https://www.fertstert.org/article/S0015-0282(08)01392-7/pdf

The Androgen Excess and PCOS Society criteria for the polycystic ovary syndrome: the complete task force report

Polycystic ovary syndrome (PCOS) was hypothesized to result from functional ovarian hyperandrogenism (FOH) due to dysregulation of androgen secretion in 1989-1995. Subsequent studies have supported and amplified this hypothesis. When defined as otherwise unexplained hyperandrogenic oligoanovulation, two-thirds of PCOS cases have functionally typical FOH, characterized by 17-hydroxyprogesterone hyperresponsiveness to gonadotropin stimulation. Two-thirds of the remaining PCOS have FOH detectable by testosterone elevation after suppression of adrenal androgen production. About 3% of PCOS have a related isolated functional adrenal hyperandrogenism. The remaining PCOS cases are mild and lack evidence of steroid secretory abnormalities; most of these are obese, which we postulate to account for their atypical PCOS. Approximately half of normal women with polycystic ovarian morphology (PCOM) have subclinical FOH-related steroidogenic defects. Theca cells from polycystic ovaries of classic PCOS patients in long-term culture have an intrinsic steroidogenic dysregulation that can account for the steroidogenic abnormalities typical of FOH. These cells overexpress most steroidogenic enzymes, particularly cytochrome P450c17. Overexpression of a protein identified by genome-wide association screening, differentially expressed in normal and neoplastic development 1A.V2, in normal theca cells has reproduced this PCOS phenotype in vitro. A metabolic syndrome of obesity-related and/or intrinsic insulin resistance occurs in about half of PCOS patients, and the compensatory hyperinsulinism has tissue-selective effects, which include aggravation of hyperandrogenism. PCOS seems to arise as a complex trait that results from the interaction of diverse genetic and environmental factors. Heritable factors include PCOM, hyperandrogenemia, insulin resistance, and insulin secretory defects. Environmental factors include prenatal androgen exposure and poor fetal growth, whereas acquired obesity is a major postnatal factor. The variety of pathways involved and lack of a common thread attests to the multifactorial nature and heterogeneity of the syndrome. Further research into the fundamental basis of the disorder will be necessary to optimally correct androgen levels, ovulation, and metabolic homeostasis.

/pdf/the-pathogenesis-of-polycystic-ovary-syndrome-pcos-the-38p7ugs9et.pdf

The Pathogenesis of Polycystic Ovary Syndrome (PCOS): The Hypothesis of PCOS as Functional Ovarian Hyperandrogenism Revisited.

Hirsutism: Implications, etiology, and management☆

The secretion and the blood levels of the adrenal steroid dehydroepiandrosterone (DHEA) and its sulfate ester (DHEAS) decrease profoundly with age, and the question is posed whether administration of the steroid to compensate for the decline counteracts defects associated with aging. The commercial availability of DHEA outside the regular pharmaceutical–medical network in the United States creates a real public health problem that may be resolved only by appropriate long-term clinical trials in elderly men and women. Two hundred and eighty healthy individuals (women and men 60–79 years old) were given DHEA, 50 mg, or placebo, orally, daily for a year in a double-blind, placebo-controlled study. No potentially harmful accumulation of DHEAS and active steroids was recorded. Besides the reestablishment of a “young” concentration of DHEAS, a small increase of testosterone and estradiol was noted, particularly in women, and may be involved in the significantly demonstrated physiological–clinical manifestations here reported. Bone turnover improved selectively in women >70 years old, as assessed by the dual-energy x-ray absorptiometry (DEXA) technique and the decrease of osteoclastic activity. A significant increase in most libido parameters was also found in these older women. Improvement of the skin status was observed, particularly in women, in terms of hydration, epidermal thickness, sebum production, and pigmentation. A number of biological indices confirmed the lack of harmful consequences of this 50 mg/day DHEA administration over one year, also indicating that this kind of replacement therapy normalized some effects of aging, but does not create “supermen/women” (doping).

https://www.pnas.org/content/pnas/97/8/4279.full.pdf

Dehydroepiandrosterone (DHEA), DHEA sulfate, and aging: contribution of the DHEAge Study to a sociobiomedical issue.

Publisher Summary This chapter describes the different aspects of regulation of androgen action. Androgens belong to a class of C-19 steroids secreted primarily by the testis and adrenal cortex. Hormonally active androgens promote reproductive and anabolic functions. Both reproductive and anabolic effects of androgens are mediated by their interaction with the androgen receptor (AR), a member of the steroid-thyroid hormone-retinoid-vitamin D superfamily of nuclear receptors (NRs) that function as ligand-activated transcription factors. Almost all of the androgen functions, except its conversion to estrogen by the enzyme aromatase in certain target cells are known to be mediated by the androgen receptor. The androgen receptor are coded by a single copy gene, which is located on the X chromosome. The functional relevance of the segmented domain structure of the NR superfamily is supported by the results of deletion mutagenesis and domain swapping among various receptor proteins. The interaction between the amino terminal and the steroid-binding carboxy-terminal end in the AR transactivation function was initially indicated by the finding that a segment within the hormone-binding domain exerts an inhibitory influence in the transcription regulatory activity of the AR, and the deletion of this region results in ligand-independent activation of the receptor.

Regulation of Androgen Action

An adrenal-secreted "androgen": dehydroisoandrosterone sulfate. its metabolism and a tentative generalization on the metabolism of other steroid conjugates in man.

http://www.jbc.org/content/241/1/20.full.pdf

Studies on Testosterone Metabolism III. THE SELECTIVE "5β-METABOLISM" OF TESTOSTERONE GLUCURONIDE

The isolation of the ester-sulfate of 5-androstene 3β-ol 7, 17-dione is described. This sulfate has been found in the peripheral venous blood plasma of several virilized women. Moreover, it has been isolated in 3 adrenal tumors and in the adrenal venous plasma of one of them.

Isolement dans le plasma veineux périphérique et surrénalien de l'ester-sulfate de 5-androstène 3β-ol 7,17-dione

Studies on Testosterone Metabolism V. TESTOSTERONE-3H 17-GLUCURONIDE-14C TO 5β-ANDROSTANE-3α,17β-DIOL-3H 17-GLUCURONIDE-14C, THE "DIRECT" 5β-METABOLISM OF TESTOSTERONE GLUCURONIDE

Dehydroisandrosterone-7α-3H glucuronide (specific activity 121 μc/μmole) has been synthesized and injected intravenously into 2 normal individuals, together with dehydroisoandrosterone-4-14C Dehydroisoandrosterone glucuronide is not an end product, since only 15 % was excreted unchanged in the urine “Direct” metabolic 17β-hydrogenation and Δ5(−6)-reduction was suggested by the isolation of several urinary glucuronides of 3β-hydroxysteroids-3H The formation of 3α-hydroxysteroids-3H, eg, androsterone-3H, and of dehydroisoandrosterone-3H sulfate was also observed The relative contributions of dehydroisoandrosterone glucuronide and dehydroisoandrosterone to urinary dehvdroisoandrosterone sulfate and androsterone were not identical; dehydroisoandrosterone glucuronide gave 8 times more dehydroisoandrosterone sulfate than dehydroisoandrosterone, on the basis of their contribution to androsterone Therefore, at the physiological level, the transformation of dehydroisoandrosterone glucuronide into 

Metabolism of dehydroisoandrosterone glucuronide.

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