Serum and follicular resistin levels in women with polycystic ovarian syndrome during IVF-stimulated cycles

BACKGROUND: Resistin is a hormone linking obesity and insulin resistance. The aim of this study was to compare resistin levels in serum or follicular fluid from women with polycystic ovarian syndrome (PCOS) and controls, both of whom were undergoing IVF. METHODS: We compared serum and follicular resistin levels in 21 PCOS women and in 18 healthy, normal ovulation, age- and body mass index (BMI)-matched non-PCOS women undergoing IVF. Correlations between serum or follicular fluid resistin levels and reproductive outcome were evaluated. RESULTS: There was no significant difference in either serum or follicular resistin levels between the control group and the PCOS group as a whole or those with insulin resistance [homeostasis model assessment of insulin resistance index applied to oral glucose tolerance test (HOMA(OGTT)) <4.7]. However, resistin levels in follicular fluid were unexpectedly significantly lower than serum levels (P<0.0001) in both the PCOS and control groups. No significant correlation was found between resistin levels and BMI, estradiol, LH, or fasting or 2 h glucose or insulin levels or between follicular resistin levels and fertilization rate, implantation rate, clinical pregnancy rate, or early miscarriage rate in PCOS. CONCLUSION: Resistin is unlikely to be a major determining factor in the growth and maturation of oocytes during IVF-stimulated cycles in PCOS.     

卵巢局部IGF-I系统与多囊卵巢综合征胰岛素抵抗的相关性研究

目的：研究卵巢局部胰岛素样生长因子-I系统（IGF-I系统）在伴有胰岛素抵抗多囊卵巢综合征中的作用机制。方法选择30例合并胰岛素抵抗的PCOS（polycystic ovary syndrome）患者为试验组,30例患有卵巢良性肿瘤需手术探查的患者为对照组。检测并对比血清、小卵泡液中IGF-I、胰岛素样生长因子结合球蛋白-1（IGFBP-1）与各项性激素,FI,2hI,ISI,QUICK I,卵巢超声指标,研究其与各种指标间的相关性。结果试验组小卵泡液IGF-I高于对照组（P〈0.01）,小卵泡液及血清IGFBP-1低于对照组（P〈0.05,P〈0.01）。试验组小卵泡液IGF-I水平高于血清（P〈0.01）,小卵泡液IGFBP-1水平低于血清（P〈0.05）。试验组小卵泡液IGF-I与T0、E2及卵巢体积（OV）,卵巢总面积（TA）,卵泡数（FN）,空腹胰岛素（FI）,服糖后2h胰岛素（2hI）呈正相关（P〈0.05）;血清IGF-I与胰岛素敏感指数（ISI）,体重指数（BMI）,腰臀比（WHR）呈正相关（P〈0.05）,与定量胰岛素敏感指数（QUICK I）呈负相关（P〈0.05）;试验组小卵泡液及血清IGFBP-1与FI,2hI呈负相关（P〈0.05）。结论 IR可能通过影响卵巢局部IGF-I系统,刺激卵巢分泌雄激素,引发排卵障碍,在PCOS的发病机制中起到重要作用。     

Serum and adipocyte resistin in polycystic ovary syndrome with insulin resistance

BACKGROUND: The aim of this study was to investigate the relationship between resistin and insulin resistance in patients with polycystic ovary syndrome (PCOS). METHODS: We compared serum resistin levels in 17 PCOS women and 10 lean, healthy, age-matched non-PCOS women and also compared levels of insulin receptor (IR), phosphatidylinositol-3 kinase (PI3-kinase), glucose transporter 4 (GLUT4) protein and resistin mRNA in adipocytes isolated from the omental adipose tissue of five of the PCOS patients and five age- and weight-matched, non-PCOS controls, to look for local defects in insulin action in PCOS. RESULTS: The PCOS group was hyperinsulinaemic and displayed an impaired insulin response in a 75 g oral glucose tolerance test and an abnormal homeostasis model insulin resistance index. Serum resistin levels were similar in PCOS patients and controls; however, resistin mRNA levels were 2-fold higher in adipocytes from PCOS patients. No correlation was found between serum resistin levels and either the BMI or testosterone levels. Western blot analysis showed that adipocyte levels of insulin receptor, PI3-kinase, and GLUT4 were respectively decreased by 56, 39.4 and 54% in PCOS patients compared with controls. CONCLUSIONS: These results suggest that overexpression of the resistin gene in adipocytes may be a local determinant factor in the pathogenesis of PCOS.     

Six-month treatment with low-dose dexamethasone further reduces androgen levels in PCOS women treated with diet and lifestyle advice, and metformin

BACKGROUND: The purpose of this study was to investigate the effect of low-dose dexamethasone on androgen levels in women with polycystic ovary syndrome (PCOS) treated with diet and lifestyle counselling, and metformin. METHODS: A prospective, randomized, double blind, placebo-controlled study was carried out. Thirty-eight women with PCOS were randomized to either dexamethasone 0.25 mg daily or placebo for 26 weeks. All received diet and lifestyle counselling at inclusion and metformin 850 mg three times daily during the whole study. Main outcome measures were: androgen levels, body mass index (BMI), insulin c-peptide, fasting glucose and serum lipids. Two-tailed t-tests and Pearson's statistics were used. RESULTS: Compared with the placebo, dexamethasone reduced testosterone by 27%, androstenedione by 21%, dehydroepiandrosterone sulphate by 46% and free testosterone index by 50% in women with PCOS treated with diet and lifestyle advice, and metformin. BMI, fasting glucose, insulin c-peptide and serum lipid levels were unaffected. CONCLUSIONS: Six-month, low-dose dexamethasone treatment further reduces androgen levels in metformin-treated PCOS women.     

The relationship between anti-Mullerian hormone, androgen and insulin resistance on the number of antral follicles in women with polycystic ovary syndrome

BACKGROUND: Anti-Müllerian hormone (AMH) is a biomarker that predicts the number of antral follicles and is involved in follicle arrest for women with polycystic ovary syndrome (PCOS). We investigated the association between the characteristic hyperandrogenemia, insulin resistance (IR), AMH, and the morphology and size of ovaries for women with PCOS. METHODS: A total of 99 Taiwanese women with PCOS who were willing to undergo vaginal ultrasonography were enrolled in this cross-sectional study. RESULTS: The number of antral follicles and the ovarian volume showed a significant correlation with AMH, total testosterone and the free androgen index, but not with age, body mass index (BMI) or the homeostasis model assessment of insulin resistance (HOMA-IR). AMH had a significant negative association with both BMI and HOMA-IR. Multiple stepwise regression analysis demonstrated that AMH, BMI and total testosterone were independently related to the number of antral follicles. AMH and total testosterone were the main determinants for ovarian volume in a stepwise regression model. CONCLUSIONS: Our results suggest that not only the AMH level, but also obesity, IR and elevated androgen levels may relate to the development of the large size of antral follicle pool and ovarian volume in women with PCOS. Obesity and IR may enhance the follicular excess through the dysregulation of AMH or through the pathway of hyperandrogenemia. These findings might partly explain why adequate body weight management and improvement in IR can improve the ovulatory function for women with PCOS.     

The role of insulin-like growth factor-1 (IGF-1) and IGF binding protein-1 (IGFBP-1) in the pathogenesis of polycystic ovary syndrome.

The objective of this study was to elucidate the relationship and role of insulin-like growth factor-1 (IGF-1), IGF binding protein-1 (IGFBP-1), insulin and luteinizing hormone (LH) in the pathogenesis of polycystic ovary syndrome (PCOS). In a pilot study, serum concentrations of IGF-1 were determined in women with PCOS (n = 10), hypopituitarism (n = 12) and normal controls (n = 10). In the main study, serum concentrations of IGF-1, IGFBP-1, insulin and LH in women with anovulation associated (n = 23) and not associated (n = 47) with PCOS were determined. Serum concentrations of IGF-1 were not different in women with PCOS, anovulatory non-PCOS and healthy women but were low in those with hypopituitarism. Mean serum IGFBP-1 in PCOS (33.8 +/- 21.2 micrograms/l) was decreased compared with anovulatory non-PCOS (60.0 +/- 22 micrograms/l) (P = 0.0001), and correlated negatively with insulin concentrations (r = -0.67, P = 0.0006). Patients with PCOS could be separated into those with high LH and those with high insulin levels. It was concluded that women with PCOS have normal serum IGF-1 concentrations but IGFBP-1 levels, regulated by insulin, are low. Hyperinsulinaemia and raised LH are independently capable of stimulating ovarian androgen production. Growth factors may have an important role in the pathogenesis of PCOS.     

Ultrasound examination of polycystic ovaries: is it worth counting the follicles?

BACKGROUND: This study revisited the ultrasonographic diagnostic criteria of polycystic ovary syndrome (PCOS) and studied the relationship between the major hormonal and metabolic features of PCOS and the follicle number per ovary (FNPO). METHODS: This prospective study included 214 women with PCOS compared with 112 women with normal ovaries. Main clinical, biological and ultrasonographic markers of PCOS were assessed during the early follicular phase. RESULTS: The mean FNPO of follicles 2-5 mm in size was significantly higher in polycystic ovaries than in controls, while it was similar within the 6-9 mm range. Setting the threshold at 12 for the 2-9 mm FNPO offered the best compromise between specificity (99%) and sensitivity (75%). Within the 2-5 mm follicular range, we found significant positive relationships between the FNPO and androgens. The FNPO within the 6-9 mm range was significantly and negatively related to body mass index and fasting insulin serum level. CONCLUSIONS: We propose to modify the definition of polycystic ovaries by adding the presence of > or =12 follicles measuring 2-9 mm in diameter (mean of both ovaries). Also, our findings strengthen the hypothesis that the intra-ovarian hyperandrogenism promotes excessive early follicular growth and that further progression cannot proceed normally because of hyperinsulinism and/or other metabolic influence linked to obesity.     

Adipocyte resistin mRNA levels are down-regulated by laparoscopic ovarian electrocautery in both obese and lean women with polycystic ovary syndrome

BACKGROUND: The aim of this study was to investigate serum and adipocyte mRNA expression of resistin in lean and obese women with polycystic ovary syndrome (PCOS) before and 3 months after laparoscopic ovarian electrocauterization (LOE). METHODS: Adipose tissue obtained from 12 women with PCOS (six obese and six lean, body mass index > 27 kg m(-1) as threshold point) before and after LOE was analysed. Gene expression of resistin was measured by semi-quantitative RT-PCR. Ten lean, age-matched healthy women served as controls. RESULTS: Both lean and obese women with PCOS had significantly higher fasting and 2 h insulin and homeostasis model insulin resistance index (HOMA(IR)) values and lower fasting glucose-to-insulin ratios (G(0)/I(0)) than did the controls. The serum levels of glucose and insulin and HOMA(IR) were significantly decreased, and the G(0)/I(0) ratio was significantly increased 3 months after LOE. No difference was found in serum resistin levels between controls and either obese or lean women with PCOS before LOE, nor between PCOS patients before and after LOE. However, resistin mRNA expression levels in both lean and obese women with PCOS before LOE were significantly higher than that in controls and were decreased significantly after LOE back to control levels. CONCLUSION: Local resistin activity may be actively involved in the pathogenesis of PCOS. LOE reduces insulin resistance and down-regulates resistin mRNA expression in lean and obese women with PCOS.     

Association study for single nucleotide polymorphisms in the CYP17A1 gene and polycystic ovary syndrome

Women with polycystic ovary syndrome (PCOS) are characterized by excess androgen secretion and anovulatory infertility as a cause of follicular maturation arrest, and they are also associated with insulin resistance and obesity. Recently, it was suggested that one of the etiologies for PCOS is an abnormality of steroid hormones, and excessive secretion of androgen. The endoplasmic reticular cytochrome P450, 17alpha-hydroxylase (CYP17A), plays a key role in the mechanism of steroid hormones such as adrenal and gonadal steroid biosynthesis. Therefore, we studied the association between single nucleotide polymorphisms (SNPs) of the A1 allelic variant of the CYP17 gene and PCOS in a Korean population. The study recruited 134 Korean women with PCOS and 100 healthy women as controls. Using the HapAnalyzer, the genotype of the CYP17A1 polymorphism in PCOS and control patients were analyzed. We considered a p-value lower than 0.05 to be statistically significant. After genotypic analysis, we found seven SNPs of the CYP17A1 gene in a large population of subjects. The frequency of seven SNPs had no significant association with PCOS. However, one haplotype (ht3) had a p-value of p=0.001, suggesting that it may be associated with the pathogenesis of PCOS in a Korean population.     

Androgen excess is associated with the increased carotid intima-media thickness observed in young women with polycystic ovary syndrome

BACKGROUND: We evaluated carotid intima-media thickness (CIMT) as an early marker of atherosclerosis, as well as its main determinants among androgen excess, obesity and insulin resistance, in patients with polycystic ovary syndrome (PCOS). METHODS: We selected 40 PCOS patients and 20 non-hyperandrogenic women who were similar in terms of age and grade of obesity. Complete clinical, metabolic and hormonal profiles and left common CIMT measurements were obtained. RESULTS: Patients with PCOS presented with increased mean CIMT values when compared with controls (F = 8.575; P = 0.005), and this was independent of obesity. Five PCOS patients but no controls had increased CIMT values. CIMT correlated directly with serum total and free testosterone, androstenedione and dehydroepiandrosterone-sulfate levels and mean 24-h heart rate (HR), and inversely with the insulin sensitivity index (ISI), but no correlation was observed with the body mass index (BMI). Multiple stepwise linear regression models showed that in PCOS patients, the main determinants of CIMT were serum total testosterone or androstenedione concentrations, with no influence of ISI or the mean 24-h HR. CONCLUSIONS: Compared with control women, PCOS patients present with an increased CIMT, independent of obesity and related directly to androgen excess; this suggests that hyperandrogenism is associated with atherosclerosis and cardiovascular risk in these women.     

Glucose intolerance, insulin resistance and cardiovascular risk factors in first degree relatives of women with polycystic ovary syndrome

BACKGROUND: The aim of the present study was to evaluate insulin resistance (IR), glucose tolerance status and cardiovascular risk factors in first degree relatives of patients with polycystic ovary syndrome (PCOS). METHODS: A total of 120 family members [Mothers(PCOS) (n = 40), Fathers(PCOS) (n = 38), Sisters(PCOS) (n = 25) and Brothers(PCOS) (n = 17)] of 55 patients with PCOS and 75 unrelated healthy control subjects without a family history of diabetes or PCOS (four age- and weight-matched subgroups, i.e. Control(Mothers), Control(Fathers), Control(Sisters) and Control(Brothers)) were studied. IR was assessed by homeostatic model assessment (HOMA IR), log HOMA, insulin sensivity index (ISI), the quantitative insulin sensitivity check index (QUICKI) and area under the curve for insulin during the oral glucose tolerance test (AUCI, AUCG) in with normal glucose tolerance (NGT) subjects and controls. Serum adiponectin, resistin, homocysteine and lipid levels were measured. RESULTS: The prevalence of any degree of glucose intolerance was 40% in Mothers(PCOS) and 52% in Fathers(PCOS). In total, six (15%) glucose tolerance disorders were identified in the Control(Mothers) and Control(Fathers) in first degree relatives of control subjects. The first degree relatives of PCOS patients had significantly higher serum fasting insulin, HOMA-IR, Log HOMA and AUCI levels in all subgroups than the control subjects. The control subjects had significantly elevated QUCKI, ISI levels and serum adiponectin levels compared to the first degree relatives of PCOS subjects in all subgroups. The serum Hcy and resistin levels increased significantly in both Fathers(PCOS) and Mothers(PCOS) groups but not Brothers(PCOS) and Sister(PCOS). CONCLUSION: The results of the present study support the finding that the first degree relatives of PCOS patients carry an increased risk of cardiovascular disease, as do PCOS patients.     

Serum adiponectin and lipid concentrations in pregnant women with polycystic ovary syndrome

BACKGROUND: We aimed to evaluate the serum adiponectin and lipid concentrations in normal and polycystic ovary syndrome (PCOS) women during pregnancy in order to establish whether PCOS induces abnormal lipid and adiponectin levels that could constitute potential metabolic risk factors for pregnancy complications. METHODS: Women with singleton pregnancies and of similar age were included (48 pregnant PCOS and 51 normal pregnant women). During gestational weeks 10-16 and 22-28, a 2 h, 75 g oral glucose tolerance test was performed, with measurement of glucose and insulin in each sample. Adiponectin and lipid concentrations were determined in the fasting sample. RESULTS: The incidence of gestational diabetes mellitus (GDM) was significantly higher in the PCOS group (12.2%) compared with the control group (2%). In PCOS patients, triglyceride (TG) concentrations and area under the curve of glucose and insulin were higher in both study periods and adiponectin concentrations were significantly lower in the second period, compared with normal women. Moreover, adiponectin concentrations were lower in women with GDM than in those with normal glucose tolerance in the two study periods. CONCLUSION: Low adiponectin and high insulin levels are associated with GDM in pregnant PCOS patients. High TG levels seem not to be directly related to pregnancy complications in these patients.     

多囊卵巢综合征患者性激素水平与胰岛素抵抗相关性分析

目的探讨多囊卵巢综合征(PCOS)的病因、发病机理及寻找最佳的治疗方案提供依据。方法通过放射免疫(RIA)法测患者胰岛素释放试验,酶法测糖耐量试验,电化学发光免疫分析(ECLIA)法测血清LH、FSH、E2、P、T水平。结果表明28.2%患者有胰岛素抵抗(IR),13.1%有IR和糖耐量受损,5.5%糖耐量受损。单纯IR患者中,肥胖者占35.7%;单纯糖耐量受损者中,肥胖者占36.3%;IR伴糖耐量受损者中,肥胖者占34.6%;肥胖组LH、LH/FSH、E2、T水平与非肥胖组之间无显著性差异(P0.05);而肥胖组与非肥胖的空腹血糖及空腹胰岛素水平有显著性差异(P0.05);肥胖者与非肥胖者月经周期及卵泡数目两指标有显著性差异(P0.05)。结论有较多PCOS患者存在IR或糖耐量受损;在IR和糖耐量受损的患者中,肥胖者占有较高的比重,肥胖可促进IR形成;肥胖可加重IR和生殖功能障碍。     

The role of sex hormone-binding globulin and androgen receptor gene variants in the development of polycystic ovary syndrome

BACKGROUND: Polycystic ovary syndrome (PCOS) may be programmed in utero by androgen excess. Our aim was to examine the role of the sex hormone-binding globulin (SHBG) and androgen receptor (AR) gene polymorphisms, in the phenotypic expression of PCOS. METHODS: A cohort of 180 women with PCOS and 168 healthy women of reproductive age were investigated. BMI was recorded and the hormonal profile was determined on Day 3-5 of menstrual cycle. DNA was extracted from peripheral blood leucocytes and the SHBG(TAAAA)n and AR(CAG)n polymorphisms were genotyped by PCR. RESULTS: Genotype analysis revealed six SHBG(TAAAA)n alleles with 6-11 repeats and 19 AR(CAG)n alleles with 6-32 repeats, present in both PCOS and control women. Long SHBG(TAAAA)n alleles (>8 repeats) were at greater frequency in PCOS than normal women (P = 0.001), whereas short AR(CAG)n alleles (相似文献   

Serum and follicular fluid levels of soluble Fas, soluble Fas ligand and apoptosis of luteinized granulosa cells in PCOS patients undergoing IVF

BACKGROUND: There are limited data about the levels of soluble apoptotic factors and their modulation with therapeutic regimens in IVF cycles. The aim of the current study was to determine follicular fluid, and serum levels of soluble Fas (sFas) and soluble Fas ligand (sFasL) in PCOS patients undergoing IVF/ICSI cycles; also to investigate the effects of metformin on these factors and on apoptosis of luteinized granulosa cells. METHODS: We investigated the serum and follicular fluid levels of sFas and sFasL in patients with PCOS (n = 28) and compared them with those of the patients with infertility due to male factor (n = 12) undergoing IVF cycles. Effects of metformin therapy on these parameters and apoptosis of luteinized granulosa cells were also investigated among the patients with PCOS. RESULTS: Serum levels of sFas were significantly lower in the PCOS group compared to those in women with infertility due to male factor. Metformin therapy in PCOS patients preceding IVF cycles increased serum levels of sFas and decreased follicular fluid levels of sFasL compared to those on placebo. Follicular fluid from PCOS patients demonstrated luteinized granulosa cell DNA fragmentation in agarose gel, whereas a similar pattern was not observed among PCOS patients undergoing metformin therapy. CONCLUSION: Decreased serum levels of sFas and luteinized granulosa cell DNA fragmentation is observed in patients with PCOS undergoing IVF cycles. Metformin therapy preceding IVF demonstrates an antiapoptotic effect with increased serum levels of sFas, decreased follicular fluid levels of sFasL and prevention of luteinized granulosa cell DNA fragmentation.     

Inhibin A, inhibin B and activin A concentrations in follicular fluid from women with polycystic ovary syndrome

Polycystic ovary syndrome (PCOS) is characterized by arrestedfollicle development at the early antral stage. Alterationsin inhibin production by developing follicles could be involvedin PCOS by suppressing follicle stimulating hormone concentrationsduring the follicular phase of the menstrual cycle as well asby increasing thecal androgen production. Inhibin B appearsto be more important than inhibin A during the follicular phase;however, there are no data regarding the follicular fluid concentrationsof inhibin B in PCOS. The purpose of this study was to compareinhibin A, inhibin B and activin A concentrations in the follicularfluid from regularly cycling women and women with PCOS. InhibinA, inhibin B and activin A were measured in the follicular fluidof 4–7 mm follicles from PCOS ovaries and size-matchedfollicles from normally cycling women by specific and sensitivetwo-site enzyme-linked immunosorbent assays. In both controland polycystic ovaries, inhibin B was approximately 10-foldhigher than activin A and more than 100-fold higher than inhibinA. There was no difference in activin A concentrations betweenPCOS and control follicles. In control ovaries, the inhibinB and inhibin A concentrations in dominant follicles were significantlyhigher than in cohort follicles. While inhibin A concentrationswere lower in PCOS follicles than in normal cohort follicles,there was no difference in inhibin B concentrations betweenPCOS follicles and normal cohort follicles. These data are consistentwith the concept that inhibin B is the physiologically mostimportant form of inhibin during the follicular phase of themenstrual cycle and indicate that PCOS is not associated withincreased inhibin B concentrations in follicular fluid.     

Is there a role for leptin in the endocrine and metabolic aberrations of polycystic ovary syndrome?

Immunoreactive serum leptin was analysed in 49 women with polycystic ovary syndrome (PCOS) distributed on a wide range of body mass index (BMI; kg/m2) and in 32 normally menstruating women with comparable age, BMI, physical activity and dietary habits. All women with PCOS had increased androgen concentrations and obese women with PCOS (BMI > or = 25, n=24) also showed decreased insulin sensitivity and a preferential accumulation of truncal-abdominal body fat. Anthropometric and hormonal variables, insulin sensitivity, and pancreatic beta-cell activity were investigated in all women. Percentage body fat was calculated using gender-specific regression equations based on skinfold measurements. Serum leptin concentrations were higher in obese than in non-obese women (P < 0.001), but did not differ between the women with PCOS and controls, nor did they differ between glucose intolerant and glucose tolerant, or hirsute and non-hirsute women with PCOS. Both groups showed strong correlations between serum leptin concentrations and percentage body fat, BMI, body fat distribution, fasting plasma insulin and C-peptide, early insulin secretion, the free androgen index (FAI), and the degree of insulin resistance. After correcting for percentage body fat, only the FAI in the women with PCOS remained significant (P < 0.05). However, in a multiple regression analysis with both percentage body fat and the FAI as independent variables, the FAI increased only minimally (2%) the explained variation in leptin concentrations. Thus, serum leptin concentrations are almost exclusively determined by the total amount of body fat, independent of its location, and do not confirm the hypothesis that leptin is involved in the development of the hormonal and metabolic abnormalities in the PCOS.      

Serum visfatin in relation to insulin resistance and markers of hyperandrogenism in lean and obese women with polycystic ovary syndrome

BACKGROUND: Visfatin, a protein secreted by adipose tissue, is suggested to play a role in pathogenesis of insulin resistance. In polycystic ovary syndrome (PCOS), insulin resistance might be involved in the development of endocrine and metabolic abnormalities. The aim of the study was to asses the relation between serum visfatin concentration and insulin sensitivity and markers of hyperandrogenism in lean and obese PCOS patients. METHODS: The study group consisted of 70 women with PCOS (23 lean and 47 obese) and 45 healthy women (25 lean and 20 obese). Euglycemic hyperinsulinemic clamp and the measurements of serum visfatin, sex hormones were performed. RESULTS: The PCOS group had lower insulin sensitivity (P=0.00049) and higher serum visfatin (P=0.047) in comparison to the control group. The decrease in insulin sensitivity was present in both the lean (P=0.019) and obese (P=0.0077) PCOS subjects, whereas increase in serum visfatin was observed only in lean PCOS subjects (P=0.012). In the whole group, serum visfatin was negatively correlated with insulin sensitivity (r=-0.27, P=0.004). This relationship was also observed in the subgroup of lean (r=-0.30, P=0.038), but not obese women. Additionally, in lean women, visfatin was associated with serum testosterone (r=0.47, P=0.002) and free androgen index (r=0.48, P=0.002), independently of other potential confounding factors. CONCLUSIONS: Visfatin is associated with insulin resistance and markers of hyperandrogenism in lean PCOS patients.     

Follistatin and activin A serum concentrations in obese and non-obese patients with polycystic ovary syndrome.

BACKGROUND: Activin promotes ovarian follicular development, inhibits androgen production and increases FSH and insulin secretion. Follistatin, an activin-binding protein, neutralizes activin bioactivity. Therefore, a decrease in the ratio of activin/follistatin might encourage characteristic features of polycystic ovary syndrome (PCOS). We investigated whether women with PCOS showed disordered follistatin and/or activin serum concentrations. METHODS: The study group included 24 obese and 20 non-obese (body mass index vertical line and <27 kg/m2 respectively) clomiphene-failure PCOS patients. The control group included 16 obese and 46 non-obese patients with normal ovulatory cycles. Blood samples were obtained from the patients on day 3-5 of a progesterone-induced or spontaneous cycle and were assayed for LH, FSH, testosterone, 17-hydroxy-progesterone, androstenedione, follistatin, activin A, fasting glucose and insulin. RESULTS: Follistatin concentrations were comparable between obese and non-obese PCOS patients (mean +/- SE; 1171 +/- 103 and 1045 +/- 159 pg/ml respectively) and significantly higher than their respective controls (628 +/- 61 and 592 +/- 49 pg/ml, P < 0.0001 and P < 0.02 respectively). Activin A concentrations were comparable between the four groups (590 +/- 35, 513 +/- 74, 661 +/- 87 and 595 +/- 43 pg/ml in obese and non-obese PCOS and controls respectively). Stepwise regression analyses for relationships between follistatin or activin A levels and all other variables indicated that follistatin was significantly and independently positively affected by PCOS (P < 0.0001), age (P < 0.02), androstenedione (P < 0.03) and weight (P < 0.05). Activin A was significantly and independently negatively affected by PCOS (P < 0.003) and FSH (P < 0.03), and positively affected by weight (P < 0.009) and androstenedione (P < 0.02). CONCLUSIONS: Serum follistatin is increased in PCOS patients, regardless of obesity. PCOS is the most significant variable that relates to high follistatin and low activin A serum concentration. A high follistatin/activin ratio could well contribute to the pathophysiology of PCOS.     

多囊卵巢综合征患者血清抑制素B水平的分析

目的：探讨抑制素B（inhibin,INH-B）水平在多囊卵巢综合征（PCOS）患者血清中的变化及其与体重指数（BMI）的关系。方法：筛选PCOS患者40例,根据体重指数（BMI）分为肥胖组和非肥胖组并检测血清中的抑制素B（INH-B）、胰岛素生长因子-I（IGF-I）、空腹胰岛素（In）、瘦素（leptin）、黄体生成素（LH）、卵泡刺激素（FSH）、人体催乳素（PRL）、雌二醇（E2）和睾酮（T）,另取40例排卵正常、无怀孕妇女做对照分析。结果：PCOS患者肥胖组leptin、In、LH、T水平明显高于非肥胖组,INH-B、IGF水平则明显低于非肥胖组,差异有统计学意义（P〈0.05）;且肥胖组的LH与INH-B呈负相关（r=-0.735,P〈0.05）,非肥胖组的LH与INH-B无明显相关性。非肥胖组INH-B、IGF、LH、T水平明显高于对照组,差异有统计学意义（P〈0.05）。结论：INH-B与多囊卵巢综合征（PCOS）发生有关,且作为PCOS特征的肥胖又影响着INH-B的作用和水平。