scholarly journals Current aspects of polycystic ovary syndrome I: definition, pathophysiology, clinical manifestations, diagnosis and complications

2018 ◽  
Vol 91 (1) ◽  
pp. 5-18
Author(s):  
Kun Imre Zoltán ◽  
Kun Ildikó ◽  
Kolcsár Melinda
Keyword(s):  
Insulin Resistance ◽  
Polycystic Ovary Syndrome ◽  
Polycystic Ovary ◽  
Clinical Manifestations ◽  
Human Reproduction ◽  
Ovary Syndrome ◽  
Adrenal Steroidogenesis ◽  
American Society ◽  
Genetically Determined

Abstract Polycystic ovary syndrome (PCOS) is the most frequent endocrine disease among women with childbearing potential, the best-known cause of hirsutism, with a hypothesized prevalence of 8-22%. The first part of the paper discusses the conceptional evolution of the syndrome, from its description in 1935 by Stein and Leventhal till today. It describes the changes in the criteria systems, emphasizing that the Rotterdam criteria, proposed in 2003 by the European Society for Human Reproduction and Embryology/American Society for Reproductive Medicine, are still valid today. This system basically differs from earlier (1990) NIH-criteria in one aspect: it introduced two newer phenotypes, one without hyperandrogenism and the other with ovulatory cycles, so it distinguishes 4 phenotypes. The etiology and pathogenesis of PCOS is heterogeneous, multifactorial, poorly understood. We present the 3 leading hypotheses (1 - hypothalamo-hypophyseal disturbances, 2 – primary enzyme disorders in ovarian, or ovarian/adrenal steroidogenesis, resulting primarily in hyperactivity of 17alpha-hydroxylase/17,20-lyase, 3 – insulin resistance-hyperinsulinism and other metabolic dysfunctions). We emphasize the role of genetically determined hyperandrogenism, that of insulin resistance-hyperinsulinism and the importance of reinforcing each other. Subsequently, the aggravating aspects of the frequently associated metabolic syndrome are discussed, and then the effects of the mentioned pathological processes on the endocrine and other organ structures participating in the regulation of sexual functions. We stress the hypothetical role of perinatal and pubertal androgen exposition in the pathogenesis of PCOS. The mechanisms of anovulation and those of the endometrial lesions are discussed, too. The clinical manifestations, the paraclinical and laboratory examinations, the positive and differential diagnosis and the complications are also presented. We intend to deal with the therapeutic aspects of PCOS in an upcoming paper.

scholarly journals Developmental origin of polycystic ovary syndrome - a hypothesis

2002 ◽  
Vol 174 (1) ◽  
pp. 1-5 ◽  
Author(s):  
DH Abbott ◽  
DA Dumesic ◽  
S Franks
Keyword(s):  
Insulin Resistance ◽  
Polycystic Ovary Syndrome ◽  
Polycystic Ovary ◽  
Regulatory Region ◽  
Later Life ◽  
Ovary Syndrome ◽  
Increased Risk ◽  
Genetically Determined ◽  
Lh Secretion

Polycystic ovary syndrome (PCOS) is a common but complex endocrine disorder and is a major cause of anovulation and consequent subfertility. It is also associated with a metabolic disturbance, characterized by hyperinsulinaemia and insulin resistance that carries an increased risk of type 2 diabetes in later life. Despite its prevalence little is known about its aetiology, but there is increasing evidence for an important genetic involvement. On the basis of experimental observations in the prenatally androgenized sheep and rhesus monkey, and supported by data from human studies, we propose that the clinical and biochemical features of PCOS can arise as a consequence of genetically determined hypersecretion of androgens by the ovary during, or very likely long before, puberty. The resulting hyperandrogenism results in 'programming' of the hypothalamic-pituitary unit to favour excess LH secretion, and encourages preferential abdominal adiposity that predisposes to insulin resistance. The severity of hyperinsulinaemia and insulin resistance (which has a profound influence on the phenotype of PCOS) is further influenced by both genetic factors (such as polymorphism in the insulin gene regulatory region) and environmental factors, notably obesity. This hypothesis therefore suggests a unifying, 'linear' model to explain the aetiology of the heterogeneous phenotype.

Polycystic Ovary Syndrome Is Associated With Obstructive Sleep Apnea and Daytime Sleepiness: Role of Insulin Resistance

2001 ◽  
Vol 56 (7) ◽  
pp. 418-419 ◽  
Author(s):  
Alexandros N. Vgontzas ◽  
Richard S. Legro ◽  
Edward O. Bixler ◽  
Allison Grayev ◽  
Anthony Kales ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Obstructive Sleep Apnea ◽  
Sleep Apnea ◽  
Polycystic Ovary Syndrome ◽  
Daytime Sleepiness ◽  
Polycystic Ovary ◽  
Ovary Syndrome ◽  
Obstructive Sleep

scholarly journals Role of Lipotoxicity and Contribution of the Renin-Angiotensin System in the Development of Polycystic Ovary Syndrome

2018 ◽  
Vol 2018 ◽  
pp. 1-13 ◽  
Author(s):  
Alexandre Connolly ◽  
Samuel Leblanc ◽  
Jean-Patrice Baillargeon
Keyword(s):  
Insulin Resistance ◽  
Polycystic Ovary Syndrome ◽  
Rat Model ◽  
Polycystic Ovary ◽  
Renin Angiotensin System ◽  
Ovary Syndrome ◽  
Nonesterified Fatty Acids ◽  
Insulin Resistant ◽  
Cellular Dysfunction

Polycystic ovary syndrome (PCOS) is a common and significant condition associated with hyperandrogenism, infertility, low quality of life, and metabolic comorbidities. One possible explanation of PCOS development is cellular dysfunction induced by nonesterified fatty acids (NEFAs), that is, lipotoxicity, which could explain both the hyperandrogenemia and insulin resistance that characterize women with PCOS. The literature suggests that androgen biosynthesis may be induced by overexposure of androgen-secreting tissues to NEFA and/or defective NEFA metabolism, leading to lipotoxic effects. Indeed, lipotoxicity could trigger androgenic hyperresponsiveness to insulin, LH, and ACTH. In most PCOS women, lipotoxicity also causes insulin resistance, inducing compensatory hyperinsulinemia, and may thus further increase hyperandrogenemia. Many approaches aimed at insulin sensitization also reduce lipotoxicity and have been shown to treat PCOS hyperandrogenemia. Furthermore, our group and others found that angiotensin II type 2 receptor (AT2R) activation is able to improve lipotoxicity. We provided evidence, using C21/M24, that AT2R activation improves adipocytes’ size and insulin sensitivity in an insulin-resistant rat model, as well as androgen levels in a PCOS obese rat model. Taken together, these findings point toward the important role of lipotoxicity in PCOS development and of the RAS system as a new target for the treatment of PCOS.

scholarly journals Biomediators in Polycystic Ovary Syndrome and Cardiovascular Risk

Biomolecules ◽  
2021 ◽  
Vol 11 (9) ◽  
pp. 1350
Author(s):  
Srdan Pandurevic ◽  
Djuro Macut ◽  
Flaminia Fanelli ◽  
Uberto Pagotto ◽  
Alessandra Gambineri
Keyword(s):  
Insulin Resistance ◽  
Polycystic Ovary Syndrome ◽  
Molecular Mechanisms ◽  
Polycystic Ovary ◽  
Clinical Manifestations ◽  
Molecular Heterogeneity ◽  
Ovary Syndrome ◽  
Metabolic Complications ◽  
Early Predictors ◽  
Cv Disease

Polycystic ovary syndrome (PCOS) is extremely heterogeneous in terms of clinical manifestations. The variability of the syndrome’s phenotype is derived from the genetic and molecular heterogeneity, with a great deal of environmental factors that may have long-term health consequences, such as metabolic and cardiovascular (CV) diseases. There is no doubt that women with PCOS suffer from metabolic complications more than their age-matched counterparts in the general population and at an earlier age. Obesity, low steroid hormone-binding globulin (SHBG), hyperandrogenemia, insulin resistance, and compensatory hyperinsulinemia are biomediators and early predictors of metabolic complications in PCOS. Doubts remain about the real risk of CV diseases in PCOS and the molecular mechanisms at the basis of CV complications. Based on that assumption, this review will present the available evidence on the potential implications of some biomediators, in particular, hyperandrogenism, estrogen-progesterone imbalance, insulin resistance, and low SHBG, in the processes leading to CV disease in PCOS, with the final aim to propose a more accurate CV risk assessment.

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