Polycystic ovary syndrome. Long term sequelae and management
Related Experiment Video
Updated: Oct 1, 2026

Evaluation of Hepatic Glucose Production in a Polycystic Ovary Syndrome Mouse Model
Published on: March 5, 2022
1Department of Obstetrics and Gynaecology, M.S. Hershey Medical Center Pennsylvania State, University College of Medicine, Hershey, PA, USA. RSL1@psu.edu
Abstract:
Polycystic ovary syndrome (PCOS) is one of the most common endocrinopathies in women and is defined by hyperandrogenic chronic anovulation with the exclusion of secondary causes, such as congenital adrenal hyperplasia or an androgen secreting tumor. PCOS women are uniquely insulin resistant. It is estimated that 5% of the female population is affected. The underlying genetic defect in insulin action is unknown. Obesity aggravates the underlying predisposition to insulin resistance. Diagnostic criteria which focus on menstrual irregularity are more likely to identify insulin resistant women. About 40% of PCOS women display glucose intolerance (either impaired glucose tolerance or type 2 diabetes) in response to an oral glucose challenge. Additionally women display multiple other risk factors for cardiovascular disease including dyslipidemia and elevated circulating inflammatory markers. The lack of a clear etiologic mechanism to the syndrome has led in the past to a multitude of symptom-oriented treatments with few therapies improving all aspects of the endocrine syndrome of PCOS. Recently treatments resulting in improved insulin sensitivity, either through weight loss/exercise programs or pharmaceutical, have been shown to improve both the endocrine and metabolic abnormalities in the syndrome. Anti-diabetic agents in PCOS have been examined in a number of randomized studies which have shown a treatment benefit. Further indications for these agents such as the prevention of pregnancy loss or the conversion to type 2 diabetes still need to be investigated in properly designed studies.
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