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.

scholarly journals Adiponectin and Polycystic Ovary Syndrome

2010 ◽  
Vol 12 (1) ◽  
pp. 62-72 ◽  
Author(s):  
Susan W. Groth
Keyword(s):  
Insulin Resistance ◽  
Metabolic Syndrome ◽  
Clinical Practice ◽  
Polycystic Ovary Syndrome ◽  
Disease Risk ◽  
Polycystic Ovary ◽  
Reproductive Age ◽  
Ovary Syndrome ◽  
Increased Risk

Introduction. Polycystic ovary syndrome (PCOS) has a prevalence of 5—8% in women of reproductive age. Women with PCOS have an increased risk of metabolic syndrome and associated comorbidities. Adiponectin is a circulating protein produced by adipocytes. Circulating levels of adiponectin are inversely related to adipocyte mass. Low levels occur with insulin resistance, type 2 diabetes, metabolic syndrome, and obesity-related cardiovascular disease. This article reviews the literature on the link between adiponectin and PCOS and the potential use of adiponectin as a biomarker for PCOS. Method. Data-based studies on adiponectin and PCOS and adiponectin measurement were identified through the Medline (1950—2009) and ISI Web of Knowledge (1973—2009) databases. Results. Fifteen studies related to adiponectin and PCOS met inclusion criteria and were included in this review. These studies present evidence that adiponectin is linked to insulin resistance, insulin sensitivity, body mass index (BMI), and adiposity. In women with PCOS, lower levels, as opposed to higher levels, of adiponectin occur in the absence of adiposity. Conclusion. The relationships between adiponectin and insulin resistance and sensitivity, metabolic syndrome, and BMI in women with PCOS suggest that adiponectin potentially could serve as a marker for disease risk and provide opportunity for earlier intervention if knowledge is successfully translated from laboratory to clinical practice. However, further study of the relationship between adiponectin and PCOS is required before there can be direct application to clinical practice.

Metabolic Syndrome During Menopause

2019 ◽  
Vol 17 (6) ◽  
pp. 595-603 ◽  
Author(s):  
Sezcan Mumusoglu ◽  
Bulent Okan Yildiz
Keyword(s):  
Insulin Resistance ◽  
Metabolic Syndrome ◽  
Central Obesity ◽  
Polycystic Ovary ◽  
Ovary Syndrome ◽  
Natural Menopause ◽  
The Metabolic Syndrome ◽  
Increased Risk ◽  
Aging Women

The metabolic syndrome (MetS) comprises individual components including central obesity, insulin resistance, dyslipidaemia and hypertension and it is associated with an increased risk of cardiovascular disease (CVD) and type 2 diabetes mellitus (T2DM). The menopause per se increases the incidence of MetS in aging women. The effect(s) of menopause on individual components of MetS include: i) increasing central obesity with changes in the fat tissue distribution, ii) potential increase in insulin resistance, iii) changes in serum lipid concentrations, which seem to be associated with increasing weight rather than menopause itself, and, iv) an association between menopause and hypertension, although available data are inconclusive. With regard to the consequences of MetS during menopause, there is no consistent data supporting a causal relationship between menopause and CVD. However, concomitant MetS during menopause appears to increase the risk of CVD. Furthermore, despite the data supporting the association between early menopause and increased risk of T2DM, the association between natural menopause itself and risk of T2DM is not evident. However, the presence and the severity of MetS appears to be associated with an increased risk of T2DM. Although the mechanism is not clear, surgical menopause is strongly linked with a higher incidence of MetS. Interestingly, women with polycystic ovary syndrome (PCOS) have an increased risk of MetS during their reproductive years; however, with menopausal transition, the risk of MetS becomes similar to that of non-PCOS women.

scholarly journals Potential genetic polymorphisms predicting polycystic ovary syndrome

2018 ◽  
Vol 7 (5) ◽  
pp. R187-R195 ◽  
Author(s):  
Yao Chen ◽  
Shu-ying Fang
Keyword(s):  
Polycystic Ovary Syndrome ◽  
Genetic Polymorphisms ◽  
Polycystic Ovary ◽  
Gonadal Hormones ◽  
Energy Regulation ◽  
Ovary Syndrome ◽  
Increased Risk ◽  
Number Of Genes ◽  
Hormone Biosynthesis

Polycystic ovary syndrome (PCOS) is a heterogenous endocrine disorder with typical symptoms of oligomenorrhoea, hyperandrogenism, hirsutism, obesity, insulin resistance and increased risk of type 2 diabetes mellitus. Extensive evidence indicates that PCOS is a genetic disease and numerous biochemical pathways have been linked with its pathogenesis. A number of genes from these pathways have been investigated, which include those involved with steroid hormone biosynthesis and metabolism, action of gonadotropin and gonadal hormones, folliculogenesis, obesity and energy regulation, insulin secretion and action and many others. In this review, we summarize the historical and recent findings in genetic polymorphisms of PCOS from the relevant publications and outline some genetic polymorphisms that are potentially associated with the risk of PCOS. This information could uncover candidate genes associating with PCOS, which will be valuable for the development of novel diagnostic and treatment platforms for PCOS patients.

Polycystic ovary syndrome: a contemporary clinical approach

2021 ◽  
Vol 27 ◽  
Author(s):  
Jelica Bjekić-Macut ◽  
Tamara Vukašin ◽  
Zelija Velija-Ašimi ◽  
Azra Bureković ◽  
Marija Zdravković ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Polycystic Ovary Syndrome ◽  
Polycystic Ovary ◽  
Cardiovascular Complications ◽  
Reproductive Period ◽  
Clinical Approach ◽  
Ovary Syndrome ◽  
Insulin Sensitizer ◽  
Central Type ◽  
Increased Risk

: Polycystic ovary syndrome (PCOS) is a frequent endocrine disease in women during reproductive period. It is considered a complex metabolic disorder with long-term metabolic, as well as reproductive consequences. Main pathophysiological pathways are related to the increased androgen levels and insulin resistance. Nowadays, genetic origins of PCOS are acknowledged, with numerous genes involved in the pathogenesis of hyperandrogenemia, insulin resistance, inflammation and disturbed folliculogenesis. Rotterdam diagnostic criteria are most widely accepted and four PCOS phenotypes have been recognized. Metabolic abnormalities are more common in phenotypes 1 and 2. Women with classic PCOS are more obese and typically have central type of obesity, more prevalently displaying dyslipidemia, insulin resistance and metabolic syndrome that could be associated with an increased risk of cardiovascular complications during life. Heterogeneity of phenotypes demands an individualized approach in the treatment of women with PCOS. Metabolic therapies involve a lifestyle intervention followed by the introduction of insulin sensitizers including metformin and inositols, glucagon-like peptide 1 receptor agonists (GLP-1 RA), as recently sodium glucose contransporter-2 (SGLT2) inhibitors. Addition of an insulin sensitizer to the standard infertility therapy such as CC improves ovulation and pregnancy rates. Our current review analyzes the contemporary knowledge of PCOS etiology and etiopathogenesis, its cardiometabolic risks and their outcomes, as well as therapeutic advances for women with PCOS.

scholarly journals Polycystic Ovary Syndrome, Insulin Resistance, and Obesity: Navigating the Pathophysiologic Labyrinth

2014 ◽  
Vol 2014 ◽  
pp. 1-17 ◽  
Author(s):  
Joselyn Rojas ◽  
Mervin Chávez ◽  
Luis Olivar ◽  
Milagros Rojas ◽  
Jessenia Morillo ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Polycystic Ovary Syndrome ◽  
Polycystic Ovary ◽  
Ovarian Tissue ◽  
Ovary Syndrome ◽  
Main Culprit ◽  
Exact Etiology

Polycystic ovary syndrome (PCOS) is a highly prevalent endocrine-metabolic disorder that implies various severe consequences to female health, including alarming rates of infertility. Although its exact etiology remains elusive, it is known to feature several hormonal disturbances, including hyperandrogenemia, insulin resistance (IR), and hyperinsulinemia. Insulin appears to disrupt all components of the hypothalamus-hypophysis-ovary axis, and ovarian tissue insulin resistance results in impaired metabolic signaling but intact mitogenic and steroidogenic activity, favoring hyperandrogenemia, which appears to be the main culprit of the clinical picture in PCOS. In turn, androgens may lead back to IR by increasing levels of free fatty acids and modifying muscle tissue composition and functionality, perpetuating this IR-hyperinsulinemia-hyperandrogenemia cycle. Nonobese women with PCOS showcase several differential features, with unique biochemical and hormonal profiles. Nevertheless, lean and obese patients have chronic inflammation mediating the long term cardiometabolic complications and comorbidities observed in women with PCOS, including dyslipidemia, metabolic syndrome, type 2 diabetes mellitus, and cardiovascular disease. Given these severe implications, it is important to thoroughly understand the pathophysiologic interconnections underlying PCOS, in order to provide superior therapeutic strategies and warrant improved quality of life to women with this syndrome.

scholarly journals Mechanisms Involved in Intrauterine Growth Restriction in Patients With Polycystic Ovary Syndrome: Primary and Secondary Prevention of Metabolic Syndrome and Cancer Risk in the Adult Life of Offspring

2021 ◽  
Vol 5 (Supplement_1) ◽  
pp. A741-A742
Author(s):  
Domingo Mugnolo ◽  
Erica Giraldo ◽  
Maria Perez Lana ◽  
Susana Beatriz Campeni
Keyword(s):  
Insulin Resistance ◽  
Metabolic Syndrome ◽  
Polycystic Ovary Syndrome ◽  
Fetal Programming ◽  
Intrauterine Growth Restriction ◽  
Polycystic Ovary ◽  
Adult Life ◽  
Ovary Syndrome ◽  
Intrauterine Growth ◽  
Increased Risk

Abstract Polycystic ovary syndrome (PCOS) is one of the most common hormonal disorders that affects between 5- 10% of women of reproductive age. It is currently considered a complex and multifactorial disease with metabolic, cardiovascular implications and represents per se an increased cancer risk. PATIENTS with PCOS routinely have menstrual disorders, hyperandrogenism, infertility and reproductive complications such as recurrent abortions, gestational diabetes, intrauterine growth restriction, pregnancy induced hypertension that give rise to underweight newborns and condition metabolic diseases to adult life and increased risk of cancer, especially breast and endometrial cancer. Insulin resistance and hyperandrogenism are the most important etiopathogenic factors in PCOS. On the other hand, subjects exposed to an adverse microenvironment in the intrauterine stage develop compensating responses to survive, a process called fetal programming. Prenatal exposure to androgens and/or insulin resistance may act as fetal programming factors and cause restriction of intrauterine growth, obesity and insulin resistance in offspring. Newborn may have an increased risk of metabolic syndrome, increased incidence of hypertensive, type 2 diabetes, heart disease and cerebrovascular disease. Prevention of these complications will be achieved if women with Polycystic Ovary Syndrome are treated appropriately throughout their lives, but especially before and during their pregnancy. Only in this way can the risk of them be reduced, representing a better quality and greater life expectancy.

scholarly journals A study of metabolic syndrome in women with polycystic ovary syndrome at tertiary care center

2021 ◽  
Vol 10 (6) ◽  
pp. 2427
Author(s):  
Chelsae Kuntal ◽  
Jyotsna Vyas ◽  
Asha Chaudhary ◽  
Sunita Hemani ◽  
Lata Rajoria
Keyword(s):  
Insulin Resistance ◽  
Metabolic Syndrome ◽  
Polycystic Ovary Syndrome ◽  
Urban Areas ◽  
Polycystic Ovary ◽  
Tertiary Care ◽  
Reproductive Age ◽  
Ovary Syndrome ◽  
Hormonal Profile ◽  
Increased Risk

Background: Polycystic ovary syndrome is a common endocrinopathy in women of reproductive age with prevalence of 6-10% which is characterized by hyper androgenic features and chronic oligo – anovulation and polycystic ovary morphology. Most women with polycystic ovary syndrome are also characterized by metabolic abnormalities like insulin resistance, hyperinsulinemia, dyslipidemia and abdominal obesity, these forming risk factors for metabolic syndrome. The objective of the study was to compare the clinical, biochemical and hormonal profile of polycystic ovary syndrome patients with and without metabolic syndrome.Methods: A comparative cross- sectional study was undertaken on 79 PCOS women diagnosed with PCOS according to Rotterdam criteria, in which the clinical data and hormonal profile of two groups of polycystic ovary syndrome women with and without metabolic syndrome was compared.Results: The mean age of 79 patients in this study group with and without metabolic syndrome was 26.17±3.18 and 25.57±3.41 years respectively. There were more patients from urban areas as compared to rural areas and maximum patients. Significantly higher number of PCOS women with metabolic syndrome had hirsutism and acanthosis nigricans than those without metabolic syndrome. Mean value of Waist circumference, systolic BP pressure, diastolic BP, S. Triglyceride and fasting glucose were higher and HDL levels were lower in women with metabolic syndrome than those without metabolic syndrome. Fasting insulin and HOMA-IR values were significantly higher in PCOS women with metabolic syndrome in comparison to those without metabolic syndrome.Conclusion: PCOS is not only is the most frequent cause of anovulation, but it is also associated with characteristic metabolic disturbances that may have important implications for the long term health. Metabolic syndrome is a cluster of endocrine disturbances, including insulin resistance, dyslipidemia, obesity, and hypertension. It is associated with a two-fold increased risk of cardiovascular disease and a five-fold increased risk of type 2 diabetes. This illustrates the importance of early detection of insulin resistance and metabolic syndrome with subsequent application of preventive measures in women with polycystic ovary syndrome.

scholarly journals A Narrative Review of Placental Contribution to Adverse Pregnancy Outcomes in Women With Polycystic Ovary Syndrome

2019 ◽  
Vol 104 (11) ◽  
pp. 5299-5315 ◽  
Author(s):  
Angela S Kelley ◽  
Yolanda R Smith ◽  
Vasantha Padmanabhan
Keyword(s):  
Insulin Resistance ◽  
Polycystic Ovary Syndrome ◽  
Pregnancy Complications ◽  
Polycystic Ovary ◽  
Evidence Synthesis ◽  
Developmental Programming ◽  
Androgen Excess ◽  
Ovary Syndrome ◽  
Increased Risk ◽  
Adverse Pregnancy

Abstract Context Polycystic ovary syndrome (PCOS) is the most common endocrinopathy of reproductive-aged women. In pregnancy, women with PCOS experience increased risk of miscarriage, gestational diabetes, preeclampsia, and extremes of fetal birth weight, and their offspring are predisposed to reproductive and cardiometabolic dysfunction in adulthood. Pregnancy complications, adverse fetal outcomes, and developmental programming of long-term health risks are known to have placental origins. These findings highlight the plausibility of placental compromise in pregnancies of women with PCOS. Evidence Synthesis A comprehensive PubMed search was performed using terms “polycystic ovary syndrome,” “placenta,” “developmental programming,” “hyperandrogenism,” “androgen excess,” “insulin resistance,” “hyperinsulinemia,” “pregnancy,” and “pregnancy complications” in both human and animal experimental models. Conclusions There is limited human placental research specific to pregnancy of women with PCOS. Gestational androgen excess and insulin resistance are two clinical hallmarks of PCOS that may contribute to placental dysfunction and underlie the higher rates of maternal–fetal complications observed in pregnancies of women with PCOS. Additional research is needed to prevent adverse maternal and developmental outcomes in women with PCOS and their offspring.

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