胰高血糖素样肽-1对多囊卵巢综合征的影响

多囊卵巢综合征（PCOS）是女性最常见的内分泌紊乱疾病,发病率为6％～10％.发病机制主要包括胰岛素抵抗、高胰岛素血症、糖耐量减低、肥胖以及慢性炎性反应状态等.胰高血糖素样肽／鄄1（GLP-1）及其受体激动剂通过与GLP-1受体特异性结合而发挥作用,能够改善PCOS患者胰岛素抵抗、降低体重、降低炎性反应因子的表达等,增加患者受孕几率,因此在治疗PCOS中有着广阔的应用前景.     

11β-羟类固醇脱氢酶1与胰岛素抵抗和多囊卵巢综合征

多囊卵巢综合征(PCOS)是育龄女性中常见的内分泌紊乱性疾病,主要以胰岛素抵抗和高雄激素血症为主要病理生理改变.PCOS患者中肥胖/代谢综合征的发生率显著高于正常人群.11β-羟类固醇脱氢酶1(11β-HSD1)在体内主要参与皮质酮和皮质醇之间的转换调节.11β-HSD1的表达和(或)活性增加,使局部皮质醇水平增加,影响胰岛素信号的转导,导致胰岛素抵抗和高胰岛素血症的发生.研究发现,11β-HSD1可能参与PCOS的发生、发展.     

多囊卵巢综合征研究新进展

多囊卵巢综合征(PCOS)是青春期和育龄妇女常见的一种主要累及生殖系统的慢性内分泌疾病.其发病机制涉及遗传、胰岛素抵抗、饮食、环境及精神心理等多种因素.其临床表现多变,主要包括高雄激素血症及胰岛素抵抗.PCOS的诊断标准有1990年美国国立卫生研究所(NIH)标准、2003年欧洲人类生殖与胚胎协会( ESHRE)/美国生殖医学会(ASRM)标准和2006年雄激素过多协会(AES)标准,都是根据专家会议共识制定的.治疗方法主要针对改善高雄激素血症和高胰岛素血症以恢复月经和排卵及改善内分泌代谢.     

胖和瘦的多囊卵巢综合征一样吗

多囊卵巢综合征（polycystic ovary syndrome,PCOS）是育龄妇女常见的内分泌代谢疾病,此人群中发病率介于8％ ～ 12％[1].PCOS临床异质性大,患者可以表现出月经紊乱、卵巢多囊、排卵障碍、多毛、痤疮以及糖脂等代谢异常[9].PCOS发病原因至今不清楚,已知受遗传和环境因素的双重影响[2].高雄激素血症和胰岛素抵抗、高胰岛素血症是PCOS的重要的病理生理改变.     

中西医对高胰岛素血症性闭经的认识与治疗概况

<正>闭经是多种因素引起的一种症状,其中包括多囊卵巢综合症(PCOS)II型中的高胰岛素血症。高胰岛素血症可引起排卵障碍,从而导致闭经。大部分人还可合并有肥胖、多毛、痤疮、不孕等症状。现将2004~2014年中西医对高胰岛素血症性闭经的认识与治疗综述如下。1中西医对疾病的认识1.1西医对高胰岛素血症的认识胰岛素抵抗(IR)和高胰岛素血症(HI)是PCOS患者基本的内分泌特征,发生率占PCOS患者的     

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。     

多囊卵巢综合征易感基因多态性的研究进展

多囊卵巢综合征（PCOS）是育龄期妇女常见的生殖内分泌和代谢紊乱疾病,在育龄妇女中发病率为7％左右[1],主要表现为高雄激素血症、月经紊乱、持续不排卵、多囊卵巢等临床特征.PCOS还有许多代谢方面的影响结果,包括肥胖风险增加、胰岛素抵抗、2型糖尿病、动脉粥样硬化的过早形成.PCOS发病机制至今尚不明了.有研究表明,PCOS发病可能是不同基因参与调控的遗传性内分泌疾病,因此,相关基因的研究现已成为热点.目前关注较多的是与高雄激素相关基因、胰岛素作用相关基因及慢性炎症因子基因等.现就PCOS易感基因多态性的研究进展做一综述.     

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.     

多囊卵巢综合征伴不孕子宫内膜的研究进展

多囊卵巢综合征(PCOS)是育龄妇女无排卵性不孕的主要原因之一.其主要内分泌特征为高雄激素血症、高胰岛素血症和胰岛素抵抗、LH水平和LH/FSH比值升高.目前的研究发现,即使对PCOS患者进行促排卵治疗,妊娠率仍相当低.因此,不孕的因素除了慢性不排卵外,还与子宫内膜局部环境的改变有关,其不正常的内分泌状况导致的不良子宫内膜环境对胚胎发育的影响引起研究者的普遍关注.目前,子宫内膜胰岛素受体表达已成为研究的热点.     

Incretin hormone secretion in women with polycystic ovary syndrome: roles of obesity, insulin sensitivity, and treatment with metformin

In normal subjects, the incretin hormones glucagon-like peptide-1 (GLP-1) and glucose-dependent insulinotropic polypeptide (GIP) are responsible for 70% of the insulin response during a meal; but in diabetic subjects and other insulin-resistant conditions, the incretin effect is impaired. Polycystic ovary syndrome (PCOS) is associated with insulin resistance, and the pathophysiologic mechanisms behind PCOS resemble those of type 2 diabetes mellitus; therefore, women with PCOS may have alterations in the incretin hormone response. Metformin is widely used in the treatment of both type 2 diabetes mellitus and PCOS. Metformin may exert some of its effect on glucose metabolism by increasing GLP-1 biosynthesis and secretion and thereby increasing the incretin effect. The objective of the study was to measure incretin hormone secretion in women with PCOS and to evaluate the effect of metformin treatment. Cross-sectional comparison of 40 women with PCOS (19 lean and 21 obese) and 26 healthy control women (9 lean and 17 obese) and longitudinal evaluation of the effects of 8 months of metformin 1000 mg twice daily in women with PCOS were performed. Plasma concentrations of GIP and GLP-1 were determined frequently during a 75-g glucose tolerance test, and insulin sensitivity was evaluated by the euglycemic hyperinsulinemic clamp. The incretin hormone response did not differ between subjects with and without PCOS. Subgroup analysis showed lower GIP (area under the curve [AUC]) levels in obese women with PCOS compared with obese control women (P < .05) and compared with lean women with PCOS (P < .05). Metformin increased GIP (AUC) and GLP-1 (AUC) in lean women with PCOS (P < .05), and a similar trend was seen in the obese women (P = .07). The GIP secretion is attenuated in obese women with PCOS, whereas treatment with metformin increases the levels of both GIP and GLP-1 in women with PCOS.     

The therapeutic effects of glucagon-like peptide-1 receptor agonists and metformin on polycystic ovary syndrome: A protocol for systematic review and meta-analysis

Background:Obesity and insulin resistance (IR) are common in polycystic ovary syndrome (PCOS), which contribute to reproductive and metabolic abnormalities. Metformin increases insulin sensitivity, but it is associated with unsatisfied benefits of weight loss. Recent studies have reported that glucagon-like peptide 1 (GLP-1) receptor agonists improve IR and reduce weight in women with PCOS. We conducted a systematic review and meta-analysis to compare the effects between GLP-1 receptor agonists and metformin, and between GLP-1 receptor agonist-metformin combination and GLP-1 receptor agonists in overweight/obese women with PCOS on anthropometric, metabolic, reproductive outcomes.Methods:Databases including PubMed, EMBASE, Web of Science, and Cochrane Library were selected to search for randomized controlled trials (RCTs) published in English up to March 2020. Eligible studies were identified according to the inclusion criteria. The primary outcomes included menstrual frequency, body mass index (BMI), total testosterone, and the homeostatic model assessment of insulin resistance. GRADE criteria were implemented to assess the quality of evidence for primary outcomes.Results:Seven RCTs were selected for analysis, comprising 464 overweight/obese women with PCOS. In the low-quality evidence, a meta-analysis demonstrated that GLP-1 receptor agonists showed better effects relative to metformin on the reduction of body mass index (mean difference − 1.72; 95% confidence interval −2.46 to −0.99, P < .001) and homeostatic model assessment of insulin resistance (standard mean difference −0.37; 95% confidence interval − 0.60,− 0.15, P = .001). Moreover, the combination therapy exhibited similar effects on primary outcomes relative to GLP-1 receptor agonist alone. GLP-1 receptor agonists were also found to be associated with lower abdominal girth compared to metformin. A meta-analysis of gastrointestinal discomfort showed no significant difference between GLP-1 receptor agonist and metformin therapies, and between the combination therapy and GLP-1 receptor agonist alone.Conclusions:GLP-1 receptor agonists appear to be more beneficial for weight loss and IR improvement compared to metformin for overweight/obese women with PCOS. However, the combination treatment displays comparable effects with GLP-1 receptor agonist alone. The incidence of gastrointestinal discomforts was similar in different groups. However, the quality of the body of evidence is “low.” Further prospective RCTs and cost-effectiveness analyses are also warranted to guide GLP-1 receptor agonists to treat women with PCOS.     

Secondary forms of polycystic ovary syndrome.

Hyperandrogenism and chronic anovulation are the most common endocrine disorders of premenopausal women. Most patients have polycystic ovary syndrome (PCOS), which is essentially benign, but might be associated with increased cardiovascular morbidity; PCOS is associated with specific endocrine and ultrasonographic features. Some patients exhibiting similar features to PCOS might have other underlying diagnoses, such as adrenal and ovarian steroidogenic deficiencies, adrenal and ovarian androgen-secreting tumours, other medical or endocrine disorders, and/or be on medications thought to cause PCOS, such as anti-epileptics. Unlike PCOS, some of these conditions can occasionally be life threatening and require prompt diagnosis and treatment. Here, we focus on these disorders, including their pathogenesis, and attempt to define the clinical and biochemical features that distinguish them from PCOS.     

PCOS remains a diagnosis of exclusion: a concise review of key endocrinopathies to exclude

Polycystic ovarian syndrome (PCOS) is a heterogenous disorder associated with clinical, endocrine and ultrasonographic features that can also be encountered in a number of other diseases. It has traditionally been suggested that prolactin excess, enzymatic steroidogenic abnormalities and thyroid disorders need to be excluded before a diagnosis of PCOS is made. However, there is paucity of data regarding the prevalence of PCOS phenotype in some of these disorders, whereas other endocrine diseases that exhibit PCOS‐like features may elude diagnosis and proper management if not considered. This article reviews the data of currently included entities that exhibit a PCOS phenotype and those that potentially need to be looked for, and attempts to identify specific features that distinguish them from idiopathic PCOS.     

Endocrine response determines the clinical outcome of pulsatile gonadotropin-releasing hormone ovulation induction in different ovulatory disorders

To accrue systematic information in different ovulatory disorders on the precise relationship among endocrine response, clinical outcome, and the occurrence of complications, we treated 114 patients with pulsatile GnRH (2.5-5.0 micrograms, iv, every 60 min) for 187 cycles and compared them to 20 normal menstrual cycles. Thirty of these patients had primary hypogonadotropic amenorrhea (PHA; 40 cycles), 33 had other forms of hypogonadotropic hypogonadism (HH; 55 cycles), and 51 had polycystic ovary syndrome (PCOS; 92 cycles). Daily blood samples were drawn for hormone determinations. In PCOS, 50 cycles were preceded by GnRH analog suppression. PHA treatment cycles were characterized by the reestablishment of a normal endocrine pattern, almost no dose-related endocrine differences, elevated ovulatory (93%) and conception rates (23%), and no multiple pregnancies. In the HH subjects the ovulatory (91%) and pregnancy rates (31%) were high; however, while the lower GnRH dose elicited a normal endocrine pattern, the 5-micrograms dose induced excessive folliculogenesis and high estradiol levels and was associated with most of the multiple pregnancies of this study (three of four). GnRH analog suppression was successfully used to avoid recurrence of ovarian over-stimulation in two HH subjects. Finally, GnRH analog suppression in PCOS permitted normalization of the follicular phase endocrine pattern, achievement of good ovulatory (76%) and pregnancy (28%) rates, and avoidance of multiple pregnancies; however, luteal phase steroid secretion was abnormal, and the abortion rate remained elevated (43%). Obesity was associated with a reduced ovulatory rate in PCOS, but not in hypogonadotropic, subjects. Thus, we can conclude that in pulsatile GnRH ovulation induction: 1) a profound hypogonadotropic condition, whether spontaneous as in PHA or induced with GnRH analogs as in other ovulatory disorders, is associated with optimal menstrual cycle restoration, high ovulatory and conception rates, and virtually absent risks of multiple pregnancy; 2) residual hypothalamic activity in HH may be responsible for supraphysiological pituitary-ovarian stimulation and result in multiple pregnancy unless a low GnRH dose (2.5 micrograms/bolus) or GnRH analog pretreatment is employed; 3) obesity does not affect treatment outcome in hypogonadotropic patients; and 4) the high spontaneous abortion rate in PCOS may be related to corpus luteum dysfunction.     

GLP-1 receptor agonists are growth and differentiation factors for pancreatic islet beta cells

Glucagon-like peptide-1 (GLP-1) is an incretin hormone that, when given exogenously, is capable of normalizing blood glucose in individuals with type 2 diabetes. Until recently most of the research on this compound had been related to its insulinotropic properties. However, GLP-1 also regulates insulin synthesis and proinsulin gene expression, as well as the components of the glucose-sensing machinery. In addition to regulating insulin release, it is involved in regulating the secretion of at least two other islet hormones--glucagon and somatostatin. Extraislet effects of GLP-1 include a role in the central nervous system stress response, hypothalamic-pituitary function, and the suppression of gastric emptying. Recent studies from our own and other laboratories show that GLP-1 can regulate islet growth and is a differentiation factor of the endocrine pancreas. This leads us to propose that GLP-1 and GLP-1 receptor agonists, in the context of long-term treatment of type 2 diabetes, will have broader biological action on the endocrine pancreas than was earlier anticipated. We propose that GLP-1 is a growth factor for pancreatic endocrine cells and can increase islet cell mass. Here we review those reports that have highlighted its role as a factor for islet cell growth and differentiation.     

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.