Contribution of endogenous LH secretion to hCG-stimulated androgen production in women with polycystic ovary syndrome

2010 ◽  
Vol 94 (4) ◽  
pp. S192
Author(s):  
M.A. Rosencrantz ◽  
H.I. Su ◽  
A. Ramos-Haggan ◽  
R.J. Chang
Keyword(s):  
Polycystic Ovary Syndrome ◽  
Polycystic Ovary ◽  
Ovary Syndrome ◽  
Lh Secretion

Relationship of GnRH-stimulated LH release to episodic LH secretion and baseline endocrine-metabolic measures in women with polycystic ovary syndrome

2004 ◽  
Vol 60 (1) ◽  
pp. 67-74 ◽  
Author(s):  
Ketan Patel ◽  
Mickey S. Coffler ◽  
Michael H. Dahan ◽  
Pamela J. Malcom ◽  
Reena Deutsch ◽  
...  
Keyword(s):  
Polycystic Ovary Syndrome ◽  
Polycystic Ovary ◽  
Ovary Syndrome ◽  
Lh Release ◽  
Relationship Of ◽  
Lh Secretion

scholarly journals Kisspeptin and neurokinin B interactions in modulating gonadotropin secretion in women with polycystic ovary syndrome

2020 ◽  
Vol 35 (6) ◽  
pp. 1421-1431
Author(s):  
Karolina Skorupskaite ◽  
Jyothis T George ◽  
Johannes D Veldhuis ◽  
Robert P Millar ◽  
Richard A Anderson
Keyword(s):  
Polycystic Ovary Syndrome ◽  
Clinical Research ◽  
Polycystic Ovary ◽  
Pulse Frequency ◽  
Research Facility ◽  
Neurokinin B ◽  
Ovary Syndrome ◽  
Clinical Research Facility ◽  
Lh Secretion

Abstract STUDY QUESTION What is the role of the hypothalamic neuropeptide neurokinin B (NKB) and its interaction with kisspeptin on GnRH/LH secretion in women with polycystic ovary syndrome (PCOS)? SUMMARY ANSWER Administration of neurokinin 3 receptor antagonist (NK3Ra) for 7 days reduced LH and FSH secretion and LH pulse frequency in women with PCOS, whilst the stimulatory LH response to kisspeptin-10 was maintained. WHAT IS KNOWN ALREADY PCOS is characterized by abnormal GnRH/LH secretion. NKB and kisspeptin are master regulators of GnRH/LH secretion, but their role in PCOS is unclear. STUDY DESIGN, SIZE, DURATION The NK3Ra MLE4901, 40 mg orally twice a day, was administered to women with PCOS for 7 days (n = 8) (vs no treatment, n = 7). On the last day of NK3Ra administration or the equivalent day in those not treated, women were randomized to 7-h kisspeptin-10 (4 µg/kg/h i.v.) or vehicle infusion. This was repeated with the alternate infusion in a subsequent cycle. PARTICIPANTS/MATERIALS, SETTING, METHODS Subjects were women with PCOS, studied in a Clinical Research Facility. Reproductive hormones were measured before and after NK3Ra administration. On the last day of NK3Ra administration (or the equivalent cycle day in untreated women), all women attended for an 8-h frequent blood sampling to allow analysis of the pulsatile LH secretion. MAIN RESULTS AND THE ROLE OF CHANCE NK3Ra reduced LH secretion (4.0 ± 0.4 vs 6.5 ± 0.8 IU/l, P < 0.05) and pulse frequency (0.5 ± 0.1 vs 0.8 ± 0.1 pulses/h, P < 0.05); FSH secretion was also reduced (2.0 ± 0.3 vs 2.5 ± 0.4 IU/l, P < 0.05). Without NK3Ra pre-treatment, kisspeptin-10 increased LH secretion (5.2 ± 0.5 to 7.8 ± 1.0 IU/L, P < 0.05), with a positive relationship to oestradiol concentrations (r2 = 0.59, P < 0.05). After NK3Ra administration, the LH response to kisspeptin-10 was preserved (vehicle 3.5 ± 0.3 vs 9.0 ± 2.2 IU/l with kisspeptin-10, P < 0.05), but the positive correlation with oestradiol concentrations was abolished (r2 = 0.07, ns. after NK3Ra). FSH secretion was increased by kisspeptin-10 after NK3Ra treatment, but not without NK3Ra treatment. LIMITATIONS, REASONS FOR CAUTION The study did not explore the dose relationship of the effect of NK3R antagonism. The impact of obesity or other aspects of the variability of the PCOS phenotype was not studied due to the small number of subjects. WIDER IMPLICATIONS OF THE FINDINGS These data demonstrate the interactive regulation of GnRH/LH secretion by NKB and kisspeptin in PCOS, and that the NKB system mediates aspects of oestrogenic feedback. STUDY FUNDING/COMPETING INTEREST(S) Wellcome Trust through Scottish Translational Medicine and Therapeutics Initiative (102419/Z/13/A) and MRC grants (G0701682 to R.P.M. and R.A.A.) and MR/N022556/1 to the MRC Centre for Reproductive Health. This work was performed within the Edinburgh Clinical Research Facility. J.T.G. has undertaken consultancy work for AstraZeneca and Takeda Pharmaceuticals and is an employee of Boehringer Ingelheim. R.P.M. has consulted for Ogeda and was CEO of Peptocrine. R.A.A. has undertaken consultancy work for Merck, Ferring, NeRRe Therapeutics and Sojournix Inc. J.D.V. and K.S. have nothing to disclose. TRIAL REGISTRATION NUMBER N/A.

scholarly journals Developmental origin of polycystic ovary syndrome - a hypothesis

2002 ◽  
Vol 174 (1) ◽  
pp. 1-5 ◽  
Author(s):  
DH Abbott ◽  
DA Dumesic ◽  
S Franks
Keyword(s):  
Insulin Resistance ◽  
Polycystic Ovary Syndrome ◽  
Polycystic Ovary ◽  
Regulatory Region ◽  
Later Life ◽  
Ovary Syndrome ◽  
Increased Risk ◽  
Genetically Determined ◽  
Lh Secretion

Polycystic ovary syndrome (PCOS) is a common but complex endocrine disorder and is a major cause of anovulation and consequent subfertility. It is also associated with a metabolic disturbance, characterized by hyperinsulinaemia and insulin resistance that carries an increased risk of type 2 diabetes in later life. Despite its prevalence little is known about its aetiology, but there is increasing evidence for an important genetic involvement. On the basis of experimental observations in the prenatally androgenized sheep and rhesus monkey, and supported by data from human studies, we propose that the clinical and biochemical features of PCOS can arise as a consequence of genetically determined hypersecretion of androgens by the ovary during, or very likely long before, puberty. The resulting hyperandrogenism results in 'programming' of the hypothalamic-pituitary unit to favour excess LH secretion, and encourages preferential abdominal adiposity that predisposes to insulin resistance. The severity of hyperinsulinaemia and insulin resistance (which has a profound influence on the phenotype of PCOS) is further influenced by both genetic factors (such as polymorphism in the insulin gene regulatory region) and environmental factors, notably obesity. This hypothesis therefore suggests a unifying, 'linear' model to explain the aetiology of the heterogeneous phenotype.

EVIDENCE FOR DECREASED ENDOGENOUS DOPAMINE AND OPIOID INHIBITORY INFLUENCES ON LH SECRETION IN POLYCYSTIC OVARY SYNDROME

1984 ◽  
Vol 20 (6) ◽  
pp. 643-648 ◽  
Author(s):  
D. C. CUMMING ◽  
R. L. REID ◽  
M. E. QUIGLEY ◽  
R. W. REBAR ◽  
S. S. C. YEN
Keyword(s):  
Polycystic Ovary Syndrome ◽  
Polycystic Ovary ◽  
Ovary Syndrome ◽  
Endogenous Dopamine ◽  
Lh Secretion

Role of Prolactin in the Polycystic Ovary Syndrome

1980 ◽  
Vol 25 (4) ◽  
pp. S89-S93 ◽  
Author(s):  
Emilio del Pozo ◽  
Paolo Falaschi
Keyword(s):  
Polycystic Ovary Syndrome ◽  
Polycystic Ovary ◽  
Control Mechanisms ◽  
Plasma Prolactin ◽  
Adrenal Androgen ◽  
Ovary Syndrome ◽  
Steroid Synthesis ◽  
Androgen Synthesis ◽  
Lh Secretion

Studies with a dopamine agonist (Bromocriptine) and an antagonist (Haloperidol) suggest that elevated sex steroid synthesis such as may be found in the polycystic ovary syndrome (PCO) influence the pituitary lactotrope response to endogenous control mechanisms. A distinction between PCO with occasional elevation of plasma prolactin (PRL) and the galactorrhoea-amenorrhoea syndrome (GA) associated with hyperprolactinaemia can be established on the basis of differences in circulating levels of sex steroids and in the pattern of response to lactotrope cell stimulation. Thus, adrenal androgen synthesis can be strengthened in GA whereas in PCO both pathways, adrenal and ovarian, may be overstimulated. Also blunted PRL response to TRH or dopaminergic blockade is often seen in GA. The use of bromocriptine in patients with PCO and elevated PRL plasma levels has been shown to restore ovulation. The possible implications of dopaminergic mechanisms in the control of LH secretion independent of PRL release are discussed.

LH in polycystic ovary syndrome: reproducibility and pulsatile secretion

1989 ◽  
Vol 121 (1) ◽  
pp. 185-191 ◽  
Author(s):  
A. P. Murdoch ◽  
P. J. Diggle ◽  
M. C. White ◽  
P. Kendall-Taylor ◽  
W. Dunlop
Keyword(s):  
Polycystic Ovary Syndrome ◽  
Polycystic Ovary ◽  
Ovary Syndrome ◽  
Blood Samples ◽  
Significant Difference ◽  
Early Follicular Phase ◽  
Within Subjects ◽  
Complicated Pattern ◽  
Normal Women ◽  
Lh Secretion

ABSTRACT Serum concentrations of LH are increased in polycystic ovary syndrome (PCOS). We have investigated two aspects of LH secretion which have not previously been reported: its reproducibility within individuals and the pattern of superimposed pulses of LH secretion. In nine patients with PCOS the mean concentration of LH was calculated from 24 blood samples taken at 15-min intervals for 6 h on two or three occasions over 1 year. Results showed differences in mean LH between subjects but reproducible concentrations within subjects over that period. It has been shown that LH is secreted in a complicated pattern of superimposed pulses which can be characterized by using the statistical methods of time-series analysis. To evaluate these pulse patterns of LH we studied nine patients with PCOS and compared the results with those of 12 normal women in the early follicular phase of the ovarian cycle. Blood samples were taken at either 5-min intervals for 6 h or 1-min intervals for 1 h. Pulses were detected in both groups at frequencies of about 1 h and 2 to 3 min. There was no significant difference in the pulse frequencies between the patients and controls but the amplitude of both groups of pulses was increased in the PCOS patients. Journal of Endocrinology (1989) 121, 185–191

Retention of estradiol negative feedback relationship to LH predicts ovulation in response to caloric restriction and weight loss in obese patients with polycystic ovary syndrome

2004 ◽  
Vol 286 (4) ◽  
pp. E615-E620 ◽  
Author(s):  
Eveline W. C. M. van Dam ◽  
Ferdinand Roelfsema ◽  
Johannes D. Veldhuis ◽  
Simone Hogendoorn ◽  
Jos Westenberg ◽  
...  
Keyword(s):  
Weight Loss ◽  
Body Weight ◽  
Polycystic Ovary Syndrome ◽  
Body Fat ◽  
Negative Feedback ◽  
Polycystic Ovary ◽  
Obese Patients ◽  
Ovary Syndrome ◽  
Fat Depots ◽  
Lh Secretion

The present study tests the hypothesis that specific endocrine, metabolic, and anthropometric features distinguish obese women with polycystic ovary syndrome (PCOS) who resume ovulation in response to calorie restriction and weight loss from those who do not. Fifteen obese (body mass index 39 ± 7 kg/m2) hyperandrogenemic oligoovulatory patients undertook a very low calorie diet (VLCD), wherein each lost ≥10% of body weight over a mean of 6.25 mo. Body fat distribution was quantitated by magnetic resonance imaging. Hormones were measured in the morning at baseline, after 1 wk of VLCD, and after 10% weight loss. To monitor LH release, blood was sampled for 24 h at 10-min intervals before intervention and after 7 days of VLCD. Responders were defined a priori as individuals exhibiting two or more ovulatory cycles in the course of intervention, as corroborated by serum progesterone concentrations ≥18 nmol/l followed by vaginal bleeding. At baseline, responders had a higher sex hormone-binding globulin (SHBG) concentration but were otherwise indistinguishable from nonresponders. Body weight, the size of body fat depots, and plasma insulin levels declined to a similar extent in responders and nonresponders. Also, SHBG increased, and the free testosterone index decreased comparably. However, responders exhibited a significant decline of circulating estradiol concentrations (from 191 ± 82 to 158 ± 77 pmol/l, means ± SD, P = 0.037) and a concurrent increase in LH secretion (from 104 ± 42 to 140 ± 5 U·l-1·day-1, P = 0.006) in response to 7 days of VLCD, whereas neither parameter changed significantly in nonresponders. We infer that evidence of retention of estradiol-dependent negative feedback on LH secretion may forecast follicle maturation and ovulation in obese patients with PCOS under dietary restriction.

scholarly journals Acupuncture for ovulation induction in polycystic ovary syndrome: a randomized controlled trial

2013 ◽  
Vol 304 (9) ◽  
pp. E934-E943 ◽  
Author(s):  
Julia Johansson ◽  
Leanne Redman ◽  
Paula P. Veldhuis ◽  
Antonina Sazonova ◽  
Fernand Labrie ◽  
...  
Keyword(s):  
Polycystic Ovary Syndrome ◽  
Polycystic Ovary ◽  
Controlled Trial ◽  
Acupuncture Group ◽  
Sex Steroid ◽  
Control Group ◽  
Controlled Clinical Trial ◽  
Ovary Syndrome ◽  
Randomized Controlled ◽  
Lh Secretion

Acupuncture has been demonstrated to improve menstrual frequency and to decrease circulating testosterone in women with polycystic ovary syndrome (PCOS). Our aim was to investigate whether acupuncture affects ovulation frequency and to understand the underlying mechanisms of any such effect by analyzing LH and sex steroid secretion in women with PCOS. This prospective, randomized, controlled clinical trial was conducted between June 2009 and September 2010. Thirty-two women with PCOS were randomized to receive either acupuncture with manual and low-frequency electrical stimulation or to meetings with a physical therapist twice a week for 10–13 wk. Main outcome measures were changes in LH secretion patterns from baseline to after 10–13 wk of treatment and ovulation frequency during the treatment period. Secondary outcomes were changes in the secretion of sex steroids, anti-Müllerian hormone, inhibin B, and serum cortisol. Ovulation frequency during treatment was higher in the acupuncture group than in the control group. After 10–13 wk of intervention, circulating levels of estrone, estrone sulfate, estradiol, dehydroepiandrosterone, dehydroepiandrosterone sulfate, androstenedione, testosterone, free testosterone, dihydrotestosterone, androsterone glucuronide, androstane-3α,17β-diol-3-glucuronide, and androstane-3α,17β-diol-17-glucuronide decreased within the acupuncture group and were significantly lower than in the control group for all of these except androstenedione. We conclude that repeated acupuncture treatments resulted in higher ovulation frequency in lean/overweight women with PCOS and were more effective than just meeting with the therapist. Ovarian and adrenal sex steroid serum levels were reduced with no effect on LH secretion.

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