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PubMed1996

Role of progesterone deficiency in the development of luteinizing hormone and androgen abnormalities in polycystic ovary syndrome.

The aetiology of polycystic ovary syndrome (PCOS) is unknown. It is uniquely characterized by oligomenorrhoea or amenorrhoea associated with normal or high oestrogen levels. This prospective clinical study was designed to examine the possible role of the lack of cyclical exposure to progesterone in the development of gonadotrophin and androgen abnormalities in PCOS. Gonadotrophin, androgen and oestrogen levels were measured in 15 PCOS patients and 10 normal subjects untreated and following treatment with the progestogen medroxyprogesterone acetate (MPA). When compared to control subjects, PCOS patients had significantly higher luteinizing hormone (LH) pulse height, pulse amplitude, integrated LH levels, LH response to gonadotrophin-releasing hormone (GnRH) and LH/FSH ratio; LH pulse frequency was similar in the two groups. In addition, the testosterone/sex hormone binding globulin ratio (T/SHBG), androstenedione and oestrone concentrations in the plasma were significantly higher in PCOS than in control subjects. When PCOS patients were treated with MPA for 5 days, there were significant decreases (p < 0.02-0.001) to values no longer different from normal: from 8.7 +/- 1.2 to 5.6 +/- 0.8 IU/l for integrated LH levels (untreated and MPA-treated PCOS); from 31.2 +/- 3.5 to 12.9 +/- 1.5 IU/l for LH response to GnRH; from 2.4 +/- 0.26 to 1.3 +/- 0.2 for LH/FSH ratio; and from 10.4 +/- 0.63 to 8.5 +/- 0.7 nmol/l for androstenedione. Significant decreases (p < 0.05-0.005) to values that still remained significantly higher than in normal subjects occurred for: LH pulse height, 11.05 +/- 1.3 to 6.88 +/- 0.79 IU/l (untreated and MPA-treated PCOS); LH pulse amplitude, 2.8 +/- 0.5 to 1.8 +/- 0.2 IU/l; total testosterone, 2.5 +/- 0.2 to 2.0 +/- 0.2 nmol/l; T/SHBG ratio, 14.1 +/- 1.7 to 11 +/- 1.5; and oestrone, 265 +/- 24 to 208 +/- 29 pmol/l. These results are consistent with the concept that ovulation failure and progesterone deficiency play a facilitatory role in the development of the hypothalamic-pituitary abnormality giving rise to disordered LH secretion in PCOS.

Androgens↗

PubMed2005

Evidence for altered adipocyte function in polycystic ovary syndrome.

BACKGROUND: Adipocytokines are produced by adipose tissue and have been thought to be related to insulin resistance and other health consequences. We measured leptin, adiponectin, and resistin simultaneously in women with polycystic ovary syndrome (PCOS) and age- and weight-matched controls. Our hypothesis was that these simultaneous measurements would help determine whether adipocytokine secretion is abnormal in PCOS independent of body mass and whether these levels are related to insulin resistance as well as other hormonal changes. METHODS: Fifty-two women with PCOS and 45 normal ovulatory women who were age- and weight-matched were studied. Blood was obtained for adipocytokines (leptin, adiponectin, and resistin) as well as hormonal parameters and markers of insulin resistance as assessed by the quantitative insulin-sensitivity check index. Body mass index (BMI) was stratified into obese, overweight, and normal subgroups for comparisons between PCOS and controls. RESULTS: Adiponectin was lower (P < 0.05) and resistin was higher (P < 0.05) while leptin was similar to matched controls. Breakdown of the groups into subgroups showed a strong body mass relationship for leptin with no changes in resistin although adiponectin was lower in PCOS, even controlling for BMI. In controls, leptin and adiponectin and leptin and resistin correlated (P < 0.05) but not in PCOS. In controls, all adipocytokines correlated with markers of insulin resistance but not in PCOS. CONCLUSIONS: When matched for BMI status, decreased adiponectin in PCOS represent the most marked change. This alteration may be the result of altered adipose tissue distribution and function in PCOS but no correlation with insulin resistance was found.

Adipocytes↗

PubMed2006

Association of dehydroepiandrosterone-sulfate with endothelial function in young women with polycystic ovary syndrome.

OBJECTIVE: The aim of this study was to assess non-invasively endothelial function of young women with polycystic ovary syndrome (PCOS) in comparison with healthy age-matched women and a group of young women with idiopathic hirsutism (IH). The possible role of metabolic and hormonal parameters on endothelial function was also examined. DESIGN: Descriptive clinical trial. METHODS: Fifty-six women, 27 with PCOS, 16 with IH and 13 healthy age-matched women were studied. Endothelial function of resistance arteries was assessed by venous occlusion plethysmography. Metabolic and hormonal parameters were estimated in this study population. RESULTS: The duration of reactive hyperemia (durRH) was shorter in PCOS group when compared with normal controls (63.75 +/- 13.33 s vs 113.18 +/- 20.92 s, P = 0.036). A similar finding was observed when PCOS were compared with IH group (63.75 +/- 13.33 s vs 105 +/- 17.20 s, P = 0.05). The durRH did not differ between IH and control group (105 +/- 17.20 s vs 113.18 +/- 20.92 s, ns). A significant positive linear correlation was found between the durRH and dehydroepiandrosterone-sulfate (DHEA-S) levels (r = +0.48, P = 0.04) in the PCOS group. The basal insulin resistance index (HOMA) differed significantly between PCOS, IH and control groups. There was no significant correlation between durRH and HOMA index or testosterone levels in the PCOS group. CONCLUSIONS: Endothelial dysfunction may be an early sign of cardiovascular system abnormalities in young PCOS women. It is possible that increased DHEA-S levels may offer a cardioprotective advantage that attenuates the effects of cardiovascular risk factors that accompany PCOS.

Adult↗

PubMed2006

[Polycystic ovary syndrome associated neoplasms].

Polycystic ovary syndrome (PCOS) is the most common endocrine disease in women on reproductive age. PCOS is characterized by the presence of anovulation, infertility and hyperandrogenism and is associated with obesity and insulin resistance. A major risk for neoplasms of the reproductive tract, like endometrial, breast and ovary cancer seems to be related to PCOS. While several studies have shown an increased risk for endometrial hyperplasia and cancer in PCOS patients, the variability of the selection criteria for PCOS has been recognized as a potential bias for these data. PCOS women also present clinical characteristics that are related to risk factors for breast cancer and some epidemiological evidences have been described on this issue. However, until now, a clear association between the presence of PCOS and breast carcinoma has yet not been found. Finally, high local steroid and growth factor concentrations are considered risk factors for ovary carcinoma, and are frequently observed in PCOS women. In turn, few studies have addressed the possibility of a link between PCOS and ovarian cancer and the results are conflicting but suggest that this association is unlikely.

Breast Neoplasms↗

PubMed2004

Positive correlation of serum leptin with estradiol levels in patients with polycystic ovary syndrome.

Patients with polycystic ovary syndrome (PCOS) usually are obese, insulin resistant and hyperinsulinemic. The known association between leptin, obesity and insulin action suggests that leptin may have a role in PCOS but this has only been addressed peripherally. This study was designed to assess the relationship between serum leptin and the anthropometric, metabolic and endocrine variables of obese (body mass index, BMI (3)30 kg/m(2)) and non-obese (BMI <30 kg/m(2)) PCOS patients. Twenty-eight PCOS patients and 24 control women subdivided into obese and non-obese groups were evaluated. Leptin, androgens, lipids, gonadotrophins and insulin-glucose response to the oral glucose tolerance test were measured by radioimmunoassay in all participants. The assays were done all in one time. The areas under the insulin curve (AUC-I) and the glycemia curve were calculated to identify patients with insulin resistance. Mean leptin levels were not significantly higher in patients with PCOS compared to the control group (21.2 +/- 10.2 vs 27.3 +/- 12.4 ng/ml). Leptin levels were found to be significantly higher in the obese subgroups both in patients with PCOS (26.9 +/- 9.3 vs 14.1 +/- 7.0 ng/ml) and in the control group (37.3 +/- 15.5 vs 12.9 +/- 5.8 ng/ml). The leptin of the PCOS group was correlated with BMI (r = 0.74; P < 0.0001) and estradiol (r = 0.48; P < 0.008) and tended to be correlated with the AUC-I (r = 0.36; P = 0.05). Of the parameters which showed a correlation with leptin in PCOS, only estradiol and probably insulinemia (AUC-I) did not show a significant correlation with BMI, suggesting that the other parameters were correlated with leptin due to their correlation with BMI. Estradiol correlated with leptin in PCOS patients regardless of their weight.

Adolescent↗

PubMed2006

In vitro evidence that hyperglycemia stimulates tumor necrosis factor-alpha release in obese women with polycystic ovary syndrome.

Women with polycystic ovary syndrome (PCOS) are often insulin resistant and have chronic low-level inflammation. The purpose of this study was to determine the effects of hyperglycemia in vitro on tumor necrosis factor (TNF)-alpha release from mononuclear cells (MNC) in PCOS. Twelve reproductive-age women with PCOS (six lean, six obese) and 12 age-matched controls (six lean, six obese) were studied. Insulin sensitivity (IS(HOMA)) was estimated from fasting levels of glucose and insulin and percent truncal fat was determined by dual energy absorptiometry (DEXA). TNFalpha release was measured from MNC cultured under euglycemic and hyperglycemic conditions. IS(HOMA) was higher in obese women with PCOS than in lean women with PCOS (student's t-test; 73.7 +/- 14.8 vs 43.1 +/- 8.6, P < 0.05), but similar to that of obese controls. IS(HOMA) was positively correlated with percent truncal fat (r=0.57, P < 0.04). Obese women with PCOS exhibited an increase in the percent change in TNFalpha release from MNC in response to hyperglycemia compared with obese controls (10 mM, 649 +/- 208% vs 133 +/- 30%, P < 0.003; 15 mM, 799 +/- 347% vs 183 +/- 59%, P < 0.04). The TNFalpha response directly correlated with percent truncal fat (r=0.45, P < 0.03) and IS(HOMA) (r=0.40, P < 0.05) for the combined groups, and with plasma testosterone (r=0.60, P < 0.05) for women with PCOS. MNC of obese women with PCOS exhibit an increased TNFalpha response to in vitro physiologic hyperglycemia. MNC-derived TNFalpha release may contribute to insulin resistance and hyperandrogenism, particularly when the combination of PCOS and increased adiposity is present.

Abdominal Fat↗

PubMed2026

Exploring the Genetic Link between Irritable Bowel Syndrome and Polycystic Ovary Syndrome: Bidirectional Mendelian Randomization and Machine Learning Approaches.

BACKGROUND: Research has shown a certain correlation between polycystic ovary syndrome (PCOS) and irritable bowel syndrome (IBS). The study aims to determine the directionality and underlying biological processes influencing the relationship between these two disorders. METHODS: We explored the causal relationship between IBS and PCOS by conducting a comprehensive bidirectional Mendelian randomization (MR) analysis using five different methods and conducted robustness assessments. We extracted differentially expressed genes from the IBS and PCOS datasets for Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) enrichment analysis. Additionally, we developed a protein-protein interaction (PPI) network and applied the Least Absolute Shrinkage and Selection Operator (LASSO) and Support Vector Machine (SVM) methodologies to pinpoint key diagnostic markers. Diagnostic efficacy was further assessed through Receiver Operating Characteristic (ROC) curve analysis for selected genes. Finally, single-sample gene set enrichment analysis (ssGSEA) was carried out to examine immune cell infiltration in IBS and PCOS. RESULTS: MR analysis identified a causal effect of PCOS on IBS (IVW, OR = 1.034, 95% CI: 1.003-1.065, P = 0.029). Conversely, no relationship between IBS and PCOS was observed in the reverse analysis. Furthermore, integrative bioinformatics and machine learning analyses identified CD14 and CASP1 as key diagnostic biomarkers for both IBS and PCOS, which were significantly associated with immune cell infiltration. CONCLUSION: MR analysis has demonstrated a significant positive causal relationship between PCOS and IBS, though the reverse causality from IBS to PCOS appeared non-significant. The genes CD14 and CASP1 emerged as potential shared diagnostic markers between these two conditions.

Polycystic Ovary Syndrome↗

PubMed2000

Sonographic parameters and hormonal status in lean and obese women with polycystic ovary syndrome.

A total of 34 patients with the diagnosis of polycystic ovary syndrome (PCOS) were recruited for this study. Weight distribution in lean PCOS women (n = 17) was 93.5% to 110.5% of normal weight for height and age. In obese women (n = 17) this distribution was 119.5 to 146.5%. Serum testosterone (T), dehydroepiandrosterone sulfate (DHEA-S), delta 4-androstendione (delta 4-A), sex hormone binding globulin, (SHBG), 17-hydroxyprogesterone (17-OH PRG), 17b oestradiol (17b-E2), cortisol (CORT), follicle stimulating hormone (FSH), luteinizing hormone (LH), prolactin (PRL) and insulin (INS) were measured. Serum SHBG levels were lower in obese PCOS women (72.9 +/- 16.2 nmol/l) than in lean PCOS women (99.6 +/- 10.5) (p < 0.001). Fasting insulin levels were higher in obese PCOS women (30.4 +/- 4.5 mUI/ml) than in lean PCOS women (14.2 +/- 7.6 mUI/ml) (p < 0.001). Mean ovarian volume did not differ significantly between lean and obese PCOS women (12.5 +/- 3.7 ml vs 16.1 +/- 5.3, p > 0.5). Endometrial thickness was roughly similar between the two groups. Endometrial surface area in lean PCOS women (7.6 +/- 2.2 cm2) was lower than in obese PCOS women (10.1 +/- 1.9 cm2) and the difference was significant (p < 0.01).

Adolescent↗

PubMed2003

[Association study between a polymorphism of aldosterone synthetase gene and the pathogenesis of polycystic ovary syndrome].

OBJECTIVE: To investigate the relationship between -344T polymorphism in aldosterone synthetase (CYP11B2) gene promoter region and the pathogenesis of polycystic ovary syndrome (PCOS). METHODS: Ninety two patients with PCOS and controls were genotyped according to the fragment length (273 bp and or 202 bp) of CYP11B2 gene promoter by the technique of polymerase chain reaction-restriction fragment length polymorphism. The levels of luteinizing hormone, follicular stimulating hormone, estrodiol, progesterone, prolactin, testosterone, plasma renin activity (PRA), plasma angiotensin II (PANG II) and aldosterone in the basal state were also determined. Different genotypes between PCOS were compared about their levels of PRA, PANG II, aldosterone and testosterone. RESULTS: (1) The C allele frequencies of CYP11B2 gene in control and PCOS was 22% and 36%, respectively. (2) The frequency of variants (TC, CC) of CYP11B2 gene -344T polymorphism site in PCOS (57%) was significantly higher than that of control subjects (37%). (3) The level of PRA, PANG II, aldosterone, testosterone were all significantly higher in the genotype of -344CC than in that of -344TT in PCOS and normal women (P < 0.01). CONCLUSIONS: (1) The variants (T-->C) of -344T polymorphism site of CYP11B2 gene predisposes increased risk of PCOS. (2) The genotype of -344CC, -344TC may be susceptible genotype of PCOS and has related to the enhanced functional activity of ovarian renin angiotensin system in PCOS.

Adult↗

PubMed2003

Absence of profound hyperinsulinism in polycystic ovary syndrome is associated with subtle elevations in the plasminogen activator inhibitor system.

In order to describe potential hypofibrinolytic tendencies in young (< 35 years) polycystic ovary syndrome (PCOS) patients, we studied plasminogen activator inhibitor (PAI-1) system components in women without laboratory evidence of hyperinsulinism or hyperandrogenism. The study was a prospective, observational comparison and took place in a major urban infertility referral center. Age, body mass index, ovulatory status, selected androgen levels, fasting insulin and plasma lipids were measured in subjects with PCOS (n = 39) and normal control subjects (n = 20). Women with PCOS had higher mean serum total testosterone and androstenedione levels compared with controls (56.4 versus 40.3 ng/dl, p = 0.03, and 179 versus 133 microg/ml, p = 0.03, respectively). Mean fasting insulin levels were higher among PCOS women (p < 0.01) and were strongly correlated with PAI-1 antigen (Ag) (r = 0.46), PAI-1 activity (r = 0.43), and tissue plasminogen activator (t-PA) (r = 0.5). Correlations were evident in both PCOS and control subjects. Mean PAI-1 Ag, PAI-1 activity, and t-PA levels were significantly elevated (p = 0.003, 0.001, and 0.001, respectively) in PCOS. ANOVA was performed to control for insulin effect; a trend toward elevated PAI-1 in PCOS persisted but was no longer statistically significant (p = 0.24). PAI-1 activity elevation remained in PCOS women with mean fasting insulin levels < 10 mIU/ml (p = 0.02), yet the difference became less significant when insulin was controlled (p = 0.38). Although these data confirm known associations between insulin and PAI-1 derangements, this is the first study to quantify discrete PAI-1 elevations that persist in the setting of PCOS even with normal or low ambient insulin levels. Additional prospective studies are needed to determine whether this altered PAI-1 state is associated with a clinically important hypofibrinolytic condition and subsequent poor reproductive outcome.

Adult↗

PubMed2003

Obesity is the major factor determining an insulin sensitivity and androgen production in women with anovulary cycles.

Aim of this study was to test the hypothesis that obesity promotes the insulin-sensitivity and ovarian hyperandrogenism in anovulating women independently of the polycystic ovary syndrome (PCOS). We examined 80 women of reproductive age (19-38 years, mean 28.5 +/- 0.6 years) with anovulary cycles. 45 subjects had PCOS and 35 had chronic anovulation without hormonal and ultrasound criteria of PCOS. The control group consisted of 12 healthy females with normal ovulary menstrual cycle (age 26.4 +/- 0.6 years). We evaluated plasma insulin level baselines (I0); 120 min after oral administration of 75g of glucose (I120), we examined FSH, LH, prolactin, testosterone, 17 OH progesterone and DHEAS and calculated indexes of insulin sensitivity, i.e. FIRI and G/I. Women with anovulary cycles yielded a significant increase in I0 (p < 0.01), I120 (p < 0.01), FIRI (p < 0.01), FSH, LH (both p < 0.05) and testosterone (p < 0.01), and a significantly decrease in G/I (p < 0.01) in comparison to controls with normal weight. There was a significant correlation between BMI and insulin levels, BMI and FIRI, and between WHR or waist circumference and FIRI, or G/I. The highest levels of insulinemia and the highest degree of insulin resistance were found in obese women (BMI > 30 kg/m2). In the group of obese anovulating women we found a positive correlation between I0 and testosterone (p < 0.01). In PCOS group, we found a negative correlation between I0 and LH (p < 0.01), and FIRI and LH (p < 0.01). In the group of obese PCOS women there were significantly higher levels of plasma insulin, and lower insulin sensitivity as compared to lean PCOS patients. However, lean PCOS women were more hyperinsulinemic and insulin resistant than the control group of lean women. Our results indicate, that obesity is the important factor determinating the insulin sensitivity and hyperinsulinemia in PCOS women. Moreover, the body weight is the major determinant of insulinemia, insulin sensitivity and ovarian hyperandrogenism, independently of PCOS. (Tab. 5, Fig. 4, Ref. 23.).

Adult↗

PubMed2005

[Expression of leptin mRNA in luteinized granulosa cells and leptin levels in serum and follicular fluid of non-obese infertile patients with polycystic ovary syndrome].

OBJECTIVE: To investigate the expression of leptin mRNA in luteinized granulose cells and the leptin level in serum and follicular fluid of non-obese patients with polycystic ovary syndrome (PCOS). METHODS: Granulosa cells were collected from the puncture fluid of follicle of 16 obese infertile patients with PCOS to undergo external fertilization. Fasting venous blood was collected while collecting the ova. RT-PCR was used to detect the expression of leptin mRNA in the granulosa cells. ELISA was used to detect the leptin level in the serum and follicular fluid. Twenty normal women undergoing external fertilization because of male infertility of their husbands were used as controls. RESULTS: The expression of leptin mRNA (A value) was 1.5 +/- 0.4 in the obese infertile patients with PCOS and was 1.8 +/- 0.6 (P > 0.05) in the controls. Both the leptin levels of serum and follicular fluid were not different between the obese infertile patients with PCOS and controls (both P > 0.05). The leptin level in follicular fluid was significantly correlated with both the serum leptin level in the obese infertile patients with PCOS (r(s) = 0.838, P = 0.000) and the control group (r(s) = 0.712, P = 0.000). The expression level of leptin mRNA in the luteinized was not correlated with the leptin level of follicular fluid in both the obese infertile patients with PCOS and the control group (both P > 0.05). The fertility rate was not different between the obese infertile patients with PCOS (7/16) and the controls (9/24) (P = 0.693). CONCLUSION: The expression of leptin mRNA is normal in the follicular fluid of the obese infertile patients with PCOS. The leptin levels in serum and follicular fluid of the obese infertile patients with PCOS are similar to those of normal women. The leptin level in follicular fluid depends mainly on the circulating leptin level.

Adult↗

PubMed2005

[Expression of insulin receptor substrate 1 and phosphorylation of tyrosine in adipose tissue of polycystic ovary syndrome].

OBJECTIVE: To study expression of insulin receptor substrate 1 (IRS-1) and phosphorylation of tyrosine in adipose tissue of polycystic ovary syndrome (PCOS) to approach the mechanism of insulin resistance (IR) in PCOS at tissue and cellular level. METHODS: IRS-1 expression and tyrosine phosphorylation of adipose tissue were studied with immunoprecipitation, Western-blot and ECL immunoblotting. RESULTS: The differences of IRS-1 expression in adipose tissue among the obese PCOS group (82 +/- 15)%, the non-obese PCOS group (79 +/- 18)%, the obese control group (75 +/- 19)% and the non obese control group (70 +/- 19)% were not significant (P > 0.05). IRS-1 tyrosine phosphorylation in adipose tissue in the obese PCOS group [(52 +/- 23)%, P < 0.001], the obese control group [(45 +/- 22)%, P < 0.01] and non-obese PCOS group [(70 +/- 25)%, P < 0.05] were markedly lower than that in the non-obese control group (88 +/- 12)%. The obese control group had more reduction than non-obese control group (P < 0.05). The differences between the obese PCOS group and the obese control group or the two PCOS groups were not significant (P > 0.05). CONCLUSION: IRS-1 tyrosine phosphorylation in adipose tissue in the two PCOS groups decreased markedly than in the non-obese control group. It might be involved in the disorder of insulin-signaling transduction downstream of insulin receptor and the occurrence of IR.

Adipose Tissue↗

PubMed2005

[Polymorphism in insulin receptor gene exon 17 in women with polycystic ovary syndrome].

OBJECTIVE: To investigate insulin receptor (INSR) genotype exon 17 frequencies in women with polycystic ovary syndrome (PCOS) and to elucidate its role in the pathogenesis of PCOS. METHODS: The study involved 33 women with PCOS and 28 healthy control women who were genotyped for polymorphism of INSR gene exon 17 by single strand conformation polymorphism (SSCP) analysis. Body mass index (BMI), insulin sensitive index (ISI), the expression of INSR beta subunit, and serum concentration of luteinizing hormone (LH), total testosterone between the genotypes were compared. RESULTS: (1) The T-to-C mutation was observed in the INSR gene exon 17 (1008 bp). The frequency of the C/C genotype was significantly higher in patients (39%) than in the controls (11%) (P < 0.05). There was no significant difference in the distribution of genotypes between obese PCOS and non-obese PCOS, and between PCOS with insulin resistance (IR) and PCOS without IR. (2) In comparison of mutation genotype groups with wild genotype (T/T), ISI was significantly decreased (C/C genotype, P < 0.01; C/T genotype, P < 0.05), and no significant difference was observed in the other indices. CONCLUSIONS: There is polymorphism in INSR gene exon 17 in patients with PCOS. This variant leads to increased risk of IR in women with PCOS. It does not influence the expression of INSR beta subunit.

Adult↗

PubMed2005

[Correlation between 4G and 5G genetypes distribution of plasminogen activator inhibitor-1 gene polymorphism in its promoter region with polycystic ovarian syndrome].

OBJECTIVE: To investigate the correlation of 4G and 5G genetypes distribution of plasminogen activator inhibitor-1 (PAI-1) gene polymorphism in its promoter region with polycystic ovary syndrome (PCOS). METHODS: In 101 Chinese PCOS patients and 42 women as control, 4G and 5G polymorphisms of PAI-1 gene were detected with PCR-restriction fragment length polymorphism (RFLP). Pregnant history, body mass index (BMI), waist-hip ratio (WHR) were collected and Homastasis Model Assessment score for insulin resistant (Homa-IR) and insulin sensitive index (ISI) in PCOS groups were calculated. RESULTS: The distributions of PAI-1 gene polymorphisms 4G type (4G/4G genetype) and 5G type (5G/5G, 4G/5G genetype) were different between the PCOS group and the control. The PCOS group had higher 4G type 57% (58/101) distribution than that of the control group 38% (16/42); 5G type is vise verse (P < 0.05). PCOS patients were divided into obese and non-obese sub-groups according to BMI. There were significant lower Homa-IR and higher ISI in non-obese subgroup than that in obese group (P < 0.05; P < 0.01). 68% (36/53) 4G type distribution in the non-obese is higher than that [48% (23/48)] in obese sub-group (P < 0.05). There were higher 4G type distribution 79% (11/14) and lower 5G type distribution 21% (3/14) in spontaneous miscarriage group than that of in non-spontaneous miscarriage group 38% (5/13) and 62% (8/13) among patients who impregnated at least once (n = 27, P < 0.05). CONCLUSION: PAI-1 gene polymorphism 4G genetype may be correlated with PCOS in Chinese women, especially in PCOS patients with non-obese PCOS and spontaneous miscarriage.

Blood Glucose↗

PubMed2006

The frequency of insulin resistance calculated upon the basis of a fasting glucose to insulin ratio and characteristics of insulin resistant women with polycystic ovary syndrome.

BACKGROUND: The Polycystic Ovary Syndrome (PCOS) is a common endocrine and metabolic disorder of women of reproductive age, characterized by hyperandrogenism and chronic anovulation. Peripheral insulin resistance (IR) has a crucial role in the pathogenesis of this disorder. A fasting glucose to insulin (G/I) ratio is a simple, reliable, sensitive and specific measurement of insulin sensitivity and is a useful test for the identification of IR in women with PCOS, who have to be treated with insulin sensitizers. OBJECTIVE: To calculate the frequency of IR among patients with PCOS, using the fasting G/I ratio, and to compare the clinical and biochemical parameters between insulin-resistant and insulin-sensitive groups. PATIENTS AND METHODS: The study comprised 62 patients of reproductive age (18-40) with PCOS. The diagnosis PCOS was determined according to the diagnostic criteria from Rotterdam 2003, i.e. the presence of two of the following three criteria: oligo-ovulation and/or anovulation; clinical and/or biochemical hyperandrogenism; and polycystic ovaries. All other states associated with hyperandrogenism had been previously excluded. An inclusion criterion for the study was the body mass index (BMI) >or=25 (kg/m2). After calculating the fasting glucose(mg/dl) / insulin(microU/ml) ratio, the patients were separated in two groups, i.e. an insulin-resistant group with a fasting G/I ratio of < 4.5(mg/10(-4) U) and an insulin-sensitive group with a fasting G/I ratio of >/=4.5(mg/10(-4) U). RESULTS: In our study, 58.06% of women with PCOS and BMI >or=25 (kg/m2) were insulin-resistant. There was no significant difference between the two groups in age or BMI. Sex hormone binding globulin (SHBG) levels were significantly lower in the insulin-resistant group (17.83 +/- 8.38 vs. 42.66 +/- 27.65 (nmol/l); p=0.0036) and they had a higher free testosterone index (19.38 +/- 8.91 vs. 9.55 +/-3.51(%); p=0.001) in comparison with the insulin-sensitive group. Progesterone levels were significantly lower in the IR group (2.41 +/- 2.50 vs. 7.05 +/- 8.04 (ng/ml); p=0.034). CONCLUSION: A fasting glucose to insulin ratio is a simple and useful test for identifying insulin-resistant obese women with PCOS. SHBG and progesterone (oligo-ovulation/anovulation) can be useful markers for long-term health risks in women with PCOS (diabetes mellitus type 2 and cardiovascular diseases). In this way we could identify the group of PCOS subjects and its subgroups, which would benefit from therapy with insulin sensitizers, with respect to the reduction of risks of chronic complications.

Adolescent↗

PubMed2006

[Peritoneal fluid leptin concentration and endocrine hormone in patients with polycystic ovarian syndrome].

OBJECTIVE: To determine whether the infertile patients with polycystic ovarian syndrome (PCOS) is related to dysregulation of peritoneal fluid and serum leptin concentration, and to investigate the relationship between the leptin and some endocrine hormones in PCOS. METHODS: Twenty subjects with PCOS and 20 control women were included in the study. Peritoneal fluid and serum concentration of leptin, insulin, insulin-antibody, testosterone (T), estrogen (E(2)), and progestogen (P) were measured by radioimmunoassay (RIA). RESULTS: Peritoneal fluid concentrations of leptin, insulin, T and insulin-antibody in PCOS patients were significantly higher than those of the control group (P<0.05). There was no statistically significant difference in peritoneal fluid E(2) and P between PCOS and the control group (P>0.05). The serum concentrations of leptin and T in PCOS were significantly higher than those of the control group (P<0.05), but the levels of insulin, E(2), P and insulin-antibody were not significantly different between the 2 groups (P>0.05). With the BMI> or =23 kg/m(2) subgroup in PCOS patients, the peritoneal fluid and serum concentrations of leptin, insulin and T were significantly higher than those of BMI 23 kg/m(2) subgroup (P<0.01). There was no significant difference in E(2)and insulin-antibody between the 2 subgroups (P>0.05). Pearson correlation analysis indicated that peritoneal fluid and serum leptin levels were positively correlated with BMI, insulin, T and insulin-antibody, but negatively correlated with E(2), with no significant correlation with P. Multiple stepwise regression analysis indicated that the factors that influenced the peritoneal fluid and serum leptin levels were BMI, insulin, T and E(2) ordinally. CONCLUSION: Peritoneal fluid and serum leptin concentration and insulin,T, Ins-antibody level are abnormal in PCOS patients. Leptin may play an important role in the pathogenesis of PCOS. BMI is the main factor to correlate with leptin.

Adult↗

PubMed2006

Significance of Doppler ultrasonography in the diagnosis of polycystic ovary syndrome.

OBJECTIVE: To investigate the importance of transvaginal color Doppler ultrasonography of uterine and intraovarian arteries in the clinical diagnosis of polycystic ovary syndrome (PCOS). MATERIAL & METHOD: This study was planned as a cohort, controlled, prospective study. A total of 80 participants (40 with PCOS and 40 as a control group) were enrolled in the study. A Doppler system with a 6.0 MHz transvaginal probe was used when performing ultrasonography (USG) and Doppler examinations. Ovarian size and volume, number of follicles and stromal echogenity were evaluated by USG. Doppler flow studies were targeted to uterine and intraovarian arteries and the pulsatility index (PI) was assessed. The concentrations of luteinizing hormone (LH), follicle stimulating hormone (FSH), total testosterone (T) and dihydroepiandrostenedione sulphate (DHEAS) were measured by immunometric methods. RESULTS: The mean values of the number of follicles and the ovarian volume of both the right and left ovaries were higher in the group with PCOS than the control group (p < 0.05). The mean PI values of the right and left ovaries, respectively, were 0.84 +/- 0.23 and 1.09 +/- 1.17 in the group with PCOS, and 0.88 +/- 0.14 and 0.92 +/- 0.15 in the control group. The mean PI values of the right and left uterine arteries, respectively, were 3.25 +/- 0.98 and 3.33 +/- 1.12 in the group with PCOS, and 3.17 +/- 0.93 and 3.2 +/- 1.38 in the control group (p > 0.05). The correlation analysis of the ovarian volume, the number of follicles and Doppler parameters revealed that there was a positive correlation and statistically significant difference between the right ovarian volume and right uterine artery PI in the group with PCOS and the left ovarian volume and left uterine artery PI in the control group (p > 0.05). The mean stromal PI of the ovarian and uterine arteries were 0.96 +/- 0.61 and 3.29 +/- 1.02 in the group with PCOS and 0.9 +/- 0.12 and 3.19 +/- 1.14 in the control group, respectively (p > 0.05). In the group with PCOS, the mean ovarian volume and the mean number of follicles were 11.46 +/- 4.43 and 13.91 +/- 4.11, respectively, whereas they were 7.63 +/- 2.44 and 5.55 +/- 2.34 in the control group (p < 0.05). CONCLUSION: It is not beneficial to use color Doppler transvaginal ultrasonography in the clinical diagnosis of patients with PCOS.

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