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Infertility seriously endangers the reproductive health of women at childbearing age. It is defined as the failure to achieve successful pregnancy after 1 year or more of regular unprotected intercourse. Broadly defined, infertility includes two aspects – failure to conceive or have a live birth. This guideline only addressed content relevant to the former. It was proposed by the gynecological endocrine group of the Chinese Society of Obstetrics and Gynecology, Chinese Medical Association, based on relevant guidelines of the World Health Organization, the American Society for Reproductive Medicine, the National Institute for Health and Clinical Excellence, as well as the clinical practice in China. The guideline was reviewed by experts and doctors from medical institutions at all levels, which is applicable to the diagnosis of infertility by physicians in obstetrics, gynecology, and andrology at various medical institutions nationwide.

A relationship between albuminuria and obstructive sleep apnea (OSA) has been documented in previous studies. Nevertheless, the impact of continuous positive airway pressure (CPAP) treatment on albuminuria in subjects with OSA is debated. This meta-analysis was carried out to investigate whether or not CPAP treatment affected urinary albumin-to-creatinine ratio (UACR) in subjects with OSA. A comprehensive literature search was conducted on Web of Science, Embase, and PubMed from January 1990 to December 2020. Information on patients’ characteristics, features of the studies, and UACR of pre- and post-CPAP treatment was collected. For estimation of the pooled effects, standardized mean difference (SMD) was applied. This meta-analysis included 6 articles and 211 subjects. The pooled analysis suggested that CPAP therapy exerted a favorable effect on the decrease of UACR in subjects with OSA (SMD = 0.415, 95% CI = 0.026 to 0.804, z = 2.09, p = 0.037). Subgroup analyses revealed that the CPAP treatment effect was not influenced by sample size, BMI, age, or AHI. The present meta-analysis indicated that UACR was significantly reduced by CPAP therapy in subjects with OSA. Further well-designed randomized controlled trials with large sample size are required to confirm the benefits.

Objective To document the possible effect of tyrosine kinase autophosphorylation on erythrocyte insulin-receptor after 12 weeks of metformin administration from the women with polycystic ovary syndrome (PCOS). Methods Thirty non-obese (BMI 2 ) healthy women with normal reproductive cycles were evaluated by conventional criteria as the control, 30 non-obese women with PCOS were categorized as nob-PCOS group, 40 obese women with PCOS (BMI ⩾ 25 kg/m 2 ) were categorized as ob-PCOS group. Subjects with PCOS were given metformin 850 mg/d for 12 weeks. The autophosphorylation of insulin receptor pY1158, pY1162/1163 and insulin receptor-β subunit (IR-β) from the solubilised erythrocyte were detected by ELISA. Results 1) Only the autophosphorylation level of pY1158 in nob-PCOS and ob-PCOS groups was lower (P 0.05), even insulin-stimulated insulin receptor (P>0.05) from both of PCOS groups. 2) After metformin administration, the pY1158, pY1162/pY1163 autophosphorylation levels were increased (P 0.05). In summary, oral administration of metformin led to an significant increase in tyrosine kinase activity in both groups of PCOS. Conclusion The impairment of tyrosine autophosphorylation at pY1158 may contribute to insulin resistance, the tyrosine kinase activity per receptor of solubilised erythrocytes were significantly increased by metformin administration and the effect of metformin on insulin-receptor tyrosine kinase activity appeared to be independent of either of these variables.

Low-grade chronic inflammation is commonly found in patients with polycystic ovary syndrome (PCOS) who exhibit hyperandrogenism or hyperandrogenemia. Clinical studies have shown that hyperandrogenemia is closely correlated with low-grade chronic inflammation. However, the mechanism underlying this correlation remains unclear. Recent studies have suggested that adipocytes increase the production of proinflammatory mediators such as interleukin-6 (IL-6) and macrophage chemotactic protein-1 (MCP-1) when the inflammatory signal transduction cascade system is activated by external stimuli. The present study aimed to evaluate the effects of testosterone on the innate signalling and expression of proinflammatory mediators in 3T3-L1 adipocytes, which were or were not induced by lipopolysaccharide (LPS). The effects of testosterone on the expression of proinflammatory mediators, nuclear factor-κB (NF-κB), and extracellular signal-regulated kinase 1/2 (ERK1/2) signalling pathways were investigated using an enzyme-linked immunosorbent assay, reverse transcriptase-polymerase chain reaction, western blot analysis and an electrophoresis mobility shift assay. Testosterone induces IL-6 and MCP-1, and enhances LPS-induction of IL-6 and MCP-1. However, the effects are not simply additive, testosterone significantly enhanced the effects of LPS-induced inflammation factors. Testosterone induces the phosphorylation of ERK1/2 and NF-κB. The effect of testosterone on the expression of IL-6 and MCP-1 is inhibited by PD98059 , an ERK1/2 inhibitor, and PDTC, an NF-κB inhibitor. The results indicate that testosterone enhances LPS-induced IL-6 and MCP-1 expression by activating the ERK1/2/NF-κB signalling pathways in 3T3-L1 adipocytes.

To explore the regulation of insulin sensitivity in liver cells by androgen signaling.Eleven adult female C57BL/6 mice were injected daily with testosterone (group T) for 24 weeks. And 10 control mice received sesame oil only (group Con). HepG2 liver cells were initially pretreated with different doses of testosterone (10(-9)-10(-5) mol/L ) for 0-36 h or with 10(-7) mol/L testosterone for 0-96 h followed by a stimulation of 100 nmol/L insulin for 15 min. Later HepG2 cells were pretreated with 10(-7) mol/L testosterone for 36 h followed by a stimulation of 100 nmol/L insulin for 15 min and then a restimulation of 100 nmol/L insulin for 15 min at 4 h and 6 h interval respectively. Phosphorylation and protein expression of Akt and GSK3β in C57BL/6 mice liver tissues and HepG2 cells were analyzed by Western blot.The 24-week treatment of testosterone decreased the phosphorylation of Akt and GSK3β in C57BL/6 adipose and liver tissues (43.1% ± 3.2% vs 77.1% ± 6.7%, 14.7% ± 6.7% vs 82.3% ± 2.0% respectively, P0.05). Pretreatment with 10(-8)-10(-6) mol/L testosterone within 36 h obviously increased the phosphorylation of Akt and GSK3β (P0.05). However pretreatment with 10(-5) mol/L within 36 h or with 10(-7) mol/L for 96 h had no effect on the phosphorylation of Akt and GSK3β compared with control group (P0.05). Pretreatment with 10(-7) mol/L testosterone for 36 h followed by insulin stimulation and restimulation after 6 h interval obviously decreased the phosphorylation of Akt and GSK3β (P0.05).Androgen signaling may contribute to insulin resistance in liver cells.

Polycystic ovary syndrome (PCOS) is a state of altered steroid hormone production and activity. Chronic estrogen exposure or lack of progesterone due to ovarian dysfunction can result in endometrial hyperplasia and carcinoma. A key contributor to our understanding of progesterone as a critical regulator for normal uterine function has been the elucidation of progesterone receptor (PR) expression, regulation, and signaling pathways. Several human studies indicate that PR-mediated signaling pathways in the nucleus are associated with progesterone resistance in women with PCOS. The aim of this review is to provide an overview of endometrial progesterone resistance in women with PCOS; to present the PR structure, its different isoforms, and their expression in the endometrium; to illustrate the possible regulation of PR and PR-mediated signaling in progesterone resistance in women with PCOS; and to discuss current clinical treatments for atypical endometrial hyperplasia and endometrial carcinoma in women with PCOS and accompanying progesterone resistance.

Rats treated on Day 5 of life with testosterone propionate (TP) were tested for their ovulatory response to pregnant mare's serum gonadotropin (PMSG) on the 30th day of life with and without cardiac puncture under ketamine/xylazine anesthesia. TP without cardiac puncture in doses of 0.625, 1.25, or 2.5 microg did not inhibit ovulation, but 5.0 microg of TP inhibited ovulation in 15 of 16 rats. When cardiac puncture was performed at 1900 hr in rats not given TP, seven of eight ovulated on Day 33. However, none of the rats that received either 1.25 or 2.5 microg of TP ovulated after cardiac puncture at 1900 hr, and only one of seven given the 0.625-microg dose ovulated. Thus, the stress of bleeding greatly enhanced the inhibitory effect of otherwise ineffective doses of TP. The preovulatory luteinizing hormone (LH) surge was delayed and diminished by neonatal TP in a dose-related manner in animals from which blood was drawn from a previously inserted catheter. When blood drawn from similarly TP-treated animals by cardiac puncture, serum levels of LH were further reduced. Progesterone, given at 1100 hr on Day 32, was capable of partially overcoming the inhibitory effects of the combined treatments on both ovulation and serum LH levels at all but the highest dose of TP tested (5.0 microg). We conclude that neonatal exposure to androgen sensitizes rats to ovulation-inhibiting factors, such as bleeding, in a manner which appears to delay as well as inhibit the preovulatory release of LH. Such early exposure to androgen, therefore, may determine the susceptibility of individuals to reproductive failure in adult life.

To study the efficacy and safety of estradiol and drospirenone tablets (Angeliq) in treatment of menopausal symptoms among postmenopausal Chinese healthy women.Total 244 postmenopausal Chinese healthy women who had moderate to severe hot flushes were randomly assigned into estradiol and drospirenone (observation group, n = 183) or placebo group (n = 61) by the ratio of 3:1 for 16 weeks in this randomized multi-center double-blind placebo-controlled study. During the trial, the follow-up visits were conducted at week 4, 8, 12, 16 of treatment and 2 weeks after treatment respectively. Height, weight, vital signs, hot flushes, other relevant menopausal symptoms and vaginal bleeding were observed in each follow-up visit, while the clinical global impression scale was assessed at 16 weeks as well.It showed that hot flushes were reduced significantly more in observation group than that in placebo group (P0.01), although both treatments were effective. The absolute values of mean severity index of total hot flushes decreased by -0.6 ± 0.5 in observation group and -0.4 ± 0.4 in placebo group from baseline respectively, which reached significant difference (P0.05). However, the absolute values of mean severity index of moderate to severe hot flushes decreased by -0.6 ± 0.8 in observation group and -0.3 ± 0.6 in placebo group from baseline respectively, which had no significant difference (P0.05). After 16 weeks treatment, it also showed that estradiol and drospirenone had significant better efficacy than placebo on moderate to severe sweating, vaginal dryness and clinical global impression scale (P0.01). During the trial, blood pressure in observation group was stable. The rate of vaginal bleeding in observation group was higher than that in the placebo group, especially during the week 4 to week 8 when 48.9% (87/178) in observation group and 10.7% (6/56) in placebo group of patients bled. Although the cumulative amenorrhea rate of observation group was lower than that of placebo group in each cycle (28 days), it increased gradually along with duration of the treatment. The commonest adverse event in observation group was breast tenderness which accounted for 12.0% (22/183). The level of serum potassium was in the normal range in observation group mostly.Meanwhile, the other adverse events rate was low. Serious adverse events reported in this trial were assessed as not study drug related or as unlikely study drug related.Estradiol and drospirenone tablets which could effectively alleviate menopausal symptoms in postmenopausal Chinese healthy women is a novel hormone replacement therapy regimen with high safety and efficacy.

To investigate the clinical features, reproductive endocrine and metabolic abnormalities in adolescent girls with polycystic ovary syndrome (PCOS).A total of 325 adolescent girls with normal menstruation, 18 obese (OB-CON) and 307 non-obese (NOB-CON), were enrolled as controls from multiple middle schools in Shanghai, China. A total of 167 adolescent girls with PCOS, 90 obese (OB-PCOS) and 77 non-obese (NOB-PCOS), were also recruited. All cases were evaluated for their clinical manifestations, reproductive endocrine and metabolic parameters. Hyperandrogenism was determined by serum testosterone (T), free androgen index (FAI) and dehydroepiandrosterone sulfate (DHEA-S). Insulin sensitivity was measured by fasting insulin (FINS) and homeostasis model assessment of insulin resistance (HOMA-IR).(1) Menarche was significantly earlier in adolescent PCOS than in controls. The incidence of obesity was significantly higher in adolescent PCOS than that in control group. (2) T, FAI and DHEA-S were significantly higher in adolescent PCOS group than those in control group. FAI was higher in OB-PCOS group than in NOB-PCOS group. LH and LH/FSH were higher in PCOS groups than those in controls. LH and LH/FSH were also much higher in NOB-PCOS group than those in OB-PCOS group. (3) HOMA-IR and FINS were significantly higher in PCOS group than those in control group. Incidence of acanthosis nigricans, FINS, HOMA-IR and triglyceride were significantly higher in OB-PCOS group than those in NOB-PCOS group. (4) 95.21% PCOS girls presented with an ultrasonic morphological evidence of polycystic ovarian.The essential features of adolescent PCOS are an earlier onset of menarche, a persistent menstrual disorder over 2 years after menarche, a higher incidence of obesity, marked hyperandrogenism and insulin resistance and disorderly gonadotropin secretion in comparison with control subjects. Hyperandrogenism and insulin resistance are much more severe in obese adolescent PCOS.

To investigate the correlations between adipocytokines and insulin resistance in women with polycystic ovary syndrome.Sixty women with polycystic ovary syndrome aged 19-34 years old were divided into 2 groups: group A [n = 36, BMIor = 25 kg/m(-2) or WHR (waist height ratio)0.85] and group B (n = 24, BMI25 kg/m(-2) and WHRor = 0.85). Twenty-six healthy infertile women with a mean age of 26 + or - 8 years old served as controls and they were named as group C (n = 26, BMI25 kg/m(-2) and WHRor = 0.85). Anthropometric measurements, hormonal profiles and metabolic profiles were compared between three groups. Plasma leptin, CRP and free fatty acid were measured by enzyme-linked immunosorbent assay (ELISA). Adiponectin, interleukin-6 (IL-6) and tumor necrosis factor-alpha (TNF-alpha) were measured by radioimmunoassay. Insulin resistance was estimated by homeostasis model assessment (HOMA).(1) Adiponectin and TNF-alpha levels were significantly higher in group B (17 + or - 9) mg/L and (1.0 + or - 0.3) mg/L respectively than in group A (10 + or - 7) mg/L and (0.8 + or - 0.2) mg/L respectively. Leptin was lower in group B (24 + or - 13) microg/L and group C than in group A (42 + or - 21) microg/L (all P0.01). IL-6 was higher in group A (173 + or - 184) ng/L and group B (184 + or - 44) ng/L than in group C (P0.05 and P0.01 respectively). No significant difference of circulating level of CRP was found between these 3 groups. (2) Leptin was positively correlated with BMI, WHR and HOMA-IR (all P0.01) whereas adiponectin was negatively correlated with BMI, WHR and HOMA-IR (P0.01; P0.01, P0.05 respectively). Multivariate regression showed that adiponectin was the most significant predictor of HOMA-IR and it explained 16.5% of variance.The higher levels of leptin and TNF-alpha, the lower level of adiponectin in obese PCOS and the higher level of TNF-alpha and IL-6 in non-obese PCOS suggested different adipocytokines play different roles of insulin resistance in PCOS.

To investigate the role of androgen in TNF-alpha and MCP-1 expression in RAW264.7 macrophage and its molecular mechanism.(1) RAW264.7 macrophage was treated with 10(-9) mol/L or 10(-7) mol/L testosterone (T) and then subjected to the measurement of: 1) the cellular expression of TNF-alpha and MCP-1 mRNA by RT-PCR; 2) the expression of TNF-alpha and MCP-1 in cell culture supernatant by ELISA; (2) The expression of phospho-NF-kappaB after treatment with T was measured by Western blot. (3) Cells were pre-incubated with 10(-4) mol/L PDTC (an inhibitor of NF-kappaB) for 1 hour, followed by T treatment. Expression of mRNA and supernatant levels of TNF-alpha and MCP-1 were measured by RT-PCR and ELISA.(1) 1) After a 6 h treatment with 10(-9) mol/L or 10(-7) mol/L T, the expression of TNF-alpha mRNA increased by 1.78 and 1.87 folds, MCP-1 by 1.58 and 1.66 folds respectively (all P0.05). 2) Incubated with both concentration of T for 6 h showed no significant changes of supernatant levels of TNF-alpha and MCP-1. After a 24 h treatment, the levels of TNF-alpha and MCP-1 increased significantly (all P0.05) while more significant increase was found in 10(-7) mol/L T group (P0.05). (2) The expression of phospho-NF-kappaB (ser276) increased significantly after cells were treated with 10(-7) mol/L T for 30 min (P0.05) and peaked at 60 min. (3) With 1 h PDTC pre-incubation, T (10(-9) mol/L or 10(-7) mol/L) treatment for 6 h led to a lower mRNA expression and 24 h led to lower supernatant levels of TNF-alpha and MCP-1 than those without (P0.05). However, both cellular and supernatant expression of TNF-alpha and MCP-1 with PDTC pre-incubation were still higher than those of blank controls (all P0.05, except for TNF-alpha in 10(-9) mol/L T treatment).Testosterone can increase TNF-alpha and MCP-1 expression in RAW264.7 macrophage in vitro. Activation of cellular NF-kappaB by testosterone may be one of underlying molecular mechanisms.

To explore the effects of androgen upon the production of inflammatory Cultured factors in 3T3-L1 adipocytes and to investigate the mechanism at the molecular level.pre-adipocytes from 3T3-L1 cell line were induced to differentiate into adipocytes. Mature adipocytes were treated with testosterone at a concentration of 10(-9) to 10(-15) mol/L for either short (0 to 30 min) or long (12, 24 and 48 h) treatment course. Secretion of inflammatory factors, i.e., interleukin-6 (IL-6) and monocyte chemoattractant protein-1 (MCP-1), in the culture medium were determined by enzyme-linked immunosorbent assay (ELISA). The mRNA expression of IL-6 and MCP-1 were determined by reverse transcriptase PCR. Phosphorylation of NF-KB was analyzed by Western blot with beta-actin as the reference gene. In another experiment, adipocytes were manipulated according to the same protocol except being pretreated with PDTC (inhibitor of NF-KB) for 2 h prior to the addition of testosterone. The results of two experiments were compared.(1) The secretion of IL-6 and MCP-1 in the culture medium were higher in the testosterone-treated groups than in the control groups (P0.05). The highest concentration of IL-6 and MCP-1 were observed in the group treated with 10(-5) M testosterone for 24 h. The mRNA expression of IL-6 and MCP-1 were higher in the groups treated with testosterone for 12 h, especially with testosterone of 10(-5) mol/L; (2) With a short treatment course of testosterone, more NF-kappaB were phosphorylated than in control, especially with testosterone of 10(-5) mol/L. More NF-kappaB was phosphorylated following the 12 h testosterone treatment (10(-9), 10(-7) and 10(-5) mol/L), especially with a testosterone concentration of 10(-9) and 10(-5) mol/L. (3) When pretreated by NF-kappaB inhibitor and followed by 10(-5) mol/L testosterone for 24 h, the secretion of IL-6 and MCP-1 in the culture medium decreased significantly (P0.01). Likewise, when pretreated by NF-kappaB inhibitor and followed by 10(-5) M testosterone for 12 h, the mRNA expression of IL-6 and MCP-1 decreased significantly.Within the certain scope, testosterone could increase the expression of inflammatory factors in adipocytes through the activation of NF-kappaB.

To investigate the relationship of dynamic quantitative changes between insulin and testosterone in polycystic ovary syndrome (PCOS).Peripheral blood samples were collected in the third to fifth day menstrual cycle from 97 PCOS patients, aged (24 +/- 6), 47 being obese (with BMI25 kg/m(2)) and 50 being non-obese (with BMI/= 25 kg/m(2)), and 27 women with oviductal sterility (control group). The serum testosterone was measured. All the subjects underwent oral glucose tolerance test (OGTT) with the glucose load of 75 g, and the plasma insulin levels 30, 60, 120, and 180 minutes later were measured. Curve fitting of 11 kinds of equations was used to estimate the optimization degree of relationship between testosterone and insulin.(1) The correlation between testosterone and insulin was the most perfect when the T and insulin levels 120 min later of the obese and non-obese PCOS patients and the controls were expressed by Compound equation with the Rsq values of 0.84, 0.79, and 0.894 respectively. (2) The Compound function curves corresponding to the data of the 3 groups showed significantly different parameters.(1) Compound equation is the optimized equation to express the quantitative change relationship between the testosterone and insulin levels in OCOS. (2) The difference in homeostasis ability to T and insulin may be related to the difference in the various parameters derived by Compound equation.

To investigate the influence of rapid nongenomic effect of androgen on the insulin sensitivity of mature adipocytes and the molecular mechanism thereof.Fetal mice [corrected] preadipocytes of the line 3T3-L1 were cultured to develop into mature adipocytes. 3T3-L1 adipocytes were pretreated with testosterone of the concentration of 10-9 to approximately 10(-5) mol/L for a short-time 0-30 minutes) or a long-time (24 hours). Insulin (Ins) 200 microl at the concentration 100 micromol/L and 2-deoxy [3H] glucose were added to examine the glucose uptake. Phosphorylation and protein expression of Ins receptor (InsR) and its downstream signaling molecules (Akt and GSK3beta) were analyzed by Western blotting.The Ins-stimulated glucose uptake after the pretreatment of testosterone for 30 min and 24 h decreased gradually in response to the increasing of the concentration of testosterone with the nadir both at the testosterone concentration of 10(-5) mol/L (both P0.05). The phosphorylation levels of InsR, Akt, and GSK3Pbeta were significantly down-regulated by adding of testosterone at the concentration of 10(-6) mol/L for 3-30 minutes (all P0.05) or by adding of testosterone at the concentrations of 10(-7) - 10(-6) mol/L for 24 hours (all P0.05). The protein expression levels of InsR, Akt, and GSK3Pbeta, however, were not significantly affected by testosterone treatment.Rapid nongenomic effect of androgen may contribute to the insulin resistance in adipocytes.

BACKGROUND: Atypical endometrial hyperplasia usually is treated with high-dose progestin or hysterectomy but the latter deprives the patient of future child bearing. CASES: Two women with atypical endometrial hyperplasia complicating polycystic ovary syndrome (PCOS) had failed to respond to high-dose progestin therapy. They were both obese insulin-resistant and nulliparous with a desire to preserve fecundity. Metformin and oral contraceptives were administered as alternatives. Endometrial curettage performed 3 months later demonstrated a proliferative endometrium without evidence of residual pathology. CONCLUSION: Insulin resistance might play a role in the occurrence of atypical endometrial hyperplasia complicating PCOS. Metformin and oral contraceptives could be an alternative treatment in the presence of progestin resistance.

To investigate the influences of fetal growth retardation (FGR) and postnatal high fat diet (HF) on the development of insulin resistance (IR), puberty development and fertility problems in female rat offspring.FGR model was induced by maternal low protein diet. 32 newborn FGR rats and 32 control rats were randomly divided into two equal groups: FGR/HF group (with the mother rats given with high fat diet for 3 weeks after delivery), FGR/N (with the mother rats given with normal diet), C/HF group (control newborn rat group with the mother rats given with high fat diet), and C/N group (control newborn rat group with the mother rats given with normal diet). The pups were fed by mother milk. All pups were weaned at the 4th week of age and then fed with the diet the same diet as that during the lactation period until the end of experiment. From day 30 onwards, vaginal opening and oestrous cycle were inspected daily on 10 pups in each group. At the 13th week, body weight, length and perirenal fat weight/body weight (Fw/Bw) were recorded for 10 pups in each group. At the same time, fasting plasma glucose (FPG), fasting insulin (FINS), and testosterone level were measured. From the 13th week onwards, mating test was performed for 6 pups in each group.At the 13th week, there was an obesity tendency in the FGR/N, FGR/HF and C/HF groups. The FINS levels were all higher, and insulin sensitivity index (ISI) levels were all significantly lower in these three groups than in the C/N group (all P0.05). The homeostasis model assessment insulin resistance index (HOMA-IR) levels of the FGR/N and FGR/HF groups were significantly higher than that of the C/N group (both P0.05), the FINS and HOMA-IR of the FGR/HF group were significantly higher than that of the FGR/N group (both P0.05). There was oligoovulation in the FGR and high fat diet rats, the pregnancy rate of the FGR/HF group was significantly lower than that of the C/N group (P0.05). FGR/HF group had the most serious obesity, IR and fertility problems.There are puberty disturbance, oligoovulation and IR in FGR and high fat diet rats. IR, puberty development and fertility problems are linked and occur independently of the postnatal nutrition, but can be exacerbated by postnatal high fat diet.

To investigate the clinical presentation, hormonal profile and metabolic abnormalities in subgroups of women with PCOS and explore a reasonable classification for PCOS.A cross-sectional study of 192 women with PCOS (14 - 38 years of age) was performed. The patients were divided into 3 groups of A, B and C according to the revised 2003 consensus on diagnostic criteria and also divided into 2 groups according to body mass index (BMI): group A (n = 110), long term anovulation, clinical and biochemical evidence of high androgen level, ovary enlargement with its size larger than 10 ml or number of small follicles of 2 - 9 mmor= 12 under ultrasound with exclusion of other diseases caused by high androgen; group B (n = 46), long term anovulation, clinical and biochemical evidence of high androgen level; group C (n = 36), long term anovulation, ovary enlargement with its size larger than 10 ml or number of small follicles of 2 - 9 mmor= 12 under ultrasound with exclusion of other disease caused by high androgen; obesity PCOS group (OB-PCOS, n = 70), BMIor= 25 (kg/m(2)); no obesity PCOS group (NOB-PCOS, n = 122), BMI25 (kg/m(2)). One hundred and four women with bilateral tubal block factor caused infertility served as control group. Anthropometric measurements, Ferriman Gallwey hirsutism scoring, presence of acne and acanthosis nigricans were noted. Hormonal profile was assessed by measuring follicle-stimulating hormone (FSH), luteinizing hormone (LH), free testosterone (FT), prolactin (PRL), sex hormone binding globulin (SHBG). The metabolic profile was investigated by measurements of oral glucose tolerance test (OGTT), serum lipid levels, including total cholesterol (Chol), triglycerides (TG), high-density lipoprotein (HDL), and low-density lipoprotein (LDL). Hyperinsulinemia was estimated by measurement of fasting insulin (FINS) and insulin area under the curve (IAUC). The extent of insulin resistance (IR) and hyperandrogenism was estimated by homeostasis model assessment (HOMA) and free androgen index (FAI) respectively.(1) Clinical phenotypes: the presence of obesity was 36.4% (70/192), among which 80.0% (56/70) were central obesity. Higher rates of acanthosis nigricans were observed in OB-PCOS group (35.7%, 25/70) compared with NOB-PCOS group (7.4%, 9/122; P0.01). Waist to hip ratio (WHR) was lower in group C than those in groups A and B (P0.05). (2) Endocrinology: FAI level was higher in OB-PCOS group than in NOB-PCOS group (P0.01), whereas LH/FSH ratio was lower in OB-PCOS group compared with NOB-PCOS group (P0.01). FAI level was higher in groups A and B than in group C (P0.01). SHBG, LH/FSH ratio did not differ between groups A, B, and C. (3) Metabolism: the prevalence of IR was 43.2% (83/192). A higher prevalence was observed in group OB-PCOS (82.8%, 58/70) compared with group NOB-PCOS (20.5%, 25/122; P0.01). FINS, HOMA-IR, glucose area under the curve (GAUC), IAUC and TG were higher in group OB-PCOS than in group NOB-PCOS (P0.01), whereas HOMA-IR, lipid profile did not differ between groups A, B, and C.The classification according to the revised 2003 consensus on diagnosis reflects the basic characteristics of PCOS; while the classification based on obesity shows the severity of hyperandrogenism and degree of IR, and thus has substantial significance for evaluation of metabolic complications.

To investigate the molecular mechanism of the influence of testosterone (T) on insulin sensitivity.Preadipocytes of the line 3T3-L1 and myoblasts of the line C2C12 were cultured to develop into mature adipocytes and skeleton muscle cells. Testosterone of the concentration of 10(-9) mol/l was added into the culture fluids for 0, 4, 8, 12, 24 and 40 hours. And testosterone of the concentrations increased by 10 times from 10(-12) mol/L, 10(-5) mol/L was added for 24 hours. Then the cell protein was extracted and the expression of insulin receptor substrate-1 (IRS-1) and glucose transporter 4 (GLUT4) in were measured by Western blotting.(1) Treated with T of the concentration of 10(-9) mol/L, the IRS-1 expression in the 3T3-L1 adipocytes increased along with the treatment time, peaked 12 hours later with a peak value 1.42 +/- 0.42 times that at the 0 h, and the values 4, 8, and 24 hours later were 1.13 +/- 0.03, 1.19 +/- 0.05, and 1.08 +/- 0.02 times that at the 0 h (all P0.05). The expression of IRS-1 in the C2C12 cells increased along with the treatment time of the testosterone of the concentration of 10(-9) mol/L too, peaked 24 hours later, with the values 8, 12, and 24 hours later 1.41 +/- 0.18, 1.53 +/- 0.14, and 1.50 +/- 0.14 times that at the 0 h (all P0.05). The GLUT4 expression value in the 3T3-L1 adipocytes increased since 4 hours after the treatment, peaked 24 hours after the treatment (3.22 +/- 0.10 that at the 0 h) (all P0.05). The GLUT4 expression value in the C2C12 cells increased since 4 hours after the treatment, peaked 24 hours after the treatment (5.17 +/- 1.06 that at the 0 h) (all P0.05). (2) The IRS-1 expression in the 3T3-L1 adipocytes and C2C12 cells increased dose-dependently along with the increase of the T concentration and peaked when the T concentration was 10(-9) mol/l (4.23 +/- 0.27 and 3.16 +/- 0.15 times that of blank controls respectively, both P0.05), and then turned to decrease. (3) The GLUT4 expression in the C2C12 cells increased along with the increase of the T concentration, peaked when the T concentration was 10(-7) mol/L (2.99 +/- 0.15 times that of the blank control, P0.05), and then remained at the similar level. (4) The GLUT4 expression in the 3T3-L1 adipocytes was highest when treated with 10(-11) mol/L testosterone (2.58 +/- 0.02 times that of the blank control, P0.05), and then decreased along with the increase of the T concentration (P0.05).Testosterone has bidirectional dose- and time-dependent effects on the cellular expression of IRS-1 and GLUT4, which increase with low dose and short time testosterone treatment and decrease with higher dose and longer time treatment.

To investigate and analyze the clinical presentation, hormonal profile, and metabolic abnormalities of obese women with polycystic ovary syndrome (PCOS).The data of the anthropometric measurements, clinical manifestations of hyperandrogenism, serum levels of luteinizing hormone (LH), follicle stimulating hormone (FSH), estradiol (E(2)), testosterone (T), prolactin (PRL), dehydro-epiandrosterone sulfate (DHEAS), sex-hormone-binding globulin (SGBG), and 17-oxyhydroprogesterone (17-OHP), fasting plasma glucose (FPG) and fasting insulin (FINS) detected after oral glucose tolerance test (OGTT), serum lipid levels, including total cholesterol (Chol), triglycerides (TG), high-density lipoprotein (HDL), and low-density lipoprotein (LDL), homeostasis model assessment (HOMA) and area under curve (AUC) so as to assess the insulin resistance (IR), free androgen index (FAI) to estimate the extent of hyperandrogenism, HOMA IS and DeltaI(30)/DeltaG(30) used to assess the function of islet beta cells, were collected from 192 women with PCOS, aged 24 +/- 6, that were divided into 2 groups according to the body mass index (BMI): Group A (n = 70) with the BMIor = 25 kg.m(-2) and Group B (n = 122) with the BMI2 5 kg.m(-2), and 65 age-matched bilateral tubal block factor infertile women served as controls that were divided into 2 groups as well: Group C (n = 25) with the BMIor = 25 kg.m(-2); and Group D (n = 79) with the BMI25 kg.m(-2), and underwent a cross-sectional study.(1) Clinical phenotype: The presence of obesity was 36.46% (70/192) of which 80.00% (56/70) was central obesity. The incidence of acanthosis nigricans was 17.18% (33/192), 35.71% in Group A and 6.56% in Group B. (P0.01). Groups A and C showed increased frequency of acanthosis nigricans compared with Group B. The value of FAI of Group A was 3.40 +/- 1.84, significantly higher than those of Group B (1.75 +/- 1.20) and Group C (1.65 +/- 0.90), (both P0.01). The LH/FSH ratio of Group B was 2.41 +/- 1.13, significantly higher than those of Groups A, C, and D (all P0.01). (2) Hormonal profile: The IR rate was 43.23% in the 192 patients, 82.86% in Group A and 20.49% in Group B. The LH and LH/FSH ratio were significantly higher in Group B than in Groups A, C, and D (all P0.01); T level was higher in Groups A and B than in Group C and D (all P0.05). SHBG was lower in Group A (108.70 +/- 81.35 nmol.L(-1)) and Group C (150.34 +/- 106.23 nmol.L(-1)) compared with Group B (192.49 +/- 98.30 nmol.L(-1)) and Group D (231.84 +/- 90.09 nmol.L(-1)) (P0.01 and P0.05). FAI level was 3.40 +/- 1.84 in Group A, significantly higher than those of Groups B (1.75 +/- 1.20), C (1.65 +/- 0.90), and D (0.84 +/- 0.45) (all P0.01). The FINS, TG, and HOMA IR of Groups A and C were all significantly higher than those of Groups B and D (all P0.01). The OGTT GAUC was significantly higher than those of Groups B, C, and D (P = 0.006, 0.028, and 0.031 respectively). (3) Metabolic profile: The prevalence of IR was 43.23% (83/192) with a higher prevalence rate in Group A (82.76%, 58/70) compared with Group B (20.49%, 25/122). The values of FINS, HOMA IR, GAUC, IAUC, and TG were all higher in Group A than in Group B (all P0.01). BMI and WHR were positively correlated with FAI and HOMA-IR (all P0.01), whereas negatively correlated with LH/FSH ratio (r = -0.345, -0.260, P0.01). There were no significant differences in HOMA-IS and DeltaI(30)/DeltaG(30) among these groups (all P0.05).Obese PCOS women have more severe hyperandrogenism, IR and hyperinsulinism than normal-weight PCOS women, which may have some health implications later in life.

To evaluate the laparoscopic operation for early ovarian malignant tumor with low risk.Ten patients with ovarian malignant tumor who underwent laparoscopic total hysterectomy, pelvic lymph nodes dissection, bilateral adnexectomy, ovarian aortic and vein high ligation, omentectomy, and additional appendectomy. Eleven patients with the same diagnosis who underwent operation by laparotomy were served as control group. The operation time, intraoperative blood loss, number of pelvic lymph nodes excised, and postoperative recovery were analyzed retrospectively.Frozen section method during operation proved the diagnosis of ovarian malignant tumor and cytological examination proved a negative result of the peritoneal irrigation liquid. The operation time was 298 min +/- 60 min for the laparoscopy group and 182 min +/- 43 min for the laparotomy group (P0.05). The intraoperative blood loss was 280 ml +/- 156 ml for the laparoscopy group and 346 ml +/- 170 ml for the laparotomy group (P0.05). The number of pelvic lymph node resected was 25 +/- 5 and 27 +/- 7 for the laparoscopy group and laparotomy group respectively (P0.05). The postoperative illness rate was 20.0% and 72.7% for the laparoscopy group and laparotomy group respectively (P0.01). Seven patients and 1 case in the laparoscopy group and laparotomy group left their beds 48 hours after operation (P0.05). The right obtuator nerve was injured and was sutured on 1 patient in the laparoscopy group.The whole procedure of total hysterectomy, bilateral adnexectomy, pelvic lymph node dissection, ovarian aortic and vein high ligation, omentectomy, and additional appendectomy may be performed under laparoscope in the treatment of early stage ovarian malignant tumor with lower risk. The laparoscopic operation has the advantage of less intraoperative bleeding, less morbidity and rapid recovery.

To investigate the role of laparoscopy in diagnosis and treatment of infertile women with endometriosis.Totally 314 infertile cases were diagnosed as having endometriosis by laparoscopy, and 58, 173, 68 and 15 cases were assigned to stage I, II, III and IV groups respectively according to the revised classification American Fertility Society (r-AFS). Laparoscopic treatment included excision of ovarian endometriosis lesions, lysis of adhesions, endocoagulation of pelvic endometriosis lesions with controlled heating (100 degrees C) and lavaging of the peritoneal cavity. The duration of follow-up after laparoscopic surgery was censored at 36 weeks. Women who became pregnant were followed up to 20 weeks' gestation. The U and chi(2) tests were used to determine significance of difference in the rate of pregnancy and spontaneous abortion between all clinical stages.Of all the 314 cases, 254 became pregnant within 36 weeks after surgery. The cumulative numbers of pregnancy were 50 (86.2%, 50/58), 141 (81.5%, 141/173), 52 (76.5%, 52/68) and 11 (73.3%, 11/15) in stage I-IV groups respectively. The accumulative pregnancy rates were, however, not significantly different among stages I-IV (P0.05). The accumulative pregnancy rate within 24 weeks after surgery (93.7%, 238/254) was higher than that within 25 - 36 weeks after surgery (6.3%, 16/254). Of 254 cases who were pregnant, 12 had miscarriage. There was no significant difference of miscarriage rate between all stages (P0.05). While the rate of miscarriage was higher within 12 weeks of gestation (83.3%, 10/12) than that of after 12 weeks of gestation (P0.05).Early lesions of endometriosis and pelvic factors for infertility can be found by laparoscopy. And pregnancy rate of endometriosis-associated infertility can be improved by laparoscopic surgery. To clean the menstrual blood pool and ablate peritoneal lesion with endocoagulation as completely as possible have significant importance for enhancement of fecundity in infertile women with endometriosis, especially for stage I-II cases.