胰高血糖素样肽1受体激动剂在肥胖型PCOS不孕患者中的应用进展

多囊卵巢综合征(polycystic ovary syndrome,PCOS)以高雄激素血症、稀发/无排卵、卵巢多囊样改变以及生育力下降为主要特征,是造成育龄期女性无排卵性不孕最常见的原因,且PCOS患者多伴有肥胖,而肥胖本身对女性生育力同样有负面影响.胰高血糖素样肽1(glucagon-like peptide-1,...     

胰高血糖素样肽-1类似物-Exenatide对多囊卵巢综合征大鼠的治疗作用

目的:探讨胰高血糖素样肽-1(GLP-1)对多囊卵巢综合征(PCOS)大鼠糖代谢及生殖内分泌变化的影响。方法:选择23日龄清洁级雌性SD大鼠80只,按照随机分组原则,分为实验组60只、对照组20只,实验组颈部皮下注射脱氢表雄酮(DHEA)建立PCOS模型,对照组在同期皮下注射油剂。予Exenatide和二甲双胍(metformin)药物干预模型大鼠,观察各组大鼠卵巢相对重量及光镜形态学改变,放射免疫分析法测定睾酮(T)、促黄体生成素(LH)、促卵泡生成素(FSH)、空腹血糖(FBG)、空腹血浆胰岛素(Fins)含量、并计算胰岛素抵抗指数(HOMA-IR)的变化。结果:Exenatide干预后:1卵巢重量显著降低,差异有统计学意义(P<0.01),卵巢颗粒细胞层增厚,多个黄体及不同发育阶段的卵泡。2血清T、LH、FBG、Fins及HOMA-IR显著降低,FSH显著升高,差异有统计学意义(P<0.01)。结论:GLP-1及其类似物-Exenatide在PCOS模型大鼠糖代谢方面及生殖内分泌变化中起部分调节作用,并与胰岛素抵抗有关。     

腹腔镜下卵巢部分皮质切除术治疗多囊卵巢综合征临床疗效观察

正多囊卵巢综合征(PCOS)主要表现为月经稀发、高雄激素血症、不孕、卵巢增大并呈多囊样改变,同时因其伴有肥胖、胰岛素抵抗、血脂异常等代谢异常,成为心脑血管疾病、Ⅱ型糖尿病发病的高危因素[1]。PCOS的发病原因复杂,致病机制尚不清楚。部分PCOS患者促排卵治疗效果不佳或促排卵失败,大大增加了治疗的难度[2]。本研究探讨腹腔镜下卵巢部分皮质切除术治疗肥胖型多囊卵巢综合征     

多囊卵巢综合征病因与发病机制的研究进展

<正>多囊卵巢综合征(PCOS)是育龄期妇女常见的生殖内分泌代谢疾病,发病率为5%~10%~([1])。其临床特点为与高雄激素血症相关的临床表现、不孕、长期无排卵、卵巢多囊样改变,常伴有胰岛素抵抗和肥胖。该病是育龄期妇女常见的、涉及诸多因素的终身性疾病,也是育龄妇女月经紊乱及不孕的原因之     

多囊卵巢综合征的发病概况

多囊卵巢综合征(polycystic ovary syndrome,PCOS)以稀发排卵或无排卵、雄激素分泌过多及卵巢多囊样改变为特征,是育龄期女性最常见的内分泌/代谢性疾病。患者不仅常出现不孕、如男性多毛、肥胖、月经紊乱,而且一系列代谢紊乱和远期并发症的发生风险增加,如高胰岛素血症、胰岛素抵抗、糖耐量异常、糖尿病前期和/或糖尿病、血压升高、血脂谱异常、心血管疾病、子宫内膜癌、乳腺癌、结肠癌等。因此,准确掌握人群中PCOS的发生情况,对于疾病的预防以及患者的生殖和远期健康均十分必要。     

达英-35治疗多囊卵巢综合征30例临床观察

多囊卵巢综合征（PCOS）是妇科内分泌常见的疾病，其临床特征是慢性无排卵、闭经或月经稀发、不孕、肥胖、多毛、卵巢多囊性增大。该病以持续无排卵、高雄激素血症为特征。     

多囊卵巢综合征患者饮食二三事

正多囊卵巢综合征(PCOS)是女性常见的内分泌紊乱性疾病之一,6%~10%的育龄妇女深受其影响。PCOS主要以不孕、多毛、痤疮和卵巢多囊样改变为主要特征,患者常伴有胰岛素抵抗、肥胖(以腹型肥胖多见)。肥胖型PCOS患者容易存在远期并发症,如并发2型糖尿病、高血压、血脂异常、脂肪肝、心血管疾病等,且某些肿瘤如子宫内膜癌、卵巢癌和乳腺癌等疾病的发生率高。饮食调控已成为肥胖     

PCOS早期病因——妊娠期母体雄激素过高

多囊卵巢综合征（polyeystic ovarysy ndrome，PCOS）是引起育龄妇女不孕的主要原因之一，临床上以月经稀发或闭经、不育、多毛、痤疮、肥胖和卵巢多囊性变为主要特征。近年来动物实验揭示出生前暴露于母体过高雄激素中，可导致雌性胎儿于青春期产生PCOS样改变，包括高雄激素血症、LH／FSH比值升高、高胰岛素血症和无排卵等。因此，有的学者提出妊娠飙母体雄激素过高可能是PCOS的早期致病因素。     

肥胖型PCOS患者的生物学特征和临床特征

多囊卵巢综合征（polycystic ovary syndrome,PCOS）是一种内分泌代谢紊乱综合征,临床表现高度异质性。肥胖是PCOS异质性临床表现之一,超过50%的PCOS患者超重或肥胖。肥胖型PCOS主要表现为高雄激素血症、中心型肥胖和糖脂代谢紊乱,非肥胖型PCOS主要表现为黄体生成激素（luteinizing hormone,LH）水平异常升高。尽管肥胖型和非肥胖型PCOS均存在内分泌代谢异常,然而肥胖可加重PCOS糖脂代谢紊乱;肥胖型PCOS还表现脂肪代谢的异常。综述肥胖型PCOS患者的临床特征、性激素水平、糖脂代谢特征,旨在为肥胖型和非肥胖型PCOS患者新的分型诊治提供参考。     

多囊卵巢综合征及卵巢打孔术

多囊卵巢综合征（polycystic ovarian syndrome,PCOS）是一种内分泌紊乱性疾病,是无排卵性不孕的主要病因。氯米芬（clomifene citrate,CC）是无排卵PCOS的首选一线促排卵治疗。随着腹腔镜手术的发展,腹腔镜下卵巢打孔术（laparoscopic ovarian drilling,LOD）已成为治疗无排卵PCOS广泛应用的微创治疗方式,当CC抵抗时LOD可作为首选促排卵方法。LOD术中需特别强调穿刺针应垂直卵巢,充分冲洗卵巢,预防医源性粘连。PCOS患者LOD术后,卵巢功能、月经及内分泌可得到明显改善。研究显示显著肥胖、雄激素过多症、长时间不孕可能预测LOD抵抗。术前黄体生成激素（LH）高水平LOD术后排卵妊娠的概率更高。LOD较促性腺激素治疗避免了多胎妊娠、卵巢过度刺激综合征（OHSS）等并发症。     

PAI-1基因4G/5G多态性与肥胖型多囊卵巢综合征的相关性研究

目的：通过研究肥胖型多囊卵巢综合征（PCOS）纤溶酶原激活物抑制因子1（PAI-1）基因启动子区4G/5G多态性的分布及其与胰岛素敏感性、PAI-1水平的相互关系,以期找到治疗肥胖型PCOS的新方法。方法：选取135例PCOS患者和124例正常对照者,计算体重指数（BMI）和腰臀比（WHR）;PCOS组又根据体质指数（BMI值）分出肥胖型与非肥胖型两组。用PCR方法测定PAI-1基因启动子区4G/5G基因多态性分布;ELISA法检测血浆PAI-1水平、空腹胰岛素（INS）、空腹血糖（G）,并计算胰岛素抵抗指数（Homa-IR）、胰岛素敏感指数（ISI）。结果：4G/5G基因多态性分布在PCOS组和正常对照组间有显著差异,PCOS组中4G/4G基因型频率47.41%高于正常对照组的16.13%,比较差异有统计学意义（P〈0.05）。PCOS组PAI-1水平高于对照组,肥胖型PCOS组PAI-1水平、WHR、空腹INS、Homa-IR均高于非肥胖组,比较差异均有统计学意义（P〈0.05）,但两组间4G/5G基因型分布无显著性差异。结论：PCOS尤其是肥胖型PCOS有较高的PAI-1水平。PAI-1基因启动子区4G等位基因可增加血浆PAI-1水平。PAI-1基因启动子区4G基因型频率高可能和PCOS发病有关,但与PCOS肥胖发病无关。抗PAI-1的研究可能提供一个新的治疗肥胖型PCOS的方法。     

肥胖与女性不孕症关系的研究进展

女性肥胖尤其是腹型肥胖可使其生育力降低,育龄期的肥胖妇女大多表现为月经失调、排卵稀发和雄激素过多.肥胖能够导致内分泌改变、影响血清性激素水平、改变其分泌方式和代谢途径及其在靶器官的作用水平,也是引起多囊卵巢综合征、高雄激素和代谢异常的关键因素.性激素分泌紊乱可能是引起肥胖并表现为不同类型和心血管代谢综合征的重要因素,故通过减轻体重可改善性激素紊乱的状况,降低雄激素水平,同时提高肥胖女性生育力.     

脑-肠轴与多囊卵巢综合征发病关系的研究进展

多囊卵巢综合征（polycystic ovary syndrome，PCOS）是一种常见的复杂内分泌紊乱性疾病，常伴有高雄激素血症、排卵障碍、胰岛素抵抗和肥胖。近年来临床上大量研究发现肥胖与PCOS关系密切，超过60%的PCOS患者表现为超重或肥胖。食欲调控和能量摄入对维持能量平衡和体质量至关重要。脑-肠轴是肠内细菌与大脑间的双向通信系统，胃肠道系统可通过产生脑肠肽参与到脑-肠互动中，主要包括生长激素释放多肽、胰高血糖素样肽-1、酪酪肽和胆囊收缩素。另外，肠道菌群的改变以及其与脑-肠轴之间的相互作用可能参与PCOS的发病。重点阐述脑-肠轴参与PCOS发病的可能机制及探讨与之相关的PCOS新型治疗方法。     

Evidence-based lifestyle and pharmacological management of infertility in women with polycystic ovary syndrome

Polycystic ovary syndrome (PCOS) is the most prevalent endocrine disorder in women of reproductive age and by far the most common cause of anovulatory infertility. Lifestyle change alone, and not in combination with pharmacological ovulation induction such as clomifene citrate or metformin, is generally considered the first-line treatment for the management of infertile anovulatory women with PCOS who are overweight or obese. Clomifene citrate should be considered as a first-line pharmacological therapy to improve fertility outcomes. Second-line medical treatments may include ovulation induction with gonadotropins (in clomifene citrate-resistant or clomifene citrate failure women) or laparoscopic ovarian drilling (in clomifene citrate-resistant women) or possibly with metformin combined with clomifene citrate (in clomifene citrate-resistant women). There is currently insufficient evidence to recommend aromatase inhibitors over that of clomifene citrate in infertile anovulatory women with PCOS in general or specifically in therapy-naive or clomifene citrate-resistant women with PCOS.     

Comparison of Dietary Intake and Physical Activity between Women with and without Polycystic Ovary Syndrome: A Review

Polycystic ovary syndrome (PCOS) is a prevalent endocrine disorder affecting women of reproductive age worldwide. In addition to deleterious effects on fertility imparted by PCOS, women with PCOS are at increased risk of obesity, diabetes, cardiovascular disease, depression, and certain cancers. Hormonal and metabolic aberrations in PCOS have the potential to influence dietary intake and physical activity levels. There are emerging global data that women with PCOS have different baseline dietary energy intakes compared with women without PCOS. These alterations in diet may exacerbate clinical symptoms and compound risk of chronic disease in patients. Few studies have compared baseline physical activity levels between women with and without PCOS. Although comparisons between studies are confounded by several factors, the data point to no differences in activity levels among PCOS and non-PCOS groups. This review provides an assessment of the current literature on baseline dietary intake and physical activity levels in women with PCOS. Future recommendations to strengthen research in this area are provided, given the implications to aid in the development of effective nutrition-focused interventions for PCOS.     

肥胖与非肥胖型多囊卵巢综合征患者血清C反应蛋白水平及意义

[目的]探讨肥胖与非肥胖型多囊卵巢综合征(PCOS)患者血清中C反应蛋白(CRP)的变化及与胰岛素抵抗的关系。[方法]将56例PCOS患者按体重指数(BMI)分为非肥胖PCOS组(22例)和肥胖PCOS组(34例),46例正常妇女分为非肥胖对照组(19例)和肥胖对照组(27例)。测定血清卵泡刺激素(FSH)、黄体生成素(LH)、泌乳素(PRL)、雌二醇(E2)、睾酮(T)、空腹血糖(FPG)、空腹胰岛素(FINS)、CRP浓度。[结果]PCOS组LH、LH/FSH、T、FINS显著高于对照组,胰岛素敏感指数(ISI)显著低于对照组,两组CRP水平无统计学差异。肥胖PCOS组和肥胖对照组血清CRP水平均显著高于各自的非肥胖组。血清CRP水平与BMI、FINS呈正相关,与ISI呈负相关。[结论]PCOS患者不存在慢性亚临床炎症,心血病风险仅限于合并肥胖或胰岛素抵抗的PCOS患者。     

瘦素与多囊卵巢综合征的研究进展

多囊卵巢综合征是一种病因未明的疾病,其临床常见代谢异常的表现,包括超重或肥胖,胰岛素抵抗,糖耐量减低或2型糖尿病,血脂异常和罹患心血管疾病的危险增加.瘦素是一种新型的脂肪源性的肽类激素,其与肥胖、不孕和胰岛素间有着密切的关系.肥胖的多囊卵巢综合征患者瘦素水平改变,瘦素与多囊卵巢综合征的胰岛素抵抗/高胰岛素血症及2型糖尿病间相互影响,多囊卵巢综合征血脂异常及并发心血管疾病的患者瘦素也有变化.所以,瘦素可能参与了多囊卵巢综合征的代谢,引起多囊卵巢综合征代谢异常.     

有生育要求的多囊卵巢综合征患者的治疗

多囊卵巢综合征(polycystic ovary syndrome,PCOS)是无排卵性不孕常见的原因,有多种非药物性和药物性方法帮助有生育要求的PCOS患者排卵并怀孕。一线疗法包括改变生活方式和克罗米芬治疗。对于克罗米芬抵抗的PCOS患者可采用二线疗法:使用促性腺激素(Gonadotrophin,Gn)、腹腔镜下卵巢打孔术(laparoscopic ovarian drilling,LOD)或者胰岛素增敏剂。如果治疗无效或合并其他不孕因素,可采用三线疗法——辅助生殖技术(assisted reproductive technology,ART)。本文重点介绍每种疗法的特点和治疗进展,以便为PCOS患者制定更加个性化的治疗方案提供参考。     

Dietary Intake,Eating Behavior,Physical Activity,and Quality of Life in Infertile Women with PCOS and Obesity Compared with Non-PCOS Obese Controls

To personalize lifestyle advice for women with polycystic ovary syndrome (PCOS) and obesity, detailed information regarding dietary intake, eating behavior, physical activity levels, and quality of life (QoL) may be useful. We aimed to investigate in a post-hoc cross-sectional analysis within a large multicenter randomized controlled trial in women with infertility whether there are significant differences in dietary intake (vegetables, fruits, sugary drinks, alcoholic beverages, savory snacks, and sweet snacks); eating behavior (emotional eating, external eating, and restricted eating); physical activity; and QoL between women with PCOS and obesity and non-PCOS obese controls. Participants were asked to complete the food frequency questionnaire (FFQ), the Dutch Eating Behavior Questionnaire (DEBQ), the Short QUestionnaire to ASsess Health-enhancing physical activity (SQUASH), and the 36-item Short Form Health Survey (SF-36) at study entry (PCOS: n = 170; non-PCOS: n = 321, mean BMI: 36). Linear and binary (multinomial) logistic regressions were used, and the analyses were adjusted for age, waist–hip circumference ratio, and homeostasis model assessment of insulin resistance (HOMA-IR). No statistically significant differences in dietary intake or physical activity were observed between the two groups. The overall score of emotional eating was 34.6 ± 11.2 in the PCOS group and 34.1 ± 11.3 in the non-PCOS group (p = 0.11). QoL scores (physical and mental) did not differ between PCOS and non-PCOS women. These findings suggest that infertile women with PCOS and obesity and infertile non-PCOS obese controls do not have different dietary habits and have similar mental and physical QoL.