), and steroid sulfotransferase (SULT2A1) play an important role in the regulation of adrenal androgen production. Specifically, adrenal production of DHEA-S is correlated with reticularis expression of SULT2A1 and CYB5. In contrast, HSD3B2 has an inverse correlation with adrenal androgen production likely due to its unique ability to remove precursors from the pathway leading to DHEA. Therefore, its expression is limited to the adrenal glomerulosa/fasciculata but not in reticularis. The differential expression of these three proteins appears to be critical for reticularis function. In this review, we focus on studies that have begun to define the mechanisms regulating the transcription of these genes. Understanding the mechanisms controlling differential expression of these proteins should provide novel information about the human adrenal reticularis and its production of DHEA and DHEA-S. KeywordsAdrenal; Androgen; Cytochrome b5; DHEA-sulfotransferase; 3β-hydroxysteroid dehydrogenase II. Background & SignificanceThe fetal adrenal produces large amounts of dehydroepiandrosterone (DHEA) and DHEAsulfate (DHEAS) during fetal development (Fig. 1). DHEA-S concentrations are also high in the newborn (Fig. 1) [1]. However, by age 1, the specialized fetal zone is lost and replaced by the definitive adrenal cortex, which initially synthesizes little DHEA-S (Fig. 1). Hence, DHEA-S production declines precipitously during the first months of life and remains low until adrenarche commences at about age 6-8 [2]. This rise in the circulating concentrations of DHEA and DHEA-S is the biochemical hallmark of adrenarche [3]. Importantly, the rise in DHEA-S occurs prior to the increase of either estrogens or androgens associated with puberty [4]. Circulating DHEA-S concentrations continue to rise and peak during the second decade of life, with levels being higher in males than in females (Fig. 1) [3,5]. While circulating concentrations of DHEA and DHEA-S rise progressively in adrenarche, cortisol and ACTH concentrations do not change significantly in this period, indicating that adrenarche is not simply a global activation of the pituitary-adrenal axis.Correspondence and reprint requests addressed to: William E Rainey, Ph.D. Department of Physiology, Medical College of Georgia, 1120 15th Street, Augusta, GA 30912,, Email: E-mail: wrainey@mcg.edu. Publisher's Disclaimer: This is a PDF file of an unedited manuscript that has been accepted for publication. As a service to our customers we are providing this early version of the manuscript. The manuscript will undergo copyediting, typesetting, and review of the resulting proof before it is published in its f...

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Section: Background and Significancementioning

confidence: 96%

Section: Background and Significancementioning

confidence: 99%

Regulation of the adrenal androgen biosynthesis

Rainey

Nakamura

2008

The Journal of Steroid Biochemistry and Molecular Biology

144

107

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“…Importantly, the rise in DHEA-S occurs prior to the increase of either oestrogens or androgens associated with puberty (Ducharme et al ., 1976). Circulating DHEA-S concentrations continue to rise and peak during the second decade of life, with levels being higher in males than in females (Smith et al ., 1975;Orentreich et al ., 1984). While circulating concentrations of DHEA and DHEA-S rise progressively, cortisol and ACTH concentrations do not change significantly, indicating that adrenarche is not simply a global activation of the pituitary-adrenal axis.…”

Section: Hormonal Changesmentioning

confidence: 99%

“…More generally, DHEA-S production declines inexorably with ageing, such that circulating DHEA-S concentrations in octogenarians are not much higher than those in preadrenarchal children (Smith et al, 1975;Orentreich et al, 1984). This decline in DHEA-S production has been termed 'adrenopause', although cortisol and aldosterone production do not decline as casual interpretation of this term might suggest.…”

Section: Clinical Impact Of Dhea-s Deficiencymentioning

confidence: 99%

Adrenarche – physiology, biochemistry and human disease

Auchus¹,

Rainey

2003

Clinical Endocrinology

258

148

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SummaryAdrenarche refers to the onset of dehydroepiandrosterone (DHEA) and DHEA-sulphate (DHEA-S) production from the adrenal zona reticularis that can be detected at around 6 years of age. The phenotypic result of adrenarche is pubarche or the development of axillary and pubic hair that occurs in both girls and boys at about age 8. The phenomenon of adrenarche is unique to human beings and to some Old World primates, and a reversal of adrenarche appears to occur in the ageing process. Premature and exaggerated adrenarche can be indicative of future onset of adult diseases, thus increasing the clinical relevance of adrenarche. The physiological triggers of adrenarche and the role(s) of DHEA-S remain speculative. However, the biochemical pathways that define adrenarche have been characterized in detail, and the appearance of key enzymes and cofactors in the adrenal zona reticularis track with the progression of adrenarche. This article reviews the clinical manifestations of adrenarche, the biochemistry of the enzymes involved in DHEA-S production, and the cell biology of the adrenal zona reticularis.Glucocorticoids and mineralocorticoids secreted by the adrenal glands are essential for the maintenance of vascular tone and carbohydrate metabolism or of blood volume and sodium balance, respectively. The testes and ovaries, by contrast, generate the sex steroids that are required for gametogenesis, secondary sexual characteristics and reproduction. However, the adrenal glands of adult human beings secrete generous quantities of the C 19 steroids dehydroepiandrosterone (DHEA) and DHEA-sulphate

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“…RIA (28) 5·1-12·3 Table 2. Part of the poor performance for urinary 17-oxogenic and 17-oxosteroids may be due to the infrequency with which some laboratories perform these assays.…”

Section: Fr-oxosteroidsmentioning

confidence: 99%

Urinary 17-Oxogenic and 17-Oxosteroids: A Case for Deletion from the Clinical Chemistry Repertoire

Rudd

1983

Ann Clin Biochem

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The principal glucocorticoid secreted by the human adrenal cortex is cortisol, at a rate of about 60 !Lmol/ day ( Fig. 1). Less than 1 % of the secreted cortisol is excreted unchanged in the urine. Cortisol is metabolised in the liver, and the metabolites are excreted as water-soluble glucuronides (Fig. 2). Approximately 80 % of cortisol is excreted as 17-hydroxy-corticosteroids, and between 5 %and 10 %undergoes further catabolism and is excreted as ll-oxygenated 17-oxosteroids. In normal subjects, a small amount of the precursors of cortisol is secreted. 17ot-Hydroxyprogesterone is metabolised mainly to pregnanetriol and to 17ot-hydroxypregnanolone, while l l-deoxycortisol is metabolised mainly to tetrahydro ll-deoxycortisol and to pregnanetetrol. In pathological conditions where there is a deficiency of21-or l l-hydroxylase, the metabolites of 17ot-hydroxyprogesterone and l I-deoxycortisol form the major component of the 17-hydroxycorticosteroid metabolites excreted. As with cortisol metabolism there is some further catabolism of these steroids to give ll-deoxy 17-oxosteroids.17-0xosteroids arise not only from the metabolism of adrenal steroids and from adrenal secretion but also from the ovary and testis. 17-0xosteroids in urine therefore comprise a mixture of ll-oxy and ll-deoxy 17-oxosteroids of adrenal origin as well as l l-deoxy 17-oxosteroids of gonadal origin.

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A radioimmunoassay for the estimation of serum dehydroepiandrosterone sulphate in normal and pathological sera

Cited by 73 publications

References 11 publications

Regulation of the adrenal androgen biosynthesis

Regulation of the adrenal androgen biosynthesis

Adrenarche – physiology, biochemistry and human disease

Urinary 17-Oxogenic and 17-Oxosteroids: A Case for Deletion from the Clinical Chemistry Repertoire

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