Hyperandrogenaemia in adolescent girls: origins of abnormal gonadotropin‐releasing hormone secretion

Solorzano, CM Burt; McCartney, CR; Blank, SK; Knudsen, K.; Jc, Marshall

doi:10.1111/j.1471-0528.2009.02383.x

Cited by 46 publications

(41 citation statements)

References 41 publications

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“…About 24% PCOS women were hirsute and 8% showed symptoms of acne. An increased conversion of testosterone to dihydrotestosterone via the enzyme 5 alpha reductase (5α-R) within the pilosebaceous unit may be one of the root causes for hirsutism [24] . 5-α reductase acts as an amplifier of the androgen signal [25] .…”

Section: Table 6: Multivariate Logistic Regression Analysis On Associmentioning

confidence: 99%

A Case-controlled Comparative Hospital-based Study on the Clinical, Biochemical, Hormonal, and Gynecological Parameters in Polycystic Ovary Syndrome

Thangavelu¹,

Godla²,

Gódi³

et al. 2017

pharmaceutical-sciences

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Maheswari, et al.: A Case-controlled Comparative Study on Polycystic Ovary SyndromeThe objective of this study was to evaluate and compare the clinical, biochemical, hormonal and gynaecological aspects of polycystic ovary syndrome at a hospital in South India. The observational, case-controlled study was conducted from April 2011 to January 2014 and recruited 192 polycystic ovary syndrome patients and 205 normal women. Clinical history and biochemical and hormonal analysis were carried out. Correlation was tested between testosterone and other clinical findings. Variables were further analysed using logistic regression with adjusted odds ratio with a 95% confidence interval. About 16% of polycystic ovary syndrome women were obese and 91% reported to have an increased waist/hip ratio. Oligomenorrhea was observed in 74% women with polycystic ovary syndrome. The tested variables revealed that body mass index, waist/hip ratio, hirsutism, testosterone, insulin, ovarian volume and follicular count were elevated in polycystic ovary syndrome patients compared to the control subjects. Increased testosterone levels correlated positively with luteinizing hormone/follicle-stimulating hormone ratio (p=0.023), hirsutism (p=0.001) and antral follicular count (p=0.004) in polycystic ovary syndrome patients in the studied population. Waist/hip ratio could possibly be a better risk indicator than body mass index. Increased testosterone levels, ovarian volume and antral follicular count or combination of these have been considered to be risk factors in developing polycystic ovary syndrome patients.

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Section: Table 6: Multivariate Logistic Regression Analysis On Associmentioning

confidence: 99%

A Case-controlled Comparative Hospital-based Study on the Clinical, Biochemical, Hormonal, and Gynecological Parameters in Polycystic Ovary Syndrome

Thangavelu¹,

Godla²,

Gódi³

et al. 2017

pharmaceutical-sciences

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show abstract

“…Excess LH secretion in PCOS is partly related to relative GnRH pulse generator resistance to the negative feedback actions of progesterone (Burt Solorzano et al 2010). This defect is reversed in adult PCOS by the androgen-receptor blockade (Eagleson et al 2000), suggesting that hyperandrogenemia per se contributes to abnormal neuroendocrine function in PCOS.…”

Section: Obesity and Hyperandrogenemia In Peripubertal Girlsmentioning

confidence: 99%

Obesity and the pubertal transition in girls and boys

Solorzano

McCartney²

2010

Reproduction

355

295

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Childhood obesity has become a major health concern in recent decades, especially with regard to metabolic abnormalities that impart a high risk for future cardiovascular disease. Recent data suggest that excess adiposity during childhood may influence pubertal development as well. In particular, excess adiposity during childhood may advance puberty in girls and delay puberty in boys. Obesity in peripubertal girls may also be associated with hyperandrogenemia and a high risk of adolescent polycystic ovary syndrome. How obesity may perturb various hormonal aspects of pubertal development remains unclear, but potential mechanisms are discussed herein. Insulin resistance and compensatory hyperinsulinemia may represent a common thread contributing to many of the pubertal changes reported to occur with childhood obesity. Our understanding of obesity's impact on pubertal development is in its infancy, and more research into pathophysiological mechanisms and longer-term sequelae is important.

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“…These data raise the possibility that dysfunctional coordination of the KNDy network may underlie neuroendocrine defects in clinical reproductive disorders, including PCOS . Adolescents with PCOS show disruption in the regulation of the GNRH pulse generator, characterized by rapid LH pulse frequency (Burt Solorzano et al 2010). To date, the limited investigations have focused on the early neurobiological mechanisms underlying pubertal regulation of the GNRH/LH pulsatile release by kisspeptin and NKB in adolescents with PCOS.…”

Section: Introductionmentioning

confidence: 99%

Prenatal androgen excess enhances stimulation of the GNRH pulse in pubertal female rats

Yan¹,

Yuan²,

Zhao³

et al. 2014

Journal of Endocrinology

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In adolescent girls with polycystic ovary syndrome (PCOS), neuroendocrine derangements manifest after the onset of puberty, characterized by rapid LH pulse frequency. The early mechanism underlying the pubertal regulation of the GNRH/LH pulsatile release in adolescents with PCOS remains uncertain. To determine the effects of prenatal androgen exposure on the activation of GNRH neurons and generation of LH pulse at puberty, we administrated 5a-dihydrotestosterone to pregnant rats and observed serum LH levels and expression of hypothalamic genes in female offspring from postnatal 4 to 8 weeks. The 6-week-old prenatally androgenized (PNA) female rats exhibited an increase in LH pulse frequency. The hypothalamic expression of neurokinin B (Nkb (Tac2)) and Lepr mRNA levels in PNA rats increased remarkably before puberty and remained high during puberty, whereas elevated Kiss1 mRNA levels were detected only after the onset of puberty. Exogenous kisspeptin, NK3R agonist, and leptin triggered tonic stimulation of GNRH neurons and increased LH secretion in 6-week-old PNA rats. Leptin upregulated Kiss1 mRNA levels in the hypothalamus of pubertal PNA rats; however, pretreatment with a kisspeptin antagonist failed to suppress the elevated serum LH stimulated by leptin, indicating that the stimulatory effects of leptin may be conveyed indirectly to GNRH neurons via other neural components within the GNRH neuronal network, rather than through the kisspeptin-GPR54 pathway. These findings validate the hypotheses that NKB and leptin play an essential role in the activation of GNRH neurons and initiation of increased LH pulse frequency in PNA female rats at puberty and that kisspeptin may coordinate their stimulatory effects on LH release.

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Hyperandrogenaemia in adolescent girls: origins of abnormal gonadotropin‐releasing hormone secretion

Cited by 46 publications

References 41 publications

A Case-controlled Comparative Hospital-based Study on the Clinical, Biochemical, Hormonal, and Gynecological Parameters in Polycystic Ovary Syndrome

A Case-controlled Comparative Hospital-based Study on the Clinical, Biochemical, Hormonal, and Gynecological Parameters in Polycystic Ovary Syndrome

Obesity and the pubertal transition in girls and boys

Prenatal androgen excess enhances stimulation of the GNRH pulse in pubertal female rats

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