{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,11,4]],"date-time":"2026-11-04T23:55:23Z","timestamp":1793836523057,"version":"4.6.1"},"reference-count":41,"publisher":"The Endocrine Society","issue":"4","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":[],"published-print":{"date-parts":[[2005,4,1]]},"abstract":"<jats:title>Abstract<\/jats:title>\n                  <jats:p>The polycystic ovary syndrome (PCOS) is characterized by insulin resistance with compensatory hyperinsulinemia. Insulin resistance also plays a role in the metabolic syndrome (MBS). We hypothesized that the MBS is prevalent in PCOS and that women with both conditions would present with more hyperandrogenism and menstrual cycle irregularity than women with PCOS only.<\/jats:p>\n                  <jats:p>We conducted a retrospective chart review of all women with PCOS seen over a 3-yr period at an endocrinology clinic. Of the 161 PCOS cases reviewed, 106 met the inclusion criteria. The women were divided into two groups: 1) women with PCOS and the MBS (n = 46); and 2) women with PCOS lacking the MBS (n = 60).<\/jats:p>\n                  <jats:p>Prevalence of the MBS was 43%, nearly 2-fold higher than that reported for age-matched women in the general population. Women with PCOS had persistently higher prevalence rates of the MBS than women in the general population, regardless of matched age and body mass index ranges. Acanthosis nigricans was more frequent in women with PCOS and the MBS. Women with PCOS and the MBS had significantly higher levels of serum free testosterone (P = 0.002) and lower levels of serum SHBG (P = 0.001) than women with PCOS without the MBS. No differences in total testosterone were observed between the groups.<\/jats:p>\n                  <jats:p>We conclude that the MBS and its components are common in women with PCOS, placing them at increased risk for cardiovascular disease. Women with PCOS and the MBS differ from their counterparts lacking the MBS in terms of increased hyperandrogenemia, lower serum SHBG, and higher prevalence of acanthosis nigricans, all features that may reflect more severe insulin resistance.<\/jats:p>","DOI":"10.1210\/jc.2004-1045","type":"journal-article","created":{"date-parts":[[2005,4,6]],"date-time":"2005-04-06T19:32:44Z","timestamp":1112815964000},"page":"1929-1935","source":"Crossref","is-referenced-by-count":718,"title":["Prevalence and Characteristics of the Metabolic Syndrome in Women with Polycystic Ovary Syndrome"],"prefix":"10.1210","volume":"90","author":[{"given":"Teimuraz","family":"Apridonidze","sequence":"first","affiliation":[{"name":"Departments of Internal Medicine (T.A., P.A.E., M.J.I., J.E.N.) Richmond, Virginia 23298-0111"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Paulina A.","family":"Essah","sequence":"additional","affiliation":[{"name":"Departments of Internal Medicine (T.A., P.A.E., M.J.I., J.E.N.) Richmond, Virginia 23298-0111"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Maria J.","family":"Iuorno","sequence":"additional","affiliation":[{"name":"Departments of Internal Medicine (T.A., P.A.E., M.J.I., J.E.N.) Richmond, Virginia 23298-0111"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"John E.","family":"Nestler","sequence":"additional","affiliation":[{"name":"Departments of Internal Medicine (T.A., P.A.E., M.J.I., J.E.N.) Richmond, Virginia 23298-0111"},{"name":"Obstetrics and Gynecology (J.E.N.), Medical College of Virginia, Virginia Commonwealth University, Richmond, Virginia 23298-0111"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"80","reference":[{"key":"2020071615530683100_R1","first-page":"3078","article-title":"Prevalence of the polycystic ovary syndrome in unselected black and white women of the southeastern United States: a prospective study.","volume":"83","author":"Knochenhauer","year":"1998","journal-title":"J Clin Endocrinol Metab"},{"key":"2020071615530683100_R2","doi-asserted-by":"crossref","first-page":"356","DOI":"10.1210\/jcem-57-2-356","article-title":"Insulin resistance in nonobese patients with polycystic ovarian disease.","volume":"57","author":"Chang","year":"1983","journal-title":"J Clin Endocrinol Metab"},{"key":"2020071615530683100_R3","first-page":"577","article-title":"Cellular mechanisms of insulin resistance in polycystic ovarian syndrome.","volume":"75","author":"Ciaraldi","year":"1992","journal-title":"J Clin Endocrinol Metab"},{"key":"2020071615530683100_R4","doi-asserted-by":"crossref","first-page":"1257","DOI":"10.2337\/diab.41.10.1257","article-title":"Evidence for distinctive and intrinsic defects in insulin action in polycystic ovary syndrome.","volume":"41","author":"Dunaif","year":"1992","journal-title":"Diabetes"},{"key":"2020071615530683100_R5","first-page":"774","article-title":"Insulin resistance and the polycystic ovary syndrome: mechanism and implications for pathogenesis.","volume":"18","author":"Dunaif","year":"1997","journal-title":"Endocr Rev"},{"key":"2020071615530683100_R6","doi-asserted-by":"crossref","first-page":"733","DOI":"10.1210\/endo-123-2-733","article-title":"Insulin-like growth factor I and insulin potentiate luteinizing hormone-induced androgen synthesis by rat ovarian thecal-interstitial cells.","volume":"123","author":"Cara","year":"1988","journal-title":"Endocrinology"},{"key":"2020071615530683100_R7","doi-asserted-by":"crossref","first-page":"560","DOI":"10.1172\/JCI114745","article-title":"Insulin-like growth factor-I enhances luteinizing hormone binding to rat ovarian theca-interstitial cells.","volume":"86","author":"Cara","year":"1990","journal-title":"J Clin Invest"},{"key":"2020071615530683100_R8","doi-asserted-by":"crossref","first-page":"38","DOI":"10.1016\/0002-9343(83)90653-8","article-title":"Mediators of postreceptor action of insulin.","volume":"74","author":"Larner","year":"1983","journal-title":"Am J Med"},{"key":"2020071615530683100_R9","doi-asserted-by":"crossref","first-page":"617","DOI":"10.1056\/NEJM199608293350902","article-title":"Decreases in ovarian cytochrome P450c17 \u03b1 activity and serum free testosterone after reduction of insulin secretion in polycystic ovary syndrome.","volume":"335","author":"Nestler","year":"1996","journal-title":"N Engl J Med"},{"key":"2020071615530683100_R10","doi-asserted-by":"crossref","first-page":"33","DOI":"10.1016\/S0002-9343(99)80057-6","article-title":"Hyperandrogenic anovulation (PCOS): a unique disorder of insulin action associated with an increased risk of non-insulin-dependent diabetes mellitus.","volume":"98","author":"Dunaif","year":"1995","journal-title":"Am J Med"},{"key":"2020071615530683100_R11","doi-asserted-by":"crossref","first-page":"141","DOI":"10.2337\/diacare.22.1.141","article-title":"Prevalence of impaired glucose tolerance and diabetes in women with polycystic ovary syndrome.","volume":"22","author":"Ehrmann","year":"1999","journal-title":"Diabetes Care"},{"key":"2020071615530683100_R12","first-page":"165","article-title":"Prevalence and predictors of risk for type 2 diabetes mellitus and impaired glucose tolerance in polycystic ovary syndrome: a prospective, controlled study in 254 affected women.","volume":"84","author":"Legro","year":"1999","journal-title":"J Clin Endocrinol Metab"},{"key":"2020071615530683100_R13","doi-asserted-by":"crossref","first-page":"1595","DOI":"10.2337\/diab.37.12.1595","article-title":"Banting lecture 1988. 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