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Comparative Study
Journal Article
Research Support, Non-U.S. Gov't
Insulin sensitivity in women with polycystic ovary syndrome: relationship to hyperandrogenemia.
Fertility and Sterility 1994 April
OBJECTIVE: To evaluate the extent of decreased insulin sensitivity in relation to body mass index and its relationship to serum androgens in women with polycystic ovarian syndrome (PCOS).
DESIGN: Comparative study of endogenous glucose disposal and serum insulin responses to oral glucose load with endocrine parameters in PCOS.
SETTING: Fertility and Endocrine Clinics, North Staffordshire Hospital Centre.
PATIENTS: Forty-nine obese and 16 nonobese women with PCOS were compared with 18 obese and 16 nonobese control women with regular ovulatory cycles and no features of PCOS.
MAIN OUTCOME MEASURES: Basal concentrations of serum LH, FSH, T, androstenedione, sex hormone-binding globulin (SHBG), and free T index. Measurements of insulin sensitivity by rate of endogenous glucose disposal after i.v. bolus injection of insulin and glucose mediated insulin responses.
RESULTS: Obese women with PCOS showed decreased insulin sensitivity and hyperinsulinemia to an extent greater than can be explained by obesity alone. Serum insulin showed inverse correlation with SHBG, and therefore hyperinsulinemia increased the bioavailability of androgens in obese PCOS. In nonobese PCOS, this method of assessment failed to reveal insulin resistance.
CONCLUSION: Hyperandrogenemia and insulin resistance are independent features of PCOS. Hyperinsulinemia enhances expression of hyperandrogenemia by increasing bioavailability of androgens.
DESIGN: Comparative study of endogenous glucose disposal and serum insulin responses to oral glucose load with endocrine parameters in PCOS.
SETTING: Fertility and Endocrine Clinics, North Staffordshire Hospital Centre.
PATIENTS: Forty-nine obese and 16 nonobese women with PCOS were compared with 18 obese and 16 nonobese control women with regular ovulatory cycles and no features of PCOS.
MAIN OUTCOME MEASURES: Basal concentrations of serum LH, FSH, T, androstenedione, sex hormone-binding globulin (SHBG), and free T index. Measurements of insulin sensitivity by rate of endogenous glucose disposal after i.v. bolus injection of insulin and glucose mediated insulin responses.
RESULTS: Obese women with PCOS showed decreased insulin sensitivity and hyperinsulinemia to an extent greater than can be explained by obesity alone. Serum insulin showed inverse correlation with SHBG, and therefore hyperinsulinemia increased the bioavailability of androgens in obese PCOS. In nonobese PCOS, this method of assessment failed to reveal insulin resistance.
CONCLUSION: Hyperandrogenemia and insulin resistance are independent features of PCOS. Hyperinsulinemia enhances expression of hyperandrogenemia by increasing bioavailability of androgens.
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