Androgen parameters and their correlation with body weight in one hundred thirty-eight women thought to have hyperandrogenism

Wild, Robert A.; Umstot, Edward S.; Andersen, Richard N.; Ranney, Gipsie B.; Givens, James R.

doi:10.1016/0002-9378(83)90998-5

Cited by 113 publications

(57 citation statements)

References 12 publications

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“…[25][26][27][28] It is well known that PCOS can be associated with increased DHAS, [29][30][31][32][33] which is confirmed here, indicating increased cortical activity. In this study, we have also investigated the mRNA expression of 11b-HSD1, 11b-HSD2 and H6PDH in subcutaneous adipose tissue biopsies from lean and obese women with or without PCOS.…”

Section: Discussionsupporting

confidence: 84%

Expression of 11β-hydroxysteroid dehydrogenase 1 and 2 in subcutaneous adipose tissue of lean and obese women with and without polycystic ovary syndrome

et al. 2009

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Objective: To investigate the expression of 11b-hydroxysteroid dehydrogenase (11b-HSD) type 1 and 2 and hexose-6-phosphate dehydrogenase (H6PDH) mRNA in subcutaneous abdominal tissue from lean and obese women with and without polycystic ovary syndrome (PCOS), and to investigate the association between these enzymes and different measures of insulin sensitivity. Design: Cross-sectional study. Subjects: A total of 60 women, 36 women with PCOS, 17 lean (lean PCOS, LP) and 19 obese (obese PCOS, OP) and 24 age-and weight-matched control women, 8 lean (lean controls, LC) and 16 obese (obese controls, OC). Subcutaneous adipose tissue was collected from the abdomen. Peripheral insulin sensitivity was assessed by the euglycemic hyperinsulinemic clamp and determined as glucose disposal rate and insulin sensitivity index. Whole-body insulin sensitivity was calculated using homeostasis model assessment insulin resistance index. Body composition was evaluated by dual X-ray absorptiometry. Adipose mRNA expression of leptin and adiponectin were determined by real-time PCR. Results: Polycystic ovary syndrome (Po0.05) and obesity (Po0.05) were independently associated with increased expression of 11b-HSD1 mRNA. The subgroups LP and OC had increased 11b-HSD1 and 11b-HSD2 mRNA expression compared with LC (Po0.05, Po0.05). There were no effects of PCOS or obesity on11b-HSD2 or H6PDH mRNA expression. Decreased peripheral insulin sensitivity (Po0.001) and increased upper body fat distribution (Po0.01) were associated with increased expression of 11b-HSD1, but neither 11b-HSD2 nor H6PDH. Conclusion: Polycystic ovary syndrome and obesity are independently associated with increased expression of 11b-HSD1. This may lead to increased conversion of cortisone to cortisol in the peripheral adipose tissue and subsequently increased glucocorticoid activity. Decreased peripheral insulin sensitivity and central obesity was associated with increased expression of 11b-HSD1.

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Section: Discussionsupporting

confidence: 84%

Expression of 11β-hydroxysteroid dehydrogenase 1 and 2 in subcutaneous adipose tissue of lean and obese women with and without polycystic ovary syndrome

et al. 2009

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“…Direct assays of free testosterone are suspect; the most reliable compute free testosterone from total testosterone and sex hormone binding globulin [92]. For these reasons, the current criteria for the diagnosis of PCOS (see Box 1) permit hirsutism to serve as a surrogate for Plasma-free testosterone is the best single indicator of androgen excess [95,96]. It is high about 50% more often than the total testosterone level in hirsute women because of their relatively low sex hormone binding globulin level.…”

Section: Determining the Presence Of Androgen Excessmentioning

confidence: 99%

“…Plasma-free testosterone is the best single indicator of androgen excess [95,96]. It is high about 50% more often than the total testosterone level in hirsute women because of their relatively low sex hormone binding globulin level.…”

Section: Determining the Presence Of Androgen Excessmentioning

confidence: 99%

Polycystic Ovary Syndrome in Adolescence

Driscoll

2003

Semin Reprod Med

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Polycystic ovary syndrome (PCOS) is a syndrome of variable combinations of menstrual irregularity, hirsutism or acne, and obesity. It can be diagnosed in adolescence and has early childhood antecedents. PCOS is the single most common endocrine cause of anovulatory infertility and a major risk factor for the metabolic syndrome and, in turn, development of type 2 diabetes mellitus (T2DM) in women. Thus, it appears that PCOS increases a woman's risk of developing cardiovascular disease. Therefore, identifying girls at risk for PCOS and implementing treatment early in the development of PCOS may be an effective means of preventing some of the long-term complications associated with this syndrome. This article reviews the definition, clinical features, diagnosis, and treatment of PCOS. Definition Classic polycystic ovary syndromeThe classic syndrome originally was described in 1935 by Stein and Leventhal as the association of amenorrhea with polycystic ovaries in women, of whom about two thirds were hirsute, and one half were obese [1]. The term PCOS was introduced upon recognition of a broader spectrum of clinical symptoms and ovarian histology, including stromal hyperplasia with multiple subcapsular follicles. Approximately two-thirds of patients with classic PCOS have hirsutism (or hirsutism equivalents, acne vulgaris or pattern alopecia), two-thirds have anovulatory symptoms (manifested as amenorrhea, oligomenorrhea, dysfunctional uterine bleeding, or unexplained infertility), and one-half are obese. Thus, only about one-third of classic cases have the full-blown clinical picture (Fig. 1). The laboratory diagnostic criteria for classic PCOS require biochemical evidence of hyperandrogenism with either a polycystic ovary by ultrasound or an increased serum level of luteinizing hormone (LH) or LH to follicle-stimulating hormone (FSH) ratio. These criteria have proven to not necessarily coincide (Fig. 2). Nonclassic and atypical polycystic ovary syndromeIn 1990, the National Institutes of Health (NIH) Conference on PCOS considered the implications of recent research findings for the diagnosis [2]. Fifty percent to 60% of those present concurred that the criteria for PCOS should consist of chronic anovulation with clinical or biochemical signs of hyperandrogenism that was not explained by other etiologies. This recognized the spectrum of the syndrome to include androgen excess in the absence of ultrasonographic and gonadotropic abnormalities (here termed nonclassic PCOS). NIH-PA Author ManuscriptNIH-PA Author Manuscript NIH-PA Author ManuscriptThe androgen excess of PCOS usually results from characteristic types of functional ovarian hyperandrogenism (FOH) or functional adrenal hyper-androgenism (FAH) [3,4]. FOH is gonadotropin-dependent excessive ovarian androgen production, and it occurs in most women with classic PCOS. It is also found in an equal number of hyperandrogenic women who do not meet the criteria for classic PCOS. It is characterized by 17-hydroxyprogesterone hyper-responsiveness to gonadotropin...

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“…Several mechanisms have been proposed to explain these findings. Early studies favoured an appetite stimulating effect of androgens causing obesity (Hosseinian et al, 1976;Wild et al, 1983) although no direct data have accumulated to support this hypothesis (Rosenfield et a/., 1984). Other studies have proposed hypothalamic defects (Kopelman et al, 1980) or an adrenal source (Ho Yuen & Mincey, 1983) to account for the androgen excess in obesity.…”

Section: Obesitymentioning

confidence: 99%

“…The main finding from these early studies was, however, that it was obesity, rather than androgens, that was associated with adverse lipid profiles (Wild et a/., 1985;Wortsman & Soler, 1982;Mattsson et a/., 1984;Graf et a/., 1990;Rojanasakul et a/., 1988). Subsequent studies revealed the sex difference in the prevalence of heart disease to be due to a cardioprotective effect of oestrogens (Campos et Insulin resistance has been implicated as a risk factor for coronary artery disease in epidemiological studies (Pyorala, 1979;Welborn & Wearn, 1979;Ducimetiere et a/., 1980) which further suggested that the mechanism behind the association was through alterations of plasma lipoprotein concentrations (Stalder et a/., 1981;Peiris et al, 1989a;Modan et al, 1988;Ostlund et aE., 1990).…”

Section: Coronary Artery Diseasementioning

confidence: 99%