Objective: Oocyte maturation process characterizes polycystic ovary syndrome (PCOS). The mechanisms of this abnormality leading to chronic anovulation are under investigation. Advanced glycosylated end products (AGEs), a marker of oxidative stress linked with oocyte maturation are localized in granulosa cells and are increased in sera, in women with PCOS. The aim of this study was to investigate the relationship, whether there is an association between the anti-mullerian hormone (AMH), a hormone produced by granulosa cells and AGEs in ovulatory and anovulatory PCOS (PCOS-Anov), as well as in non-PCOS anovulatory (Non-PCOS Anov) women. Design: Cross-sectional study. Methods: Data from sixty women with PCOS (37 anovulatory and 23 regularly ovulating) were compared with eleven Non-PCOS Anov women and 25 normal women. In each subject biochemical, hormonal, and ultrasonographic parameters were studied. Results: AMH values were statistically significantly higher in PCOS-Anov (7.63G3.12) in comparison with ovulatory PCOS (PCOS-Ov; 4.92G2.50), Non-PCOS Anov (3.66G1.4), and controls (4.02G1.27 ng/ml). AGEs demonstrated a similar pattern: 8.70G1.65 in PCOS-Anov, 7.43G1.79, PCOS-Ov, 5.21G0.09, Non-PCOS Anov, and 5.85G0.89 U/ml in controls (P!0.005 for all comparison respectively). Follicle number was significantly higher in PCOS-Anov in comparison with other groups. A significant positive correlation between AMH and AGEs was observed (r: 0.326, P!0.01), and with the estimated AMH/AGEs ratio to follicle number (r: 0.42, P: 0.0001) and the presence of anovulation. Conclusions: These data suggest that an oxidative marker, AGEs, and AMH, may interact in the anovulatory mechanisms in women with PCOS.

Objectives: The aim of the present study was to evaluate the impact of polycystic ovarian morphology in the hormonal and metabolic features of the "classical" phenotypes of PCOS. Design:The study included 1275 Caucasian women with PCOS with a mean age of 24.25 ± 5.79 years and a mean BMI of 26.80 ± 7.03 kg/m 2 . Diagnosis of PCOS was based on the 2003 Rotterdam ESHRE/ASRM-Sponsored PCOS Consensus criteria. Two phenotypes, matched for age and BMI were compared: Phenotype I (n=620) which included PCOS women with biochemical hyperandrogenemia and/or clinical hyperandrogenemia, chronic anovulation and polycystic ovarian morphology on ultrasound (PCO). Phenotype II (n=400) which included PCOS women with biochemical hyperandrogenemia and/or clinical hyperandrogenemia and chronic anovulation, without PCO. These phenotypes were further subdivided in normal weight and obese PCOS women.Results: PCOS women of Phenotype I had higher LH/FSH ratio (p<0.001), higher Testosterone (p<0.01), Δ4 Androstenedione (p<0.001) and 17-OH progesterone levels (p<0.001), and higher Free Androgen Index (FAI) values (p<0.01) compared to Phenotype II. With the exception of fasting glucose levels, all other indices of insulin resistance (fasting insulin, fasting glucose/insulin ratio, QUICKI and HOMA2IR) document an association between Phenotype I and greater insulin resistance in overweight/obese PCOS women. Conclusions:In conclusion, in "classical" phenotypes of polycystic ovary syndrome (PCOS), polycystic ovarian morphology is associated with more severe hyperandrogenemia and deranged LH/FSH ratio. In overweight/obese PCOS subjects, PCO is positively correlated with insulin resistance.

No abstract

Polycystic ovary syndrome (PCOS) is a syndrome involving defects in primary cellular control mechanisms that result in the expression of chronic anovulation and hyperandrogenism. This syndrome has been for many years one of the most controversial entities in gynecological endocrinology. Polycystic ovary syndrome has been proven to be a familial condition. Although the role of genetic factors in PCOS is strongly supported, the genes that are involved in the etiology of the syndrome have not been fully investigated until now, as well as the environmental contribution in their expression. The heterogeneity of the syndrome entertains the mystery around this condition which concerns thousands of infertile women worldwide. Some genes have shown altered expression suggesting that the genetic abnormality in PCOS affects signal transduction pathways controlling steroidogenesis, steroid hormones action, gonadotrophin action and regulation, insulin action and secretion, energy homeostasis, chronic inflammation and others. The present review of the contemporary literature constitutes an effort to present all the trends in the current research for the etiology of polycystic ovary syndrome.

No abstract

The aim of this study was to monitor serum leptin concentrations after altering the levels of testosterone, by intramuscular administration of human chorionic gonadotropin (hCG), in eugonadal men. A 7-day monitoring of hCG, testosterone and leptin levels was performed after intramuscular administration of a dose of 5000 IU hCG in these men. Thirty fertile men aged 23-38 years were studied. In addition, 30 women aged 18-34 years with normal ovulatory cycles were studied, to verify reports of sexual dimorphism in serum leptin levels. These 60 individuals were divided into four groups, according to their sex and body mass index (BMI) values. In men, blood samples were collected at 09.00, after an overnight fast, for the determination of hCG, testosterone and leptin levels, and, immediately thereafter, a dose of 5000 IU hCG was administered intramuscularly. Further blood samples were collected at 24-h intervals for a period of 7 days for determination of the same hormones. In women, blood samples were collected only once, at 09.00, after an overnight fast between the 3rd and the 6th day of the menstrual cycle, for determination of serum estradiol and leptin levels. Our results showed that the mean value of leptin in thin men and women was significantly lower than that in obese men and women, respectively. The mean value of leptin in thin women was significantly higher than that in obese men. Serum leptin concentrations decreased significantly, 168 h after short-term hCG administration. There was a significant positive correlation between BMI values and serum leptin concentrations, in both men and women. Our results support the view that hCG administration in eugonadal men does not influence serum leptin levels. Moreover, a short-term increase of serum testosterone levels, after one dose of hCG, is not sufficient to affect and modify leptin secretion mechanisms in vivo.