PCOS患者血浆抵抗素与胰岛素抵抗的关系

目的探讨血浆抵抗素水平与多囊卵巢综合征（PCOS）患者胰岛素抵抗（IR）的关系。方法对35例PCOS患者及40例健康者（对照组）采用ELISA方法检测血浆抵抗素，放免法检测促黄体生成素（LH）、卵泡刺激素（FSH）及空腹胰岛素（FIN），氧化酶法检测空腹血糖（FPG），计算胰岛素抵抗指数（HOMA—IR）。结果PCOS组血浆抵抗素、LH、LH／FSH、FIN、HOMA—IR显著高于对照组（P均〈0．05）；PCOS组血浆抵抗素与FPG、FIN、HOMA—IR、LH及LH／FSH呈显著正相关（P均〈0．05）。结论抵抗素参与PCOS患者的IR发生过程，可作为一种新的敏感指标评价PCOS患者的IR程度。     

35例多囊卵巢综合征患者血清抑制素b与激活素α检测结果分析

用酶联免疫吸附法对35例多囊卵巢综合征（PCOS）患者（PCOS组）和35例不孕症患者（对照组）血清抑制素b（INHb）和激活素α（ACTα）水平进行检测。结果PCOS组INHb水平明显高于对照组，ACTα水平明显低于对照组（P均〈0．01）。提高血清INHb水平升高及ACTα水平降低可能参与了PCOS的发生；临床可根据PCOS患者血清INHb和ACTα水平制定治疗方案。     

关注多囊卵巢综合征与胰岛素抵抗

多囊卵巢综合征（PCOS）患者无论是否肥胖，均存在胰岛素抵抗（IR），可表现为高胰岛素血症和糖代谢异常。PCOS患者不仅存在IR，而且有胰岛β细胞功能障碍。PCOS患者IR的发生与胰岛素受体后信号通道缺陷有关。治疗措施包括改善不良的生活方式、减轻体重、二甲双胍等。     

罗格列酮联合枸橼酸氯米芬对多囊卵巢综合征伴假性黑棘皮病患者的疗效研究

多囊卵巢综合征（PCOS）是一种常见的内分泌紊乱性疾病，发病率约占育龄妇女的5％～10％。PCOS患者普遍存在胰岛素抵抗和高雄激素血症，由此导致糖、脂代谢异常。假性黑棘皮病（AN）是一种胰岛素抵抗、高胰岛素血症、高雄激素血症的皮肤特征性改变。在不同的胰岛素抵抗综合征中常常伴有假性黑棘皮病。本研究观察新型胰岛素增敏剂罗格列酮联合枸橼酸氯米芬治疗PCOS伴假性黑棘皮病的疗效，及其对胰岛素抵抗的影响。     

胰岛素抵抗和多囊卵巢综合征

多囊卵巢综合征（polycystic ovarian syndrome，PCOS）是育龄期妇女不孕的常见原因，发病率为6％～80A，临床表现为高雄激素血症或雄激素过多症伴排卵过少。国外研究显示PCOS患者胰岛素抵抗（IR）发生率为50％～70％，提示IR在PCOS的发病中扮演了重要角色。本文总结就胰岛素抵抗与多囊卵巢综合征的关系进行综述。     

多囊卵巢综合征与胰岛素抵抗

多囊卵巢综合征（PCOS）是妇女最常见的一种内分泌紊乱和糖代谢异常的综合征，其发生率占育龄妇女的5％～10％。而胰岛素抵抗（IR）是指胰岛素靶组织（如骨胳肌、脂肪组织、肝脏等）对胰岛素敏感性降低，对葡萄糖的利用降低及抑制肝葡萄糖输出的作用减弱。近年来许多研究发现，PCOS可能与高胰岛素血症和IR有关。而胰岛素抵抗和高胰岛素血症是PCOS和2型糖尿病的共同表现，且胰岛素敏感性下降均为35％～40％，但是卵巢功能障碍仅存在于PCOS患者，而不常见于2型糖尿病患者。这表明PCOS患者卵巢本身的糖代谢异常和胰岛素抵抗对卵巢功能改变更重要。     

多囊卵巢综合征合并代谢综合征患者血清AMH水平、窦卵泡计数变化及其意义

目的 探讨多囊卵巢综合征（PCOS）合并代谢综合征患者血清抗米勒管激素（AMH）水平及窦卵泡计数（AFC）变化及其临床意义。方法 选择PCOS合并代谢综合征患者130例（观察组）、单纯多囊卵巢综合征患者65例（对照组），采集所有研究对象外周静脉血，离心留取血清，检测血清AMH、空腹血糖（FPG）、空腹胰岛素（FINS）、TG、HDL并计算胰岛素抵抗指数（HOMA-IR），于月经第1～5天通过彩色超声诊断仪检测AFC。分析PCOS合并代谢综合征患者血清AMH水平及AFC与糖脂代谢指标的关系以及二者之间的关系。采用受试者工作特征（ROC）曲线分析血清AMH水平及AFC对PCOS合并代谢综合征的预测效能。结果 观察组与对照组血清AMH水平分别为（15.3±3.1）、（5.8±1.6）ng/mL,AFC分别为24(15,32)、8(4,15)个，观察组血清AMH水平及AFC均显著高于对照组（t/Z分别为16.021、12.041,P均<0.01）。观察组FPG、TG、FINS、HOMA-IR均高于对照组，HDL低于对照组（P均<0.05）。PCOS合并代谢综合征患者血清AMH水平及...     

多囊卵巢综合征性激素水平检测

目的：探讨血清性激素各项检测指标与不同年龄段的多囊卵巢综合征（PCOS）患者的关系及其临床意义。方法：以月经周期正常的健康妇女为对照组,采用化学发光法测定30岁以下年龄组和30岁及以上年龄组PCOS患者促黄体生成素（LH）、促卵泡生成素（FSH）、泌乳素（PRL）、雌二醇（E2）、睾酮（TESTO）、孕酮（Prog）水平,通过统计学软件进行比较分析。结果：多囊卵巢综合征患者,30岁以下年龄组和30岁及以上年龄组LH高于对照组（P〈0．01）,E2高于对照组（P〈0．05）,TESTO高于对照组（P〈0．01）。30岁以下PCOS患者组和30岁及以上PCOS患者组各检测指标之间差异无统计学意义（P〉0．05）。结论：血清中LH,E2高水平及TESTO增高可能是多囊卵巢综合征的预示因子,高LH、高E2、高雄激素血症可能是引起PCOS发生的因素之     

血清AMH水平与PCOS患者内分泌功能变化的研究进展

多囊卵巢综合征（PCOS）是以内分泌紊乱、月经稀发、肥胖、卵巢小卵泡增多为临床表现的妇科常见疾病。抗苗勒管激素（AMH）作为转化生长因子β超家族的一员，是近年临床上最常用的评估卵巢储备功能的检验指标，可更加客观地反映卵巢窦卵泡数，评估PCOS患者卵巢多囊样改变的严重程度，AMH与PCOS患者内分泌改变息息相关。     

Diane－35治疗多囊卵巢综合征的相关研究

近年研究认为,高同型半胱氨酸（Hey）血症是心脑血管疾病的独立危险因素,而血Hey水平升高也与一系列不良妊娠结局的发生密切相关。临床和流行病学研究表明,多囊卵巢综合征（PCOS）患者远期并发心血管疾病的风险性升高,两者存在相关性。本研究通过观察PCOS患者在复方醋酸环丙孕酮（Diane-35）治疗前后相关内分泌、代谢的变化,初步探讨Diane－35治疗PCOS的有效性及安全性,并探讨血浆总Hey（tHey）与PCOS的相关性。     

The biological variation of insulin resistance in polycystic ovarian syndrome

Increased insulin resistance (IR) is a cardinal feature of overweight patients with polycystic ovarian syndrome (PCOS). However, there are no data on the variability of IR for subjects with PCOS. The biological variation of IR (homeostasis model assessment model) was assessed by measuring IR at 4-d intervals on 10 consecutive occasions in 12 overweight PCOS patients (median age, 28 yr; range, 18-31 yr) and 11 weight-matched control women having regular menses and without PCOS (median age, 30 yr; range, 19-33 yr). The distribution of IR was log Gaussian in PCOS and Gaussian distribution in the control group. The IR in PCOS subjects was significantly greater than in the controls [mean (range), 5.85 U (1-42.1) vs. 1.67 U (0.48-3.49); P = 0.001]. After accounting for analytical variation, the mean intraindividual variance was also substantially greater in PCOS patients than in controls (mean, 1.19 vs. 0.23). As a consequence, at any level of IR, a subsequent sample must rise by more than 322% or fall by more than 31% to be considered significantly different from the first. IR, measured using the homeostasis model assessment model, is significantly greater and more variable for overweight patients with PCOS. Therefore, this inherent variability needs to be accounted for in studies of IR in PCOS.     

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

Polycystic ovary syndrome (PCOS) is associated with hyperinsulinemia, insulin resistance (IR), increased risk of glucose intolerance, and type 2 diabetes. Family studies have indicated a genetic susceptibility to PCOS. The aims of this study were 1) to assess glucose tolerance status, gonadotropins, and androgens in first degree relatives of patients with PCOS; and 2) to assess IR in normal glucose tolerant (NGT) family members. One hundred two family members of 52 patients with PCOS [Mothers(PCOS) (n = 34; mean age, 46.5 yr; mean body mass index (BMI), 28.8 kg/m(2)), Fathers(PCOS) (n = 24; mean age, 50.4 yr; mean BMI, 27.5 kg/m(2)), Sisters(PCOS) (n = 19; mean age, 25.1 yr; mean BMI, 22.9 kg/m(2)), and Brothers(PCOS) (n = 25; mean age, 23.7 yr; mean BMI, 22.5 kg/m(2))] and 82 unrelated healthy control subjects without a family history of diabetes or PCOS (4 age- and weight-matched subgroups, i.e. Control(MothersPCOS), Control(FathersPCOS), Control(SistersPCOS), and Control(BrothersPCOS)) were studied. Glucose and insulin (at baseline and during a 75-g, 2-h oral glucose tolerance test) were measured. IR was assessed by fasting insulin (FI), fasting glucose to insulin ratio (FGI), homeostatic model assessment (HOMA IR), and area under the curve for insulin during the oral glucose tolerance test (AUC(insulin)) in NGT Mothers(PCOS), Fathers(PCOS), Sisters(PCOS), Brothers(PCOS), and matched control subgroups. Including the prestudy-diagnosed 3 mothers and 2 fathers with diabetes, diabetes and impaired glucose tolerance (IGT) were noted in 16% and 30% of Mothers(PCOS) and 27% and 31% of Fathers(PCOS), respectively. There was no diabetes in Sisters(PCOS) and Brothers(PCOS). IGT was found in 5% of Sisters(PCOS). Impaired fasting glucose was found in 3% of Mothers(PCOS) and 4% of Brothers(PCOS). The analysis of NGT family members showed that Mothers(PCOS) had higher FI (P < 0.05), HOMA IR (P < 0.05), and AUC(insulin) (P < 0.01) and lower FGI (P < 0.05) than Control(MothersPCOS), whereas all IR parameters were comparable between Fathers(PCOS) and their matched control subgroup. Sisters(PCOS) had higher FI (P < 0.05), HOMA IR (P < 0.01), and AUC(insulin) (P < 0.05) and lower FGI (P < 0.01), and Brothers(PCOS) had higher AUC(insulin) (P < 0.01) than their matched control subgroups, respectively. Mothers(PCOS) had higher testosterone levels than Control(MothersPCOS) (P < 0.01 and P < 0.05 for pre- and postmenopausal women, respectively). Sisters(PCOS) had higher LH (P < 0.01), testosterone (P < 0.001), androstenedione (P < 0.01), and dehydroepiandrosterone sulfate (P < 0.05) levels than Control(SistersPCOS). There was no difference in gonadotropin and androgen levels in Fathers(PCOS) compared with Control(FathersPCOS) or in Brothers(PCOS) compared with Control(BrothersPCOS). Our results suggest that 1) first degree relatives of patients with PCOS may be at high risk for diabetes and glucose intolerance; 2) NGT female family members have insulin resistance; and 3) mothers and sisters of PCOS patients have higher androgen levels than control subjects. We propose that the high risks of these impairments warrant screening in first degree relatives of patients with PCOS.     

The management of insulin resistance in polycystic ovary syndrome.

Polycystic ovary syndrome (PCOS) has reproductive and metabolic implications. Insulin resistance (IR), secondary to genetic and lifestyle factors, is integral in the pathogenesis, metabolic, clinical features and the long-term sequelae in the majority of people with PCOS. Therapeutic strategies targeting IR in PCOS ameliorate clinical features and might reduce long-term sequelae including diabetes. The mainstay for improving IR is lifestyle change; however, feasibility and sustainability remain concerns. In PCOS, metformin reduces IR, improves ovarian function, regulates cycles, lowers androgens, improves clinical hyperandrogenism and potentially improves fertility. Metformin is also likely to delay diabetes onset and has a role in PCOS in those at high risk of diabetes; however, further research is needed to clarify specific target subgroups and clinical indications.     

Decreased insulin receptor (IR) autophosphorylation in fibroblasts from patients with PCOS: effects of serine kinase inhibitors and IR activators

Insulin resistance is characteristic of many patients with polycystic ovary syndrome (PCOS). Several studies have suggested that a decrease in insulin receptor (IR) autophosphorylation is a significant component of this resistance. In this study, we have used a highly sensitive ELISA to measure IR tyrosine phosphorylation in fibroblasts from patients with PCOS and healthy control women. After the stimulation of intact fibroblasts with insulin, IR tyrosine phosphorylation in cells from the PCOS patients was decreased by approximately 40% when compared with controls. However, when IR were first immunocaptured from fibroblasts and then stimulated with insulin, neither basal nor insulin-stimulated IR autophosphorylation was different between the two groups, suggesting that a factor independent of the IR was involved. To examine the role of increased serine kinase activity in decreased IR autophosphorylation in PCOS, fibroblasts from PCOS patients were pretreated with inhibitors of serine kinases before insulin stimulation. Pretreatment with H7, a nonspecific protein kinase inhibitor, completely reversed the decrease in insulin-stimulated IR autophosphorylation. Pretreatment with H89, an inhibitor of protein kinase A, partially reversed this function, whereas pretreatment with G?6983, an inhibitor of protein kinase C, was without effect. We next studied the effects of two small molecule activators of the IR tyrosine kinase: TLK16998 and Merck L7. Both TLK16998 and Merck L7 were able to reverse the impaired insulin-stimulated IR autophosphorylation. In summary, a factor(s) extrinsic to the IR cause impaired IR signaling in fibroblasts from patients with PCOS. Reversal of the impaired IR signaling by inhibitors of serine kinase activity suggests that serine kinase-mediated pathways may be involved in the insulin resistance. Moreover, the observation that TLK16998 and Merck L7 improved IR tyrosine phosphorylation in fibroblasts from patients with PCOS suggests that specific pharmacological therapies might be developed to treat the insulin resistance in PCOS.     

The impact of intensified exercise training on insulin resistance and fitness in overweight and obese women with and without polycystic ovary syndrome

Objective To evaluate mechanisms of insulin resistance (IR) in overweight and obese women with and without polycystic ovary syndrome (PCOS) and explore relationships between IR, fitness and body mass index (BMI) at baseline and following exercise intervention. Design Prospective controlled intensified exercise intervention study. Patients A total of 20 overweight (BMI > 25 kg/m²) and obese (>30 kg/m²), reproductive‐aged PCOS women and 13 non‐PCOS overweight, healthy controls of comparable BMI and age were studied at baseline. Measures were repeated in 13 PCOS and eight control women following three 1‐h exercise sessions per week over 12 weeks. Measurements Insulin resistance was measured by glucose infusion rate on euglycaemic hyperinsulinaemic clamp, and fitness was assessed by VO_2max. Results At baseline, PCOS women were 46% more insulin resistant than controls (175·6 vs 257·2 mg/m²/min, P < 0·05) with IR independently associated with VO_2max and BMI in the PCOS group only (P < 0·01). Postexercise IR improved across both groups (P < 0·01). In PCOS women, IR improved by 16% (P < 0·05) but was not restored to the same level as controls (P < 0·05). Improvement in IR and in VO_2max was related to the PCOS group (r² = 0·85, P < 0·05), yet change in IR and in fitness was not related. No associations were found in controls. Conclusions While intensified exercise improves IR in PCOS women, a higher IR persisted following exercise in PCOS women, and a clear relationship between improved IR and improved fitness was not found. Therefore, other mechanisms of, and therapies for, IR must be explored in PCOS as IR remains higher than observed in non‐PCOS controls.     

多囊卵巢综合征与胰岛素抵抗

多囊卵巢综合征(PCOS)是育龄妇女常见的内分泌失调性疾病.胰岛素抵抗是其发生、发展的重要病理生理机制.近年来,PCOS患者胰岛素抵抗具体的分子机制得到了深入研究,涉及胰岛素的分泌、代谢和各种脂肪因子等.本文即对PCOS患者胰岛素抵抗分子机制的研究进展作一综述.     

多囊卵巢综合征与胰岛素抵抗

多囊卵巢综合征(PCOS)是育龄妇女常见的内分泌失调性疾病.胰岛素抵抗是其发生、发展的重要病理生理机制.近年来,PCOS患者胰岛素抵抗具体的分子机制得到了深入研究,涉及胰岛素的分泌、代谢和各种脂肪因子等.本文即对PCOS患者胰岛素抵抗分子机制的研究进展作一综述.     

多囊卵巢综合征与胰岛素抵抗

多囊卵巢综合征(PCOS)是育龄妇女常见的内分泌失调性疾病.胰岛素抵抗是其发生、发展的重要病理生理机制.近年来,PCOS患者胰岛素抵抗具体的分子机制得到了深入研究,涉及胰岛素的分泌、代谢和各种脂肪因子等.本文即对PCOS患者胰岛素抵抗分子机制的研究进展作一综述.     

多囊卵巢综合征与胰岛素抵抗

多囊卵巢综合征(PCOS)是育龄妇女常见的内分泌失调性疾病.胰岛素抵抗是其发生、发展的重要病理生理机制.近年来,PCOS患者胰岛素抵抗具体的分子机制得到了深入研究,涉及胰岛素的分泌、代谢和各种脂肪因子等.本文即对PCOS患者胰岛素抵抗分子机制的研究进展作一综述.     

多囊卵巢综合征与胰岛素抵抗

多囊卵巢综合征(PCOS)是育龄妇女常见的内分泌失调性疾病.胰岛素抵抗是其发生、发展的重要病理生理机制.近年来,PCOS患者胰岛素抵抗具体的分子机制得到了深入研究,涉及胰岛素的分泌、代谢和各种脂肪因子等.本文即对PCOS患者胰岛素抵抗分子机制的研究进展作一综述.