title: Obesity and the polycystic ovary syndrome.
abstract: The polycystic ovary syndrome (PCOS) is a mostly hyperandrogenic disorder and is possibly the most common endocrinopathy of premenopausal women. The primary defect in PCOS appears to be an exaggerated androgen synthesis and secretion by the ovaries and the adrenal glands. In a substantial proportion of PCOS patients, the primary defect in androgen secretion is triggered by factors such as the hyperinsulinism resulting from insulin resistance and/or the secretion of metabolically active substances by visceral adipose tissue, because these factors may facilitate androgen synthesis at the ovaries and the adrenals of predisposed women. The prevalence of obesity in PCOS patients is increased when compared to the general female population and, conversely, the prevalence of PCOS is increased in overweight and obese women when compared to their lean counterparts. Obesity exerts a major impact on the PCOS phenotype, particularly on the metabolic associations and complications of the syndrome. Among others, the presence obesity is clearly related to the infertility of PCOS, and increases the risk for the metabolic syndrome and its constellation of cardiovascular risk factors in these women. This review will summarize the pathophysiological mechanisms underlying the association of obesity and PCOS, the impact of obesity on the PCOS phenotype and on the association of PCOS with metabolic disorders and cardiovascular risk factors, and the new developments in the management of obese PCOS patients.
authors.affiliation: Department of Endocrinology, Hospital Ramón y Cajal, Universidad de Alcalá, Madrid, Spain.
authors.forename: E
authors.initials: E
authors.lastname: Martínez-Bermejo
authors.forename: M
authors.initials: M
authors.lastname: Luque-Ramírez
authors.forename: H F
authors.initials: HF
authors.lastname: Escobar-Morreale
mesh_terms: D000311:Adrenal Glands / Q000378:metabolism; D000328:Adult; D000728:Androgens / Q000378:metabolism; D002318:Cardiovascular Diseases / Q000453:epidemiology / Q000209:etiology; D003278:Contraceptives, Oral, Hormonal / Q000009:adverse effects / Q000627:therapeutic use; D004032:Diet; D005260:Female; D006801:Humans; D017588:Hyperandrogenism / Q000150:complications / Q000503:physiopathology; D007333:Insulin Resistance; D008019:Life Style; D024821:Metabolic Syndrome / Q000235:genetics / Q000503:physiopathology; D008687:Metformin / Q000627:therapeutic use; D008954:Models, Biological; D009765:Obesity / Q000150:complications / Q000503:physiopathology*; D010053:Ovary / Q000378:metabolism; D011085:Polycystic Ovary Syndrome / Q000175:diagnosis / Q000209:etiology / Q000235:genetics / Q000503:physiopathology*; D011247:Pregnancy; D012307:Risk Factors
chemical_list: D000728:Androgens; D003278:Contraceptives, Oral, Hormonal; D008687:Metformin