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PubMed2005

[Microsatellite polymorphism of (tttta) n in the promoter of CYP11a gene in Chinese women with polycystic ovary syndrome].

OBJECTIVE: To investigate the distribution of (tttta) n microsatellite polymorphism in the promoter of CYP11a gene in Chinese women with polycystic ovary syndrome (PCOS) and the relationship between such polymorphism and PCOS. METHODS: Peripheral blood samples were obtained from 201 women with PCOS, aged 26 +/- 4, and 147 women without PCOS, aged 29 +/- 5. Radioimmunoassay was used to examine the levels of testosterone, follicle-stimulating hormone, luteinizing hormone, progesterone, estradiol, and prolactin. Locus-specific prime PCR was used to detect the frequencies of the CYP11a alleles. Body mass index (BMI) was calculated. RESULTS: The average BMI of the women with PCOS was 22 kg/m(2) +/- 4 kg/m(2), and that of the non-PCOS women was 22 kg/m(2) +/- 6 kg/m(2). The six-repeat allele variant genotypic distribution of CYP11a was statistically different between the women with PCOS and those without PCOS [Fisher's exact test (2-tail), P = 0.031]. The frequency of 6//6 genotype in the PCOS patients was 57.7% (116/201), significantly higher than that of the non-PCOS women [44.9% (66/147), chi(2) = 5.588, P = 0.018]. The BMI of the PCOS patients with 4//4 genotype was 19.4 kg/m(2) +/- 1.7 kg/m(2), statistically lower than those of the PCOS patients with 4//6, 6//6, and 6//8 genotypes (23.6 kg/m(2) +/- 3.3 kg/m(2), 22.5 kg/m(2) +/- 3.8 kg/m(2), 22.2 kg/m(2) +/- 4.2 kg/m(2) respectively, P = 0.0037, 0.0027, and 0.059 respectively). The PCOS patients with the allele (tttta) 6 had markedly higher BMI (22.7 kg/m(2) +/- 3.7 kg/m(2)) than those without the allele (tttta) 6 (19.4 kg/m(2) +/- 1.7 kg/m(2), P = 0.0075). No differences were observed in the serum levels of reproductive hormones among the individuals with different genotypic features in the PCOS patients. CONCLUSION: The six-repeat allele is the most common fragment of (tttta) n microsatellite polymorphism in Chinese Han woman. The 6//6 genotype is significantly more frequent and is associated with greater BMI in the women with PCOS. The six-repeat allele variant may play a certain role in the pathogenesis of PCOS.

Adult↗

PubMed2001

Tissue insulin sensitivity and body weight in polycystic ovary syndrome.

OBJECTIVE: Polycystic ovarian syndrome (PCOS) and obesity both affect insulin sensitivity. This study was designed to investigate the biochemical indices of PCOS and tissue insulin sensitivity in groups of lean and obese women with clinically equivalent degrees of the syndrome, relative to control subjects. DESIGN: A prospective study of in vivo parameters and in vitro study of adipocytes to assess insulin sensitivity. PATIENTS: Six lean and 14 overweight patients fulfilling formal diagnostic criteria for PCOS were studied. The degree of hirsutism and amenorrhoea was similar in each group. Eight control subjects were also studied. MEASUREMENTS: Endocrine and metabolic parameters were measured in lean and overweight patients with PCOS and control subjects. In vitro studies of adipocyte insulin receptor binding and adipocyte insulin action were performed. RESULTS: The mean plasma LH level was elevated in both groups of PCOS but was significantly higher in the lean group (LH levels were 25.1 +/- 3.1 and 14.5 +/- 1.6 iu/l in lean PCOS and obese PCOS, respectively (P = 0.01)). There was a strong inverse correlation between BMI and LH levels (R = - 0.70, P = 0.001). Fasting insulin levels were elevated in both lean and obese groups (11.5 +/- 2.8 and 26.8 +/- 8.1 mU/l, respectively; P = 0.068). Mean serum testosterone and serum androstenedione levels were also elevated in PCOS compared to control subjects but there was no difference between the two groups of PCOS subjects. Insulin receptor binding in amenorrhoeic subjects with PCOS was low in both lean and obese patients with PCOS but was not significantly different between the two groups (0.79 +/- 0.17% and 0.66 +/- 0.07% per 10 cm2 cell membrane, respectively). Maximally insulin-stimulated rates of 3-O-methylglucose transport were low in both groups compared to previously studied normal subjects (0.96 +/- 0.21 and 0.64 +/- 0.07 pmol per 10 cm2 membrane in lean and obese PCOS subjects, respectively; P = NS). CONCLUSIONS: Lean subjects with a given phenotypic expression of PCOS have an equivalent degree of tissue insulin resistance compared to obese PCOS subjects. This implies that the insulin resistance may be a primary feature of PCOS. If this is so, a similar clinical degree of the syndrome may be brought about by genetically determined insulin resistance in lean subjects or by insulin resistance which is secondary to obesity.

Adipocytes↗

PubMed2003

Is serum leptin level regulated by thyroid functions, lipid metabolism and insulin resistance in polycystic ovary syndrome?

Our aim was to determine whether serum leptin level is regulated by thyroid hormones, lipid metabolic products and insulin resistance status in women with polycystic ovary syndrome (PCOS). A prospective case-controlled study was carried out in Istanbul University, Cerrahpasa School of Medicine in 25 lean PCOS (L-PCOS) women, 19 obese PCOS (O-PCOS) women and 28 normal women. The diagnosis of PCOS was established according to the clinical, hormonal (elevated luteinizing hormone and serum androgens) and ultrasonographic findings. Fasting serum levels of thyroid stimulating hormone (TSH), free triiodothyronine (FT3), free thyroxine (FT4), fasting glucose, insulin, total cholesterol (TC), triglyceride (TG), high-density lipoprotein-cholesterol (HDL-C), low-density lipoprotein-cholesterol (LDL-C), very low-density lipoprotein-cholesterol (VLDL-C) and leptin were measured and compared in the three groups and the correlations between serum levels of leptin and other parameters were evaluated. Serum leptin levels were higher in the O-PCOS group, while its level was comparable between the L-PCOS and control groups. Serum levels of FT4 were significantly lower in both L-PCOS and O-PCOS groups than the control group. Women in both L-PCOS and O-PCOS groups were found to be significantly hyperinsulinemic and insulin resistant. Serum levels of TC, VLDL-C and TG were significantly higher in the O-PCOS group, while serum HDL-C level was lower. There was a poor correlation between serum leptin, and FT4, TC, TG, HDL-C and VLDL-C levels. A significant correlation was observed between serum leptin levels and both BMI and insulin resistance status in PCOS. We believe that, although thyroid hormones and lipid metabolic products do not seem to participate in the regulation of serum leptin levels, BMI and insulin resistance status may have a key role in women with PCOS.

Adult↗

PubMed2007

Effect of long-term orlistat treatment on serum levels of advanced glycation end-products in women with polycystic ovary syndrome.

UNLABELLED: BACKGROUND Women with polycystic ovary syndrome (PCOS) exhibit elevated serum advanced glycation end-products (AGE) compared with healthy subjects. Short-term administration of orlistat has been shown to reduce the postmeal increase in serum AGE levels in women with PCOS and in controls. OBJECTIVE: To evaluate the long-term effect of orlistat and a low-calorie diet on serum AGE levels, and on the hormonal and metabolic profile of obese PCOS and normal women. DESIGN: A clinical trial of 6 months of orlistat administration with an energy-restricted diet [basic metabolic rate (BMR) 600 kcal/day] in all subjects. SUBJECTS: Twenty-nine women with PCOS [aged 27.52 +/- 5.77 years; body mass index (BMI) 35.43 +/- 5.31 kg/m(2)] and 18 controls (aged 32.06 +/- 5.64 years; BMI 36.39 +/- 6.47 kg/m(2)). MEASUREMENTS: Serum AGE levels (U/ml), hormonal and metabolic profile. RESULTS: PCOS and controls did not differ in BMI (P = 0.58), waist-to-hip ratio (WHR) (P = 0.44), fasting insulin concentration (P = 0.45) and glucose-to-insulin ratio (GIR) (P = 0.34). PCOS women exhibited statistically higher AGE (P < 0.001) and testosterone levels (P < 0.001) compared with controls. After 6 months of orlistat treatment, AGE levels showed a statistically significant decrease in both groups (PCOS: baseline 9.08 +/- 1.84, post-orlistat 8.56 +/- 1.95, P = 0.001; controls: baseline 5.02 +/- 0.62, post-orlistat 4.91 +/- 0.69, P = 0.03), independently of the BMI reduction in the PCOS group. A significant reduction was observed in BMI (PCOS: P < 0.001; controls: P < 0.001), WHR (PCOS: P = 0.002; controls: P = 0.04), fasting insulin (PCOS: P < 0.001; controls: P = 0.008), and testosterone concentrations in PCOS (P < 0.001). SHBG concentration (PCOS: P = 0.004; controls: P = 0.008) and GIR (PCOS: P < 0.001; controls: P = 0.03) were significantly increased. A significant improvement was also observed in insulin resistance indices post-treatment in both groups. CONCLUSIONS: Our data suggest that orlistat has a beneficial effect in reducing elevated AGE levels and improving the hormonal and metabolic profile in women with PCOS after 6 months of treatment, independently of BMI changes.

Adult↗

PubMed1998

Augmented frequency and mass of LH discharged per burst are accompanied by marked disorderliness of LH secretion in adolescents with polycystic ovary syndrome.

The aim of this study was to quantify pulsatile LH secretion, burst frequency and mass, LH half-life, and the approximate entropy (ApEn) or (dis-) orderliness of LH release in adolescents with polycystic ovary syndrome (PCOS), combining a high-precision immunofluorimetric LH assay with deconvolution techniques. We sampled LH concentration profiles every 20 min overnight in 12 girls with PCOS (mean +/- S.E.M. age 16.4+/-0.57 years, body mass index (BMI) 24.4+/-1.6 kg/m2) and 11 eumenorrheic early-follicular-phase controls (mean +/- S.E.M. age 16.5+/-0.47 years, BMI 22.2+/-1.0 kg/m2). Fasting serum levels of androstenedione, testosterone, 17-hydroxyprogesterone (17-OHP), estrone, estradiol, FSH and sex hormone-binding globulin (SHBG) were determined. Compared with euandrogenic girls, PCOS adolescents had significantly (P<0.005) elevated serum LH/FSH ratios, 17-OHP, androstenedione, esterone and testosterone levels, decreased SHBG, and similar estradiol. PCOS subjects exhibited a 3-fold higher mean serum LH concentration with almost no overlap with controls (8.8+/-1.2 and 2.8+/-0.3 IU/l respectively, P<0.001). We initially used a conventional serum hormone concentration peak analysis method (Cluster) to evaluate the characteristics of pulsatile LH release. Cluster analysis disclosed a significant increase in serum LH concentration maximal peak height, a higher LH peak frequency and a higher mean serum LH concentration in interpulse nadirs in the PCOS group. Deconvolution analysis of mechanisms underlying the foregoing showed higher frequency in the PCOS group than the controls (7.9+/-0.4 and 5.7+/-0.6 pulses/12 h respectively, P<0.05). The mass of LH released per secretory event was also significantly higher in PCOS subjects than controls (5.4+/-0.57 and 3.4+/-0.56 IU/l respectively, P<0.05). Since the pulsatile production rate is the product of the mean mass of hormone secreted per pulse and the number of pulses per day, we estimated a significantly higher mean pulsatile production rate of (endogenous) LH in the PCOS group (41+/-4.2 IU/l per day in the PCOS group vs 18+/-2.3 IU/l per day in the controls, P<0.01). The mean estimated half-life of endogenous LH disappearance was also significantly higher in patients with PCOS than in controls (110+/-8.5 and 77+/-3.7 min respectively, P<0.01). To quantify the orderliness of LH release, we used ApEn. PCOS patients had remarkably increased disorderliness (higher ApEn) of LH release (1.09+/-0.04 vs 0.77+/-0.08 in controls, P = 0.002). Mean serum LH concentration, mass of LH secreted per burst, and LH production rate in PCOS, but not in normal adolescents, correlated positively with androstenedione (P<0.02, 0.02 and 0.05 respectively). The same parameters also correlated positively with 17-OHP (P<0.05, 0.02 and 0.05 respectively). Stepwise regression analysis unmasked a negative influence of BMI in PCOS on both mass of LH secreted per burst (r = -0.77, P<0.005) and LH production rate (r = -0.70, P<+/0.01). We conclude that PCOS adolescents secrete LH molecules with amplified frequency and burst mass and with markedly disrupted orderliness. A rise in basal (non-pulsatile) LH release, more basic LH isoforms, and/or a prolongation or asymmetry of the LH secretory burst could account for the apparently prolonged LH half-life. Determining whether disorderliness of the amplified pituitary LH release process is an intrinsic abnormality in PCOS. or reflects androgen excess, may help to clarify the pathophysiology of this oligo-ovulatory syndrome in young women.

Adolescent↗

PubMed1998

Inhibin A and inhibin B in women with polycystic ovarian syndrome during treatment with FSH to induce mono-ovulation.

OBJECTIVE: Polycystic ovary syndrome (PCOS) is characterized by the presence of numerous small antral follicles arrested at a diameter of less than 10 mm. As development of large antral follicle(s) can be stimulated by the administration of FSH, it has been suggested that the arrest of follicle development is due to a relative lack of or resistance to FSH. We have measured the concentration of FSH and LH and the ovarian hormones oestradiol, inhibin A and B, in relation to the dynamics of follicular development in women with PCOS under basal conditions and during treatment with FSH. DESIGN: The concentrations of FSH, LH, oestradiol, inhibin A and B were measured in women with PCOS who were untreated (n = 9) or following progesterone-induced menses (10 cycles in six women) and control women on day 3 of a normal cycle (n = 10). Serial measurements of the same hormones were made during induction of ovulation with low dose of exogenous FSH in the women with PCOS who had been treated with progesterone. The dynamics of follicle development were measured by serial pelvic ultrasound examinations during treatment with FSH in PCOS and in the follicular phase of control cycles. PATIENTS: Nine anovulatory untreated women with PCOS were compared with 10 normal women and six women with PCOS undergoing FSH treatment. RESULTS: The concentrations of inhibin B and LH were higher in both groups of women with PCOS than in normal control women on day 3. In untreated women with PCOS the concentration of inhibin A was also significantly elevated compared to control women (P < 0.01) but not in women pretreated with progesterone. Basal concentrations of oestradiol were also significantly higher in women with PCOS than in the early follicular phase of the normal cycle. There were no significant differences in the concentration of FSH between the groups. Treatment of women with PCOS with low doses of FSH stimulated the development of a single dominant follicle which had an identical rate of growth and secretion of oestradiol and inhibin A to that observed in spontaneous cycles in normal women. In contrast to normal women, the concentration of inhibin B rose 7-fold following FSH treatment and remained elevated until the luteal phase. CONCLUSIONS: The raised concentrations of inhibin A and B in women with PCOS probably reflects the increased number of small antral follicles characteristically present in that condition. The striking similarity in the dynamics of growth of the dominant follicle and the pattern in concentration of oestradiol and inhibin A in normal women and in women with PCOS treated with modest amounts of FSH, suggests that the arrest of follicle development in PCOS may be due to a relative deficiency of FSH which may in turn be secondary to increased secretion of either or both inhibin forms.

Adult↗

PubMed1999

The effects of metformin on insulin resistance and ovarian steroidogenesis in women with polycystic ovary syndrome.

OBJECTIVE: Polycystic ovary syndrome (PCOS) is a form of functional ovarian hyperandrogenism and affects approximately 5-10% of women of reproductive age. Insulin resistance and hyperinsulinaemia appear to be almost universal feature of the polycystic ovary syndrome. Abnormal regulation of cytochrome P450c17alpha causes the exaggerated secretion of ovarian androgens in PCOS. The aim of the present study was to determine whether reduction of insulin levels by metformin would attenuate FSH, LH, 17-Hydroxyprogesterone (17-OHP) and androstenedione hyperresponsiveness to buserelin testing in PCOS women. DESIGN: The presence of hyperinsulinaemia in 16 women with PCOS was demonstrated by an oral glucose tolerance test (OGTT) and results were compared with 13 healthy women. PCOS women were also evaluated with insulin tolerance test (ITT) for the assessment of insulin sensitivity. FSH, LH, 17-OHP and androstenedione responses to buserelin testing were measured in all the women with PCOS. PCOS patients were given metformin (500 mg, orally, two times daily) for 12 weeks and re-evaluated at the end of the treatment period. RESULTS: Women with PCOS were hyperinsulinaemic (basal insulin 92.1+/-14.3 vs. 44.0+/-4.0 pmol/l; AUCinsulin 68087.4+/-8862.3 vs. 13075.5+/-1327.6 pmol/lx120 min) compared with healthy women. Metformin therapy improved menstrual disturbances in 25% of the women with PCOS and also resulted in some improvement in insulin sensitivity and reduced basal and post glucose load insulin levels. However, FSH, LH, 17-OHP and androstenedione responses to buserelin testing were unaltered in response to metformin. CONCLUSION: It is clear that PCOS is often associated with profound insulin resistance and hyperinsulinaemia. These abnormalities explain the increased prevalence of glucose intolerance in women with PCOS and metformin has beneficial effects on insulin sensitivity in women with PCOS. Amelioration of hyperinsulinaemia has no significant effect on ovarian cytochrome P450c17alpha enzyme activity. However, it can be used in obese women with PCOS as an adjuvant therapy and long term studies should be performed to evaluate the endocrine effects of metformin in women with PCOS.

17-alpha-Hydroxyprogesterone↗

PubMed2001

Polycystic ovary syndrome: relationship between insulin sensitivity, sex hormone levels and ovarian stromal blood flow.

Polycystic ovary syndrome (PCOS) is the most common cause of menstrual disorders, and is characterized by chronic anovulation, hyperandrogenism and infertility. In recent years, it has become apparent that PCOS is also associated with hyperinsulinemia that is probably central to the pathogenesis of PCOS. As a peculiar vascular pattern has been reported to be present in PCOS, the aim of this study was to investigate intraovarian stromal vascularization in PCOS patients and its possible correlation with sex hormones, gonadotropins and insulin levels. Twenty-eight oligomenorrheic or amenorrheic patients with PCOS and 14 eumenorrheic women with a PCOS-like ovarian pattern undergoing endocrine screening and ultrasound color Doppler intraovarian blood flow were recruited to the study. Ten healthy women with regular menses represented the control group. Hormonal assays (follicle-stimulating hormone (FSH), luteinizing hormone (LH), androstenedione, testosterone, sex hormone-binding globulin (SHBG) and estradiol), oral glucose tolerance test (OGTT), baseline and glucose-induced insulin levels, and transvaginal ultrasonographic and color Doppler analysis (pulsatility index (PI), resistance index (RI) and velocity (Vmax) of ovarian stromal flow) were performed in all participants in the early proliferative phase. Endocrine values showed significant differences in PCOS patients compared with PCOS-like women and controls, while PI and RI indices were significantly higher in controls. PCOS patients were divided into hyperinsulinemic (n = 16) and normoinsulinemic (n = 12). Androstenedione was significantly higher (p < 0.01) in the hyperinsulinemic than in the normoinsulinemic patients and controls, while SHBG was significantly (p < 0.01) lower in the hyperinsulinemic group. Analysis of color Doppler intraovarian vascularization showed a significantly lower RI and a higher Vmax in the hyperinsulinemic subjects than in the normoinsulinemic PCOS patients and controls. An increased stromal blood flow was observed in the PCOS and PCOS-like patients by transvaginal color Doppler evaluation, but this technique is not able to differentiate these two similar ovarian patterns. However, hyperinsulinemic PCOS patients had an increased vascularity of the ovarian stroma. A strong correlation between hyperinsulinemia, hyperandrogenism and low SHBG levels was evidenced, and a hyperinsulinemia-induced mechanism for ovarian stromal angiogenesis is discussed.

Adult↗

PubMed2006

Epidemiology and adverse cardiovascular risk profile of diagnosed polycystic ovary syndrome.

CONTEXT: Polycystic ovary syndrome (PCOS) is associated with menstrual and reproductive abnormalities, insulin resistance, and obesity. OBJECTIVE: The objective of this study was to determine the prevalence of diagnosed PCOS and its association with cardiovascular risk factors. SETTING: The study is set in an integrated health care delivery system in northern California. PATIENTS: A total of 11,035 women with PCOS were identified by one or more outpatient diagnoses of PCOS using health plan databases. An age-matched sample of women without PCOS was also selected. OUTCOME MEASURES: Prevalence of PCOS and targeted cardiovascular risk factors [hypertension, dyslipidemia, diabetes mellitus, and body mass index (BMI)] were measured. RESULTS: During 2002-2004, the prevalence of diagnosed PCOS among female members aged 25-34 yr was 2.6% (95% confidence interval 1.6-1.7%). Women with diagnosed PCOS were more likely than those without PCOS to be obese [BMI > or = 30 mg/m(2); odds ratio (OR) 4.21, 3.96-4.47]. Furthermore, PCOS was associated with diabetes (OR 2.45, confidence interval 2.16-2.79), hypertension (OR 1.41, 1.31-1.51) and known dyslipidemia (OR 1.53, 1.39-1.68), even after adjusting for BMI and known confounders. Among women with PCOS, compared with whites, Blacks and Hispanics were more likely and Asians less likely to be obese; Asians and Hispanics were more likely to have diabetes; and Blacks were more likely and Hispanics less likely to have hypertension. CONCLUSIONS: Within a large, community-based population receiving health care, diagnosed PCOS was highly prevalent and associated with a much higher frequency of cardiovascular risk factors that varied by race/ethnicity. Our prevalence estimates likely underestimate the true prevalence of PCOS. Further studies are needed to explore racial/ethnic differences and the extent to which PCOS contributes to future cardiovascular risk.

Adult↗

PubMed1994

Insulin, C-peptide, androgens, and beta-endorphin response to oral glucose in patients with polycystic ovary syndrome.

We examined the effects of an oral glucose load on plasma insulin, androgens, and beta-endorphin (beta EP) concentrations in patients carefully selected as having polycystic ovary syndrome (PCOS) and normal glucose tolerance. Our aim was to verify whether insulin resistance is a common feature of PCOS and to differentiate the metabolic abnormalities related to PCOS from those associated with obesity. Plasma immunoreactive insulin (IRI), C-peptide (C-PR), testosterone, androstenedione, dehydroepiandrosterone sulfate, ACTH, and beta EP responses to a 3-h oral glucose tolerance test (OGTT) were evaluated in 10 obese (OB-PCOS) and 10 nonobese (NO-PCOS) patients with PCOS and in 7 obese and 7 nonobese ovulatory controls. OB-PCOS and NO-PCOS did not differ significantly from weight-matched controls in the IRI response, but had a significantly higher C-PR response in terms of mean postglucose load levels and mean incremental areas. During OGTT, mean plasma levels of testosterone, androstenedione, and dehydroepiandrosterone sulfate declined in both PCOS groups as well as in controls, and no significant correlation between the plasma androgen and IRI or C-PR responses was found. The ACTH response in OB-PCOS and NO-PCOS was similar to that in controls, with a progressive decrease until 180 min. A similar decline in plasma beta EP was found in controls, whereas no change in plasma beta EP was observed in OB-PCOS and NO-PCOS. These findings indicate that independently of the presence of obesity, PCOS patients have enhanced insulin secretion in response to OGTT and show a peculiar pattern of changes in plasma beta EP.

Administration, Oral↗

PubMed1996

A mechanism for the suppression of estrogen production in polycystic ovary syndrome.

In polycystic ovary syndrome (PCOS), follicle development arrests in the early antral stage when aromatase expression in the granulosa cells (GC) would normally occur. Despite high intrafollicular concentrations of androstenedione and bioactive FSH, in vivo estrogen biosynthesis remains low. When GC from PCOS follicles are stimulated with FSH in vitro, a marked stimulation of estrogen production occurs, suggesting that PCOS follicles contain an endogenous inhibitor of estrogen production. To test this hypothesis, GC from hyperstimulated women were cultured with increasing concentrations of follicular fluid (FF) from PCOS and normally cycling control women in the presence of androstenedione (10(-5) mol/L). FF from control women caused a small decrease (20%) in estradiol production. PCOS FF caused a dose-related inhibition of estradiol production (60%), indicating that there was significantly more inhibitory activity in PCOS FF. To determine whether abnormal androgen metabolism could play a role in inhibiting estradiol production in PCOS, we measured 5 alpha-androstane-3, 17-dione, a competitive inhibitor of aromatase activity, in serum and FF of control and PCOS women. 5 alpha-Androstane-3, 17-dione levels in serum were significantly elevated in PCOS. 5 alpha-Androstane-3, 17-dione levels were 1000-fold higher in PCOS FF than serum. Moreover, FF levels were markedly higher in PCOS follicles (P < 0.0001) than in normal dominant and cohort follicles. Dose-response studies revealed that the concentration of 5 alpha-androstane-3, 17-dione present in FF form normal dominant follicles (79.4 +/- 14.6 nmol/L) had little effect on estradiol production. In contrast, 5 alpha-androstane-3, 17-dione levels in PCOS FF (581.6 +/- 62.9 nmol/L) inhibited estradiol production by 75%. These data support the hypothesis that PCOS FF contains one or more endogenous inhibitors of aromatase activity and suggest that abnormally high 5 alpha-androstane-3, 17-dione levels in PCOS FF may be an important inhibitor of estradiol production.

Adolescent↗

PubMed1997

Inappropriate gonadotropin secretion in polycystic ovary syndrome: influence of adiposity.

In recent years, there has been uncertainty concerning the association of inappropriate gonadotropin secretion (high LH and normal FSH) and the polycystic ovary syndrome (PCOS). In the present study, we ascertained the influence of body composition on LH pulsatile parameters in 33 PCOS and 32 normal cycling (NC) women across a wide range of body mass index (BMI, 19-42 kg/m2). Twenty four-hour pulsatile parameters for serum LH (10-min sampling) and pituitary gonadotropin responses to i.v. bolus GnRH (10 micrograms) were evaluated. Fasting (0800 h) FSH and steroid hormone concentrations and 24-h mean insulin levels were determined. Insulin sensitivity (SI) was assessed by rapid i.v. glucose tolerance test in a subset of 28 PCOS and 29 NC subjects. Our results showed that BMI, an indicator of relative adiposity, had a significant negative impact on 24-h mean LH pulse amplitude (r = -0.63, P < 0.001) and the peak increment of LH in response to GnRH stimulation (r = -0.41; P = 0.02) for PCOS but not NC women. In contrast, 24-h LH pulse frequency was uniformly increased (40%) in PCOS as compared with NC women independent of BMI. In PCOS women, the blunting of pulse amplitude with increasing BMI resulted in a decline in 24-h mean LH levels (r = -0.63, P < 0.001) and the ratio of LH/FSH (r = -0.44, P = 0.02) not seen in NC. With BMI < 30 kg/m2, 24-h mean LH values for PCOS women were greater than the normal range for NC in 95% (18/19) of cases, whereas 24-h LH levels failed to discriminate PCOS from NC women in 43% (6/14) of obese (BMI > 30 kg/m2) PCOS women. Thus, the diagnostic value of LH determinations is retained for PCOS women with BMI < 30 kg/m2. For screening purposes, the mean of two LH values in samples collected at 30-min intervals was found to have a discriminatory power equal to that of the 24-h mean. These findings suggest that 1) BMI negatively influences LH pulse amplitude in PCOS women principally by an effect at the pituitary level; 2) accelerated LH pulse frequency in PCOS women is not influenced by BMI and represents a basic component of hypothalamic dysfunction in PCOS women; and 3) BMI does not influence gonadotropin secretion in normal cycling women. Thus assessments of basal LH levels and the LH/FSH ratio in hyperandrogenic anovulatory women are clinically meaningful when BMI is taken into account. Investigations to define the factor(s) that link adiposity and the attenuation of LH pulse amplitude in PCOS women would add further understanding of this complex neuroendocrine-metabolic disorder.

17-alpha-Hydroxyprogesterone↗

PubMed2006

Glucose intolerance in Japanese patients with polycystic ovary syndrome.

BACKGROUND: Hyperinsulinemia, which is related to obesity, played a pathogenic role in polycystic ovary syndrome (PCOS). However, the incidence of obesity in Japanese women with PCOS is different from that reported in patients with PCOS in Europe and USA. We should determine if insulin resistance occurs in Japanese PCOS. The purpose of this study is to assess the presence of insulin resistance in Japanese PCOS, while also considering obesity as a factor. METHODS: We divided the patients with polycystic ovary (PCO) into three groups based on body mass index and levels of gonadotropin. Nine obese PCOS, 34 normal body-weighted PCOS (luteinizing hormone (LH)/follicle stimulating hormone (FSH) >1.0) and 11 normal LH (LH/FSH </= 1.0), normal body-weighted PCO were studied. We compared those patients to 16 control subjects with normal ovulation or with hypothalamic anovulation. Eleven women in the control were normal body-weighted and five were obese. Patients were given an oral glucose tolerance test. Testosterone, plasma glucose and serum immunoreactive insulin after oral administration of 75 g dextrose were studied. We also compared glucose-intolerance [total plasma glucose (SigmaPG) and insulin (SigmaIRI), insulinogenic index (I.I.), fasting plasma glucose/immunoreactive insulin (FPG/IRI), homeostasis model assessment of insulin resistance (HOMA-R)] and testosterone among these groups. RESULTS: There were no differences in SigmaPG, SigmaIRI, I.I., FPG/IRI or HOMA-R between PCOS and controls. However, there were significant differences in SigmaPG, SigmaIRI, FPG/IRI and HOMA-R between obese and normal body-weighted patients. Similarly, there were no differences in SigmaPG, SigmaIRI, I.I., FPG/IRI or HOMA-R between PCOS and controls in the normal body-weighted group. However, there were significant differences in SigmaPG, SigmaIRI, FPG/IRI and HOMA-R between the obese and the normal body-weighted PCOS. There were also significant differences in SigmaPG and I.I. between LH-dominant, normal body-weighted PCOS and normal LH PCO. CONCLUSION: Japanese PCOS might have insulin-resistance but the factor of obesity had a stronger effect on insulin-resistance than did the existence of PCOS. The possibility of a different type of glucose-intolerance was suggested in the patients with ultrasonographical PCO in whom gonadotropin secretion was abnormal.

Adolescent↗

PubMed2000

Definition of polycystic ovary syndrome.

This article aims to answer two questions in defining polycystic ovary syndrome (PCOS): what is PCOS and how should the syndrome be recognized in clinical practice? Whether PCOS is a primary or a secondary ovarian disease remains controversial. It has been suggested for many years that the main pathophysiological factor in PCOS is dysregulation of the relationship between the hypothalamus, the pituitary and the ovary. However, PCOS also involves intraovarian morphological and functional abnormalities. With respect to clinical practice, many reports have questioned the sensitivity as well as the specificity of a high LH concentration. Similarly, the biological hyperandrogenism of PCOS cannot define the syndrome. GnRH agonist or hCG tests are not convenient for the diagnosis of PCOS in practice. Stromal hyperplasia is considered to be indicative of PCOS but it is highly dependent on the settings of the ultrasound machine, thus use of the total ovarian area, the upper normal limit of which is 5.5 cm(2), is recommended. The need for diagnostic markers of PCOS depends on the clinical presentation. In the full-blown syndrome (classic PCOS), the clinical symptoms provide the most powerful indication and the association of the three components (hyperandrogenism, anovulatory dysfunction and metabolic abnormalities) has a strong diagnostic potency. In non-classic PCOS, a cost-effective and safe work-up should be applied, which includes ultrasonography and hormonal assays (basal serum concentrations of testosterone, sex hormone binding globulin, 17-hydroxyprogesterone, LH, FSH and prolactin). Asymptomatic PCOS may be discovered incidentally during ultrasonography, and it is important to take this finding into account when designing an ovulation induction protocol. In most cases of PCOS, the diagnosis may remain presumptive providing other diagnoses have been ruled out and the follow-up does not disclose any atypical development of the condition.

Journal Article↗

PubMed2001

Polycystic ovarian syndrome and the risk of spontaneous abortion following assisted reproductive technology treatment.

BACKGROUND: A high proportion of infertile patients have polycystic ovarian syndrome (PCOS) with a reportedly greater risk of spontaneous abortion. Because of the close link between PCOS and obesity and the independent association of obesity with poor pregnancy outcomes, it is important to distinguish the possible confounding effect of body mass index (BMI) or other variables from that of PCOS. This study aims to determine the effect of PCOS status on the risk of spontaneous abortion with adjustment for body mass and several other confounding factors in a large cohort of pregnant infertile women. METHODS: The patients (n = 1018) were treated in a tertiary infertility centre. Their PCOS status was determined by standard criteria and their BMI had been taken less than 1 year before the pregnancy. Patients whose PCOS status or BMI measurements were not assessed were excluded. Student's t-test or chi2 test were used to test the difference between the PCOS and non-PCOS groups while a multivariate logistical regression model was used to assess the effect of PCOS, BMI and other confounding factors. RESULTS: Overall, the incidence of PCOS was 37% in this cohort. The overall incidence of spontaneous abortion in the study population was 21%. Univariate analysis showed that women with PCOS had a significantly greater risk of spontaneous abortion compared with non-PCOS women (25 versus 18%, P < 0.01). However, using multivariate logistic regression analysis this effect was reduced to a non-significant level [odds ratio (OR) = 1.10, 95% confidence interval (CI) 0.85-1.36] after adjusting for obesity and patients/treatment combination factor, and to nil after adjusting for all confounding factors considered in this study (OR = 0.98, 95% CI 0.75-1.28). CONCLUSION: The results of this study suggest that the higher risk of spontaneous abortion observed in women with PCOS is likely to be due to their high prevalence of obesity and the type of treatment they receive.

Abortion, Spontaneous↗

PubMed1992

The significance of a single serum LH measurement in women with cycle disturbances: discrepancies between immunoreactive and bioactive hormone estimates.

OBJECTIVE: We evaluated the significance of single serum LH estimates (as assessed by radiometric assay (IRMA) and Leydig cell in-vitro bioassay (BIO)) for the diagnosis of polycystic ovary syndrome (PCOS) in women with infertility and cycle abnormalities. DESIGN: Hormonal and clinical comparisons between subgroups were made based on classification according to (a) rigid clinical and endocrine (excluding LH) characteristics of PCOS, (b) elevated IRMA-LH concentrations, (c) BIO-LH levels. In addition, androgen modulation of LH biopotency was studied in these patients. PATIENTS: Ninety-nine women presenting at our infertility Unit with oligo/amenorrhoea. MEASUREMENTS AND RESULTS: Of the total study group, 35 women were diagnosed positive as PCOS and 42 showed elevated IRMA-LH levels. Only 51% (n = 18) of PCOS patients showed elevated IRMA-LH levels, and in PCOS significantly higher levels of BIO-LH, androstenedione, oestrone, and BIO/IRMA-LH ratios were found as compared to non-PCOS patients. In the group with elevated IRMA-LH only 43% (n = 18) of subjects were diagnosed as PCOS, and no difference in BIO/IRMA-LH ratios was found. With increasing BIO-LH levels the probability of PCOS rises sharply (P < 0.001), whereas this probability is of only marginal significance (P < 0.06) for IRMA-LH. In the total study group a correlation is observed between serum testosterone (T) levels and IRMA-LH (r = 0.47), and BIO-LH (r = 0.51) concentrations. This correlation is absent comparing serum T and BIO/IRMA-LH ratios (r = 0.15). CONCLUSIONS: Results presented in this study indicate that (1) women with infertility and oligo/amenorrhoea classified based on signs of PCOS or IRMA-LH levels, exhibit different clinical and endocrine characteristics, (2) only 51% of PCOS women exhibit elevated IRMA-LH concentrations, and only 43% of women with elevated IRMA-LH were diagnosed as PCOS, (3) IRMA-LH levels are a poor predictor of PCOS, whereas the predictive value of BIO-LH is better, (4) elevated BIO/IRMA-LH ratios in PCOS are dependent on alterations in BIO-LH, rather than IRMA-LH concentrations, and (5) no correlation was observed between serum T levels and BIO/IRMA-LH ratios.

Adult↗

PubMed1995

Insulin secretory defects in polycystic ovary syndrome. Relationship to insulin sensitivity and family history of non-insulin-dependent diabetes mellitus.

The increased prevalence of non-insulin-dependent diabetes mellitus (NIDDM) among women with polycystic ovary syndrome (PCOS) has been ascribed to the insulin resistance characteristic of PCOS. This study was undertaken to determine the role of defects in insulin secretion as well as familial factors to the predisposition to NIDDM seen in PCOS. We studied three groups of women: PCOS with a family history of NIDDM (PCOS FHx POS; n = 11), PCOS without a family history of NIDDM (PCOS FHx NEG; n = 13), and women without PCOS who have a family history of NIDDM (NON-PCOS FHx POS; n = 8). Beta cell function was evaluated during a frequently sampled intravenous glucose tolerance test, by a low dose graded glucose infusion, and by the ability of the beta cell to be entrained by an oscillatory glucose infusion. PCOS FHx POS women were significantly less likely to demonstrate appropriate beta cell compensation for the degree of insulin resistance. The ability of the beta cell to entrain, as judged by the spectral power for insulin secretion rate, was significantly reduced in PCOS FHx POS subjects. In conclusion, a history of NIDDM in a first-degree relative appears to define a subset of PCOS subjects with a greater prevalence of insulin secretory defects. The risk of developing NIDDM imparted by insulin resistance in PCOS may be enhanced by these defects in insulin secretion.

Adult↗

PubMed2005

Polycystic ovaries are common in women with hyperandrogenic chronic anovulation but do not predict metabolic or reproductive phenotype.

Polycystic ovary syndrome (PCOS) is a heterogeneous disorder of unexplained hyperandrogenic chronic anovulation. Experts have recommended including the morphology and volume of the ovary in the diagnostic criteria for PCOS. We performed this study to determine whether there was an association between the morphology and size of the ovaries and markers of insulin sensitivity as determined by dynamic testing within women with PCOS or compared with a group of control women. We then examined reproductive parameters. We studied 88 unrelated PCOS women and 21 control women, aged 17-45 yr. All were in the early follicular phase or its equivalent (no follicle with > 10 mm diameter and anovulatory serum progesterone level < 3 ng/ml). Subjects underwent on the same day a phlebotomy for baseline hormones, a 2-h oral glucose tolerance test, and transvaginal ultrasound to determine the morphology and volume of the ovaries. Ninety-five percent (84 of 88) of women with PCOS and 48% (10 of 21) of the control women had polycystic ovaries using the criteria of at least one ovary greater than 10 cm3 (PCOV) and/or polycystic ovary morphology (PCOM) using the criteria of 10 or more peripheral follicular cysts 8 mm in diameter or less in one plane along with increased central ovarian stroma. PCOM was a better discriminator than PCOV between PCOS and control women. The odds of women with PCOS having PCOM were elevated 50-fold compared with controls (odds ratio, 50; 95% confidence interval, 10-240; P < 0.0001), whereas the odds of PCOV were elevated 5-fold in women with PCOS (odds ratio, 4.6; 95% confidence interval, 1.7-12.6; P = 0.003). Neither the insulin sensitivity index, fasting or 2-h values, or any integrated measures of glucose and insulin varied in women according to either morphology or volume, nor was there an association with circulating androgen levels. Women with PCOS and PCOM had lower FSH levels than women with PCOS and non-PCOM. Women with PCOS and PCOV had a higher LH to FSH ratio than women without PCOV and PCOS. These data support the hypothesis that polycystic ovaries are an abnormal finding. However, neither the morphology nor the volume of the ovaries is associated with distinctive metabolic or reproductive phenotypes in women with PCOS.

Adolescent↗