scholarly journals Animal Models to Understand the Etiology and Pathophysiology of Polycystic Ovary Syndrome

2020 ◽  
Vol 41 (4) ◽  
pp. 538-576 ◽  
Author(s):  
Elisabet Stener-Victorin ◽  
Vasantha Padmanabhan ◽  
Kirsty A Walters ◽  
Rebecca E Campbell ◽  
Anna Benrick ◽  
...  
Keyword(s):  
Animal Models ◽  
Polycystic Ovary Syndrome ◽  
Genetic Manipulation ◽  
Polycystic Ovary ◽  
Developmental Origins ◽  
Metabolic Dysfunction ◽  
Ovary Syndrome ◽  
Naturally Occurring ◽  
High Prevalence

Abstract More than 1 out of 10 women worldwide are diagnosed with polycystic ovary syndrome (PCOS), the leading cause of female reproductive and metabolic dysfunction. Despite its high prevalence, PCOS and its accompanying morbidities are likely underdiagnosed, averaging > 2 years and 3 physicians before women are diagnosed. Although it has been intensively researched, the underlying cause(s) of PCOS have yet to be defined. In order to understand PCOS pathophysiology, its developmental origins, and how to predict and prevent PCOS onset, there is an urgent need for safe and effective markers and treatments. In this review, we detail which animal models are more suitable for contributing to our understanding of the etiology and pathophysiology of PCOS. We summarize and highlight advantages and limitations of hormonal or genetic manipulation of animal models, as well as of naturally occurring PCOS-like females.

High prevalence of multimorbidity in overweight and obese women with Polycystic Ovary Syndrome (PCOS)

2017 ◽  
Author(s):  
Hamidreza Mani ◽  
Yogini Chudasama ◽  
Danielle Bodicoat ◽  
Miles Levy ◽  
Laura Gray ◽  
...  
Keyword(s):  
Polycystic Ovary Syndrome ◽  
Polycystic Ovary ◽  
Obese Women ◽  
Ovary Syndrome ◽  
High Prevalence

scholarly journals Polycystic Ovary Syndrome: Familiar to Millions?

2020 ◽  
Vol 10 (1) ◽  
pp. 1
Author(s):  
Johannes Ott
Keyword(s):  
Polycystic Ovary Syndrome ◽  
Polycystic Ovary ◽  
Psychological Consequences ◽  
Ovary Syndrome ◽  
Endocrine Disorder ◽  
High Prevalence ◽  
Basic Characteristics

Often, articles about polycystic ovary syndrome (PCOS) start with information about the condition’s high prevalence, the basic characteristics that define this endocrine disorder, and the manifold somatic and/or psychological consequences [...]

Preliminary indication of a high prevalence of polycystic ovary syndrome in indigenous Australian women

2002 ◽  
Vol 16 (6) ◽  
pp. 443-446 ◽  
Author(s):  
S. R. Davis ◽  
S. Knight ◽  
V. White ◽  
C. Claridge ◽  
B. J. Davis ◽  
...  
Keyword(s):  
Polycystic Ovary Syndrome ◽  
Polycystic Ovary ◽  
Ovary Syndrome ◽  
Indigenous Australian ◽  
High Prevalence

scholarly journals The Role of the Brain in the Pathogenesis and Physiology of Polycystic Ovary Syndrome (PCOS)

2019 ◽  
Vol 7 (8) ◽  
pp. 84 ◽  
Author(s):  
Coutinho ◽  
Kauffman
Keyword(s):  
Animal Models ◽  
Polycystic Ovary Syndrome ◽  
Neural Circuit ◽  
Polycystic Ovary ◽  
Pulse Frequency ◽  
Reproductive Age ◽  
Neuron Activity ◽  
Ovary Syndrome ◽  
Gnrh Neurons ◽  
Reproductive Endocrine

Polycystic ovary syndrome (PCOS) is a common reproductive endocrine disorder, affecting at least 10% of women of reproductive age. PCOS is typically characterized by the presence of at least two of the three cardinal features of hyperandrogenemia (high circulating androgen levels), oligo- or anovulation, and cystic ovaries. Hyperandrogenemia increases the severity of the condition and is driven by increased luteinizing hormone (LH) pulse secretion from the pituitary. Indeed, PCOS women display both elevated mean LH levels, as well as an elevated frequency of LH pulsatile secretion. The abnormally high LH pulse frequency, reflective of a hyperactive gonadotropin-releasing hormone (GnRH) neural circuit, suggests a neuroendocrine basis to either the etiology or phenotype of PCOS. Several studies in preclinical animal models of PCOS have demonstrated alterations in GnRH neurons and their upstream afferent neuronal circuits. Some rodent PCOS models have demonstrated an increase in GnRH neuron activity that correlates with an increase in stimulatory GABAergic innervation and postsynaptic currents onto GnRH neurons. Additional studies have identified robust increases in hypothalamic levels of kisspeptin, another potent stimulator of GnRH neurons. This review outlines the different brain and neuroendocrine changes in the reproductive axis observed in PCOS animal models, discusses how they might contribute to either the etiology or adult phenotype of PCOS, and considers parallel findings in PCOS women.

scholarly journals Metabolic dysfunction in obese Hispanic women with polycystic ovary syndrome

2015 ◽  
Vol 30 (6) ◽  
pp. 1358-1364 ◽  
Author(s):  
S. Sam ◽  
B. Scoccia ◽  
S. Yalamanchi ◽  
T. Mazzone
Keyword(s):  
Polycystic Ovary Syndrome ◽  
Polycystic Ovary ◽  
Hispanic Women ◽  
Metabolic Dysfunction ◽  
Ovary Syndrome

scholarly journals High Prevalence of the Polycystic Ovary Syndrome and Hirsutism in Women with Type 1 Diabetes Mellitus1

2000 ◽  
Vol 85 (11) ◽  
pp. 4182-4187 ◽  
Author(s):  
Héctor F. Escobar-Morreale ◽  
Belén Roldán ◽  
Raquel Barrio ◽  
Milagros Alonso ◽  
José Sancho ◽  
...  
Keyword(s):  
Diabetes Mellitus ◽  
Type 1 Diabetes ◽  
Polycystic Ovary Syndrome ◽  
Type 1 Diabetes Mellitus ◽  
Polycystic Ovary ◽  
Normal Serum ◽  
Ovary Syndrome ◽  
Menstrual Dysfunction ◽  
High Prevalence

The current recommendation for strict metabolic control of type 1 diabetes mellitus requires the administration of supraphysiological doses of insulin, which might result in insulin-mediated stimulation of androgen synthesis, as occurs in insulin-resistant states. At present, the prevalence of hyperandrogenic disorders in women with type 1 diabetes mellitus is unknown. Eighty-five women with type 1 diabetes mellitus were evaluated for symptoms and signs of hyperandrogenism. In 68 of the patients, several serum androgen and hormone concentrations were measured. The polycystic ovary syndrome (PCOS) was defined by the presence of menstrual dysfunction, together with clinical and/or biochemical evidence of hyperandrogenism, and exclusion of other etiologies. Eighteen healthy women, menstruating regularly, served as controls for the androgenic profiles. Thirty-three patients (38.8%) presented hyperandrogenic disorders (16 had PCOS, and 17 had hirsutism without menstrual dysfunction). Type 1 diabetic patients with PCOS presented increased serum total and free testosterone concentrations, and serum androstenedione levels, but had normal serum sex hormone-binding globulin and dehydroepiandrosterone-sulfate levels. Hirsute type 1 diabetic women without menstrual dysfunction presented normal serum androgen levels. There were no significant differences between hyperandrogenic and nonhyperandrogenic type 1 diabetes mellitus women in clinical variables such as the duration of diabetes, age at diagnosis of diabetes, conventional or intensive insulin therapy, mean daily insulin dosage, or metabolic control. In conclusion, women with type 1 diabetes mellitus have a high prevalence of hyperandrogenic disorders, including PCOS and hirsutism.

scholarly journals Polycystic ovary syndrome: reviewing diagnosis and management of metabolic disturbances

2014 ◽  
Vol 58 (2) ◽  
pp. 182-187 ◽  
Author(s):  
Poli Mara Spritzer
Keyword(s):  
Polycystic Ovary Syndrome ◽  
Diagnostic Criteria ◽  
Polycystic Ovary ◽  
Pharmacological Therapy ◽  
Lifestyle Changes ◽  
Reproductive Age ◽  
Metabolic Dysfunction ◽  
Metabolic Disturbances ◽  
Ovary Syndrome ◽  
Individual Woman

Polycystic ovary syndrome (PCOS) is a common condition in women at reproductive age associated with reproductive and metabolic dysfunction. Proposed diagnosed criteria for PCOS include two out of three features: androgen excess, menstrual irregularity, and polycystic ovary appearance on ultrasound (PCO), after other causes of hyperandrogenism and dysovulation are excluded. Based on these diagnostic criteria, the most common phenotypes are the “classic PCOS” – hyperandrogenism and oligomenorrhea, with or without PCO; the “ovulatory phenotype” – hyperandrogenism and PCO in ovulatory women; and the “non-hyperandrogenic phenotype”, in which there is oligomenorrhea and PCO, without overt hyperandrogenism. The presence of obesity may exacerbate the metabolic and reproductive disorders associated with the syndrome. In addition, PCOS women present higher risk for type 2 diabetes and higher prevalence of cardiovascular risk factors that seems to be associated with the classic phenotype. The main interventions to minimize cardiovascular and metabolic risks in PCOS are lifestyle changes, pharmacological therapy, and bariatric surgery. Treatment with metformin has been shown to improve insulin sensitivity, lowering blood glucose and androgen levels. These effects are more potent when combined with lifestyle interventions. In conclusion, besides reproductive abnormalities, PCOS has been associated to metabolic comorbidities, most of them linked to obesity. Confounders, such as the lack of standard diagnostic criteria, heterogeneity of the clinical presentation, and presence of obesity, make management of PCOS difficult. Therefore, the approach to metabolic abnormalities should be tailored to the risks and treatment goals of each individual woman.

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