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Clustering of Cardiovascular Risk Factors Associated With the Insulin Resistance Syndrome

Assessment by principal component analysis in young hyperandrogenic women

¹ Unit of Epidemiology and Medical Statistics, Department of Public Medicine and Health, University of Verona, Verona, Italy
² Division of Endocrinology and Metabolism, Department of Biomedical and Surgical Sciences, University of Verona, Verona, Italy

Address correspondence and reprint requests to Prof. Paolo Moghetti, Divisione di Endocrinologia e Metabolismo, Ospedale Maggiore, P.le Stefani, 1, 37126 Verona, Italy. E-mail: moghetti{at}iol.it

OBJECTIVE—Hyperinsulinemia is often associated with several metabolic abnormalities and increased blood pressure, which are risk factors for cardiovascular disease. It has been hypothesized that insulin resistance may underlie all these features. However, recent data suggest that some links between insulin resistance and these alterations may be indirect. The aim of our study was to further investigate this issue in a sample of young hyperandrogenic women, who often show insulin resistance and other metabolic abnormalities typical of the insulin resistance syndrome.

RESEARCH DESIGN AND METHODS—We tested the hypothesis of a single factor underlying these features by principal component analysis, which should recognize one component if a single mechanism explains this association. The analysis was carried out in a sample of 255 young nondiabetic hyperandrogenic women. Variables selected for this analysis included the basic features of the insulin resistance syndrome and some endocrine parameters related to hyperandrogenism.

RESULTS—Principal component analysis identified four separate factors, explaining 64.5% of the total variance in the data: the first included fasting and postchallenge insulin levels, BMI, triglycerides, HDL cholesterol, and uric acid; the second, BMI, blood pressure, and serum free testosterone; the third, fasting plasma glucose, postchallenge glucose and insulin levels, serum triglycerides, and free testosterone; and the fourth, postchallenge plasma insulin, serum free testosterone, and gonadotropin-releasing hormone agonist–stimulated 17-hydroxyprogesterone.

CONCLUSIONS—These results support the hypothesis of multiple determinants in the clustering of abnormalities in the so-called insulin resistance syndrome.

Abbreviations: DHEAS, dehydroepiandrosterone sulfate • GnRH, gonadotropin-releasing hormone

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