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Journal of Clinical Endocrinology & Metabolism, doi:10.1210/jc.2005-1653
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The Journal of Clinical Endocrinology & Metabolism Vol. 91, No. 1 64-68
Copyright © 2006 by The Endocrine Society

Cross-Sectional Associations of Resistin, Coronary Heart Disease, and Insulin Resistance

Mary Susan Burnett, Joseph M. Devaney, Remi J. Adenika, Robert Lindsay and Barbara V. Howard

MedStar Research Institute (M.S.B., J.M.D., R.J.A., B.V.H.), Washington, D.C. 20010; Children’s National Medical Center (J.M.D.), Washington, D.C. 20010; and British Heart Foundation Cardiovascular Research Centre (R.L.), University of Glasgow, Glasgow G11 6NT, United Kingdom

Address all correspondence and requests for reprints to: Mary Susan Burnett, Cardiovascular Research Institute, MedStar Research Institute, 108 Irving Street NW, Room 217, Washington, D.C. 20010. E-mail: Mary.s.burnett-miller{at}medstar.net.

Context: Recently, resistin was found to be present in atherosclerotic lesions in apoE–/– mice. Resistin may be associated with inflammation and atherosclerosis in humans; however, the role of resistin in human disease remains controversial.

Objective: This study assesses cross-sectional relationships of resistin with coronary heart disease (CHD).

Design, Setting, and Participants: Blood samples from the third examination of the Strong Heart Study (SHS)—the largest study of CHD in American Indians—were used. Cases who had suffered previous myocardial infarction (n = 100) were selected randomly from the three SHS sites and matched for study site and sex with controls who had no history of cardiovascular disease (CHD or stroke) (n = 100).

Main Outcome Measure: Resistin levels by enzyme-linked immunosorbent assay method in cases and controls was the main outcome measure.

Results: Resistin levels were higher in cases than controls [median (interquartile range): 3.4 (2.5–4.7) vs. 2.8 (2.1–4.0) ng/ml; P = 0.003] and had univariate correlations with age (Spearman r = 0.21; P < 0.002), fasting insulin (r = 0.21; P = 0.003), insulin resistance by homeostasis model (r = 0.22; P = 0.04), albumin to creatinine ratio (r = 0.19; P = 0.01), and fibrinogen (r = 0.34; P < 0.0001). Cases were more likely to have diabetes (cases 67%; controls 41%; P < 0.0001) but had similar body mass index (cases 31.4 ± 5.4; controls 30.7 ± 6.3; P = 0.85). Resistin levels were higher in participants with established nephropathy (albumin to creatinine ratio >300 mg/g, n = 26) compared with those with normo- (n = 122) or microalbuminuria (n = 42). In multivariate analysis, nephropathy (P = 0.0013) but not previous myocardial infarction (P = 0.12) was significantly associated with resistin.

Conclusions: Resistin is not independently associated with CHD. Resistin is elevated in survivors of myocardial infarction; however, this reflects a novel association of raised resistin with diabetic nephropathy.




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