多囊卵巢综合征患者血清中瘦素水平与胰岛素抵抗关系的研究

目的探讨多囊卵巢综合征（PCOS）患者血清中瘦素（Leptin）与胰岛素抵抗的关系。方法测定了56例PCOS患者和30例正常妇女血清中的瘦素、血糖和胰岛素水平；用胰岛素抵抗指数（IR）和胰岛素敏感指数（ISI）以及胰岛素曲线下面积（AUC）作为评价患者胰岛素抵抗的指标，相关性分析探讨瘦素与胰岛素抵抗的关系。结果PCOS组患者血糖、胰岛素及Leptin水平明显高于对照组（P〈0．05）；PCOS纽中瘦素与FINS（r=0．655，P〈0．0I）、IR（r=0．442，P〈0．01）、AUC（r=0．520，P〈0．01）、ISI（r=0．458，P〈0．05）均呈正相关关系。结论瘦素可能参与PCOS发生、发展有关，PCOS患者血清中瘦素水平与胰岛素抵抗存在一定的相关性。     

多囊卵巢综合征患者胰岛素、雄激素分析

目的 探讨多囊卵巢综合征(PCOS)患者胰岛素及雄激素分泌特征.为PCOS的正确诊断、合理治疗提供依据.方法 随机选择PCOS患者100例,其中有胰岛素抵抗79例,无胰岛素抵抗21例;高雄激素血症57例,无高雄激素血症43例.结果 ①与无胰岛素抵抗者比较,有胰岛素抵抗者BMI、空腹和服糖后30、60、120min血糖及胰岛素明显升高;②与无高雄激素血症者比较.高雄激素血症者空腹及服糖后60min胰岛素水平明显升高.胰岛素敏感指数明显降低.而胰岛素抵抗指数明显升高.雌二醇(E2)、黄体生成素(LH)、睾酮(T)明显升高.结论 PCOS患者胰岛素抵抗与高雄激素血症具有相关性.     

多囊卵巢综合征高雄激素血症患者瘦素水平的检测及评价

目的探讨多囊卵巢综合征高雄激素血症进行患者瘦素(Leptin)水平及其与睾酮(T)、体重指数(BMI)的关系.方法采用放射免疫分析法(RIA)检测53例PCOS患者血清瘦素水平,其中非肥胖组PCOS患者36例,正常对照30例;肥胖组PCOS患者17例,正常对照20例.结果肥胖组及非肥胖组PCOS高雄激素血症患者血清瘦素水平均明显高于相当体重指数的正常对照组,有显著差异(p均＜0.01);两组瘦素水平分别与其睾酮水平进行相关性分析,均显著正相关(r=0.51,p＜0.01和r=0.58,p＜0.01);非肥胖组PCOS患者血清瘦素水平与其BMI相关分析显示,无相关性;肥胖组PCOS患者血清瘦素水平与其BMI进行相关分析,显著正相关(p=0.56,p＜0.01).结论高瘦素血症是PCOS患者的内分泌特征之一,PCOS高雄激素血症的形成与高瘦素水平有关;超重或肥胖的PCOS高雄激素血症患者存在瘦素抵抗现象.     

多囊卵巢综合征血清学指标检测的临床应用

多囊卵巢综合征（PCOS）是育龄妇女最常见的生殖内分泌紊乱疾病,主要表现为月经失调、排卵障碍、不孕和肥胖等,常伴有高雄激素血症、高胰岛素血症和胰岛素抵抗[1-2]。关于PCOS的发病机制尚未完全阐明,瘦素（leptin）是近年来发现的一种由脂肪组织分泌的蛋白类激素,有研究发现其可能参与多系统的调控,其中包括对生殖系统的调控[3]。本文对患者血清胰岛素（INS）、leptin及睾酮（T）、卵泡刺激素（FSH）、     

瘦素与多囊卵巢综合征的相关分析

目的探讨血清中瘦素（Leptin）水平与多囊卵巢综合征（PCOS）的关系。方法采用免疫化学发光法检测68例PCOS患者和32例正常妇女血清中的廋素、性激素水平,同时进行糖耐量及胰岛素释放试验。结果 PCOS组血清瘦素水平明显高于对照组（P〈0.05）;PCOS组与对照组相比,除E2水平无显著性差异（P〈0.05）外,其余各项LH、T、PRL、FSH、A4差异显著（P〈0.05）;PCOS组中非肥胖与肥胖组间,除了T、A4差异显著（P〈0.05）外,其余指标差异均无统计学意义（P〈0.05）;PCOS组中瘦素与FINS（r=0.726,P〈0.01）、IR（r=0.631,P〈0.01）、AUC（r=0.518,P〈0.01）、ISI（r=0.663,P〈0.05）均呈正相关关系。结论瘦素可能参与PCOS的发生、发展,并与胰岛素抵抗、高胰岛素血症密切相关。     

多囊卵巢综合征大鼠模型诱导的实验研究

目的建立多囊卵巢综合征（PCOS）大鼠模型。方法通过皮下埋置17-炔诺酮硅胶棒联合皮下注射HCG（Bogovich法）诱导PCOS大鼠模型。测定血清睾酮（T）空腹血糖（FPG）及胰岛素（FIns）水平。结果模型组胰岛素抵抗指数（Homa-IR）、FPG、Fins及T水平均高于对照组,24dPCOS大鼠模型构建成功。结论 Bogovich法诱导的PCOS大鼠模型存在高雄激素水平及代谢异常,是研究PCOS发病机制的理想动物模型。     

2型糖尿病患者血清瘦素水平及临床意义

目的：观察2型糖尿病（DM2）患者血清瘦素（leptin）水平及其与肥胖、血糖、血脂的关系。方法：采用放射免疫分析（RIA）测定42例DM2患者和38例正常对照组的血清leptin水平。结果：DM2组血清leptin水平明显高于对照组（P〈0．01）;血清leptin与体重指数（BMI）、血清胰岛素（INS）、总胆固醇（TC）、甘油三酯（TG）、脂蛋白LDL-C呈正相关。结论：DM2患者的高leptin血症与肥胖、血脂异常及胰岛素抵抗（IR）密切相关。     

miRNA-21在多囊卵巢综合征患者中的临床诊疗意义

目的探究mi RNA-21在PCOS患者中的临床诊疗意义。方法选择在我院妇产科检查的PCOS患者24例,其中合并肥胖患者13例。随机选取26例经诊断无雄激素过多或排卵功能异常的健康对照女性,其中有一半人群肥胖。本次研究将分为PCOS患者的观察组、女性健康对照组。所有入组的患者首先检测睾酮、雄烯二酮、雌激素、胆固醇、血糖、胰岛素和hs-CRP生化指标。q RT-PCR检测外周血mi RNA-21的表达水平。结果观察组和对照组的体重正常或肥胖患者,睾酮和雄烯二酮显著高于对照组患者(P0.05)。同时,观察组肥胖患者雌激素水平明显低于对照组肥胖患者(P0.05),而胰岛素和hs-CRP高于对照组肥胖患者(P0.05)。另外,观察组肥胖患者mi RNA-21外周血表达水平明显高于对照组肥胖患者(P0.05)。结论 PCOS患者高雄激素和肥胖相关,且促进外周血mi RNA-21的表达。雄激素特别是睾酮在mi RNA对PCOS患者的疾病发展过程中起到重要的作用。     

多囊卵巢综合征妇女激素与血脂水平的相关性研究

本文以34例PCOS妇女和20例正常月经周期妇女为研究对象,通过测定两组激素和血脂水平,了解两组血清激素和血脂的差别。同时,应用逐步回归方法,建立了Tch和HDLc的回归模型。结果表明PCOS组LH、LH/FSH、睾酮明显高于对照组(P<0.05),而E_2低于对照组黄体期水平(P<0.05)。空腹血清胰岛素与Tch高于对照组,而HDLc低于对照组(P<0.05)。PCOS妇女Tch和HDLc分别与胰岛素和睾酮呈线性关系。由此,推测PCOS妇女的高胰岛素和高雄激素水平可能分别是致Tch升高和HDLc降低的原因之一。从而为防止PCOS妇女心血管疾病危险性提供了发病学基础。     

PCOS患者血脂、激素、糖耐量和胰岛素抵抗指数及其与BMI、GAUC的相关性分析

目的 分析多囊卵巢综合征(PCOS)患者血脂、性激素、糖耐量和胰岛素抵抗指数及其与体重指数(BMI)、血糖曲线下面积(GAUC)的相关性.方法 将辽阳市第三人民医院60例PCOS患者作为研究对象,其中非胰岛素抵抗患者(31例)为对照组,胰岛素抵抗患者(29例)为研究组.比较两组激素、血脂、胰岛素抵抗指数和糖耐量的情况,并通过Pearson相关性分析胰岛素抵抗指数与胰岛素抵抗患者BMI、GAUC的关系.结果 相比对照组,研究组患者BMI、甘油三酯和高密度脂蛋白(HDL)的水平均明显升高,差异均有统计学意义(均P＜0.05),而两组患者总胆固醇和低密度脂蛋白(LDL)水平的比较,均无统计学意义(均P＞0.05);两组患者黄体生成素、雌二醇及卵泡刺激素水平的比较,均无明显差异(均P ＞0.05);相比对照组,研究组胰岛素抵抗指数、空腹血糖、空腹胰岛素及GAUC的水平均显著升高,差异均有统计学意义(均P＜0.05);PCOS胰岛素抵抗患者的胰岛素抵抗指数与BMI、GAUC均存在显著相关性(均P＜0.01).结论 PCOS胰岛素抵抗患者BMI、甘油三酯、HDL、胰岛素抵抗指数、空腹血糖及GAUC均明显升高,并且胰岛素抵抗指数与BMI、GAUC均存在显著的正相关关系,提示提高体重与葡萄糖耐量可能会增加PCOS胰岛素抵抗患者发病的可能性.     

两种SD大鼠多囊卵巢综合征模型的比较研究

目的比较两种SD大鼠多囊卵巢综合征动物模型的建模效果。方法建立两种PCOS动物模型。观察各组大鼠卵巢形态学、性激素及空腹血糖和胰岛素的变化。结果DHEA建模组大鼠的体重显著低于对照组（P〈0．05）;hCG建模组大鼠卵巢重量和体积均显著高于对照组（P〈0．05）。两建模组大鼠卵巢卵泡多呈囊性扩张,颗粒细胞层数减少,卵泡膜细胞、间质细胞增生。两建模组大鼠血清T、FINS、FBG和HOMA指数均显著高于对照组（P〈0．05）;DHEA建模组LH水平较对照组无显著性差异;hCG建模组大鼠血清LH、LH／FSH比值均显著高于对照组（P〈0．05）。DHEA建模组FSH水平显著高于对照组（P〈0．05）。结论利用hCG诱导SD幼年雌性大鼠出现了与PCOS患者极为相似的卵巢病理改变及LH、雄激素水平升高和胰岛素抵抗等典型内分泌变化,其建模效果优于DHEA。     

多囊卵巢综合征IGF-Ⅰ、IGFBP-1相关因素探讨

目的探讨多囊卵巢综合征(PCOS)患者胰岛素生长因子-Ⅰ(IGF-Ⅰ)、胰岛素生长因子结合球蛋白-1(IGFBP-1)水平与肥胖、性激素、糖代谢各项指标之间的关系。方法测定31例PCOS研究组和29例健康对照组IGF-Ⅰ、IGFBP-1水平及肥胖、性激素、糖代谢各项指标,比较两组间差异;分析研究组IGF-Ⅰ、IGFBP-1水平与其他各项指标之间相关性。结果研究组IGFBP-1,性激素结合球蛋白(SHBG)低于对照组,体重指数(BMI),臀围比值(WHR),多毛评分(F-G评分),黄体生成素(LH),黄体生成素/卵泡刺激素(LH/FSH),总睾酮(T),游离睾酮(FT),雄烯二酮(A2),硫酸脱氢表雄酮(DHEAS),空腹胰岛素(FINS),胰岛素抵抗指数(HomaIR)高于对照组,差异均有显著性(P0.001～0.05),IGF-Ⅰ,FSH,雌二醇(E2),17羟孕酮(17-OHP),泌乳素(PRL),空腹血糖(FBG)差别无显著性(P0.05)。研究组中IGFBP-1与BMI呈负相关(r=-0.372,P0.05),与FINS呈负相关(r=-0.481,P0.01),与SHBG呈正相关(r=0.504,P0.01),IGF-Ⅰ与各指标之间无明显相关性。结论 IGFBP-1与PCOS患者肥胖、空腹胰岛素水平密切相关。     

PCOS患者卵巢超声形态学改变与内分泌激素相关性的初步研究

目的探讨多囊卵巢综合征（PCOS）患者卵巢的形态学改变与内分泌激素的相关性。方法选择94例PCOS患者作为研究组,按体质量指数（BMI）分为肥胖型PCOS组（OB-PCOS）和非肥胖型PCOS组（NOB-PCOS）;同期选择69例有正常排卵的输卵管性不孕患者作为对照组,经阴道超声分别测量其卵巢总面积（A）,同时检测其黄体生成素（LH）、卵泡刺激素（FSH）、睾酮（T）、雌二醇（E2）、人体催乳素（PRL）水平,并分析其与A值之间的相关性。结果 1.PCOS组卵巢总面积明显高于对照组（P〈0.001）,LH、LH/FSH以及T水平较对照组明显升高,差异有统计学意义（P〈0.001）,FSH水平明显降低,差异有统计学意义（P〈0.05）;2.PCOS患者肥胖型组T水平较非肥胖型组升高,差异无统计学意义（P〉0.05）;3.相关性分析显示,PCOS组A值与T值呈正相关,差异有统计学意义（P〈0.05）。结论 PCOS的发病过程中,卵巢总面积的改变受内分泌激素的影响。     

PCOS患者血浆leptin和血清T、E2、FSH、LH、PRL检测的临床意义

目的：探讨多囊卵巢综合征（PCOS）患者血浆leptin和血清T、E2、FSH、LH、PRL水平的变化及临床意义。方法：应用放射免疫分析和发光法对31例PCOS患者进行了血浆leptin和血清T、E2、FSH、LH、PRL测定,并以正常妇女作对照。结果：PCOS患者血浆leptin和血清T、LH、PRL水平非常显著地高于正常妇女组（P〈0.01）,FSH、E2水平与正常妇女组比较无显著性差异（P〉0.05）,且血浆leptin水平与血清T、LH、PRL水平呈正相关（r=0.5784、0.5411、0.6082,P〈0.01）。结论：检测PCOS患者血浆leptin和血清T、E2、FSH、LH、PRL水平的变化与疾病的发生和发展密切相关。     

Hyperinsulinemia in polycystic ovary syndrome: relationship to clinical and hormonal factors

We analyzed the association between hyperandrogenism and hyperinsulinemia, and their relationship to body mass index, in a large series of patients with polycystic ovary syndrome (PCOS). A characteristic hormonal profile was sought in women with marked hyperinsulinemia. The patient group consisted of 73 women with PCOS, ranging in age from 16 to 29 years. The control group consisted of 34 healthy women with no evidence of hyperandrogenism, aged 19–30 years. None of the patients or control women had a body mass index above 27 kg/m². Follicle-stimulating hormone, luteinizing hormone, prolactin, testosterone, estradiol, androstenedione, dehydroepiandrosterone sulfate, sex hormone binding globulin, 17-hydroxyprogesterone, and free cortisol were determined by radioimmunoassay. The free testosterone index was calculated. The oral glucose tolerance test was used to analyze basal insulinemia, maximum insulin peak, and the insulinemia/glycemia index. In the group with PCOS body mass index was greater, free testosterone index was higher, and levels of dehydroepiandrosterone sulfate, testosterone, 17-hydroxyprogesterone (P < 0.001) and androstenedione (P < 0.05) were higher than in the control group. Of the insulin parameters, basal insulinemia, maximum insulin peak, and insulinemia/glycemia index were higher in the patient group (P < 0.001). In patients with marked insulinemia, free testosterone index was more markedly elevated, and gonadotrophin levels were normal. Our data confirm that a characteristic pattern of hyperinsulinemia is associated with PCOS. We found no causal relationship between hyperinsulinemia and androgen levels. A characteristic hormonal pattern was found in patients with marked hyperinsulinemia.Abbreviations BMI body mass index - 17OHP 17-hydroxyprogesterone - DHEAS dehydroepiandrosterone sulfate - FTI free testosterone index - I/G insulin/glucose ratio - OGTT oral glucose tolerance test - PCOS polycystic ovary syndrome - P_max maximun peak of insulin - SHBG sex hormone binding globulin - LH luteinizing hormone - FSH follicle-stimulating hormone     

多囊卵巢综合征妇女内源性胰岛素释放与睾酮反应的相关性研究

本研究以36例PCOS妇女和20例正常月经周期妇女为研究对象。通过测定激素基础水平,观察在糖耐量试验中胰岛素对糖负荷的反应和睾酮的变化以及分析体脂与胰岛素的关系。发现PCOS妇女有较高的空腹血糖水平、空腹血清胰岛素与空腹血清睾酮呈显著正相关(r=0.65,P<0.01)。在糖负荷期PCOS组血清胰岛素释放显著高于对照组(P<0.01),同时,总睾酮与总胰岛素呈正相关(r=0.69,P<0.01)。PCOS肥胖者总胰岛素对糖负荷的反应最大,对照非肥胖者反应最小(F=3.02,P<0.01)。PCOS妇女体脂百分率与空腹血清胰岛素呈正相关(r=0.523,P<0.05)。由此提示(1)PCOS妇女内源性胰岛素释放是PCOS雄激素增高的原因之一;(2)PCOS妇女体脂过多可能在PCOS的高胰岛素血症和胰岛素抵抗中起有部分作用。     

Influence of hypo- and hyperglycaemia on plasma leptin concentrations in healthy women and in women with polycystic ovary syndrome

BACKGROUND: Insulin resistance and obesity play an important role in the pathogenesis of polycystic ovary syndrome (PCOS). It is known that experimentally induced insulin resistance diminishes the stimulatory effect of insulin on leptin secretion. It is not yet known whether the long-term insulin resistance as found in PCOS patients alters the leptin response to hypo- and hyperglycaemia. METHODS: We induced hyper- and hypoglycaemia by glucose clamp technique in 7 patients with PCOS and 20 healthy controls. After a plasma glucose level of 8.8 mmol/l was reached, the plasma glucose level was reduced stepwise to 6.8, 4.8 and 2.8 mmol/l. RESULTS: The PCOS patients required lower glucose infusion rates to reach the glycaemic targets (P < 0.05). Serum insulin and C-peptide concentrations increased significantly during the clamp compared with the baseline in both groups (P < 0.001 for insulin, and P < 0.001, P < 0.005 for C-peptide control and PCOS, respectively) and increased significantly more in PCOS patients compared with the control group (both P < 0.05). Basal leptin levels were significantly higher in the PCOS group than in the control group (P = 0.005). In the controls, the leptin concentration increased significantly during the clamp (P < 0.001 for each glycaemic target), whereas in the PCOS group, leptin secretion increased only during hypoglycaemia (P = 0.04). CONCLUSIONS: Compared with the healthy controls, the response of leptin secretion to hyper- and hypoglycaemia was diminished in PCOS patients. Changes in leptin secretion seem not to be caused by hyper- and hypoglycaemia, but rather by hyperinsulinaemia. Reduced insulin sensitivity seems to be responsible for the diminished leptin response, which might contribute to the obesity found in PCOS patients.     

Polycystic ovary syndrome in men: Stein-Leventhal syndrome revisited

Polycystic ovary syndrome (PCOS), also referred to as Stein-Leventhal syndrome, is one of the most common endocrinopathies. It is characterized by hyperandrogenism, hyperinsulinemia, central obesity, polycystic ovaries, and anovulation. However, some of these manifestations, including the polycystic ovaries, are neither specific for the disorder, nor found in all affected individuals. PCOS appears to be due to one or more primary defects in the upstream gonadotropin/androgen and/or insulin pathway, with the polycystic ovaries being one of many downstream manifestations. Yet, the pathophysiology of PCOS is not completely elucidated. Since the primary defect underlying PCOS may be an upstream endocrine and/or metabolic disturbance, rather than a defect in the ovaries themselves, we hypothesize that this aberration can also arise in men and that the absence of polycystic ovaries in men with other stigmata of the disorder should not eliminate the diagnosis. Our hypothesis is supported by the observation that a genetic susceptibility to PCOS exists, and that PCOS-type manifestations are not limited to women. Indeed, male relatives may suffer from insulin resistance, obesity, diabetes mellitus, and cardiovascular disease. Therefore, recognition of this syndrome in men is important, since pharmacologic treatments identified for women with PCOS may alleviate metabolic problems related to insulin resistance and its sequelae in men with a similar underlying defect. We suggest that first-degree relatives of patients with PCOS should be examined not only for phenotypic features characteristic of PCOS but also for biochemical evidence of hyperinsulinemia and hyperandrogenism. In addition to examining these individuals for obesity, the women should be evaluated for hirsutism and the men should be screened for early-onset male-pattern alopecia and excess hairiness. Serologic evaluation should included the ratio of fasting levels of glucose to insulin, a glucose tolerance test, the free testosterone level and the sex hormone-binding globulin level. Finally, both male and female first-degree relatives of patients with PCOS should be tested for the underlying molecular defect(s) of this condition, once it is identified. As new treatments for PCOS emerge, e.g. insulin-sensitizing drugs, it will be important to determine if these treatments have beneficial effects on the metabolic symptoms and complications in all afflicted patients, regardless of gender.     

多囊卵巢综合征患者脂联素和C一反应蛋白与颈动脉内膜中层厚度的关系

目的观察多囊卵巢综合征(PCOS)患者血清脂联素(APN)水平和C一反应蛋白(CRP)浓度与颈动脉内膜中层厚度(IMT)的关系,探讨PCOS患者是否存在早期动脉粥样硬化。方法选择我院PCOS患者51例作为研究对象,分为肥胖组与非肥胖组,同期选择非PCOS患者50例作为对照,测定血清APN水平和CRP浓度及内分泌代谢指标,同时采用彩色多普勒显像仪测量颈总动脉IMT。结果 PCOS肥胖组及非肥胖组血清APN水平低于对照组(P<0.05),CRP浓度、颈动脉IMT均明显高于对照组(P<0.05)。PCOS肥胖组血清APN水平低于非肥胖组(P<0.05);PCOS肥胖组血清CRP浓度、IMT高于非肥胖组,差异有统计学意义(P<0.05)。相关分析显示PCOS组APN与CRP,IMT、HOMA-IR均有显著的负相关(P<0.05或P<0.01)。CRP与IMT、HOMA-IR具有显著的正相关(P<0.05或P<0.01)。结论 PCOS患者尤其伴有肥胖者血清脂联素水平降低,CRP浓度升高,胰岛素抵抗增加,IMT增加,可能存在早期动脉粥样硬化。炎症反应可能参与了PCOS患者尤其伴有肥胖者早期动脉粥样硬化的发生发展。