Journal
SEMINARS IN REPRODUCTIVE MEDICINE
Volume 32, Issue 3, Pages 202-213Publisher
THIEME MEDICAL PUBL INC
DOI: 10.1055/s-0034-1371092
Keywords
obesity; adolescent; overweight; hyperandrogenemia; polycystic ovary syndrome
Categories
Funding
- NIH [R01 HD058671, K32 HD070854, T32 DK007646]
- Eunice Kennedy Shriver National Institute of Child Health and Human Development/ National Institutes of Health as part of the Specialized Cooperative Centers Program in Reproduction and Infertility Research [U54 HD28934]
- Endocrine Fellows Foundation
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Obesity exacerbates the reproductive and metabolic manifestations of polycystic ovary syndrome (PCOS). The symptoms of PCOS often begin in adolescence, and the rising prevalence of peripubertal obesity has prompted concern that the prevalence and severity of adolescent PCOS is increasing in parallel. Recent data have disclosed a high prevalence of hyperandrogenemia among peripubertal adolescents with obesity, suggesting that such girls are indeed at risk for developing PCOS. Obesity may impact the risk of PCOS via insulin resistance and compensatory hyperinsulinemia, which augments ovarian/adrenal androgen production and suppresses sex hormone-binding globulin (SHBG), thereby increasing androgen bioavailability. Altered luteinizing hormone (LH) secretion plays an important role in the pathophysiology of PCOS, and although obesity is generally associated with relative reductions of LH, higher LH appears to be the best predictor of increased free testosterone among peripubertal girls with obesity. Other potential mechanisms of obesity-associated hyperandrogenemia include enhanced androgen production in an expanded fat mass and potential effects of abnormal adipokine/cytokine levels. Adolescents with PCOS are at risk for comorbidities such as metabolic syndrome and impaired glucose tolerance, and concomitant obesity compounds these risks. For all of these reasons, weight loss represents an important therapeutic target in obese adolescents with PCOS.
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