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Associations of Adiponectin, Resistin, and Tumor Necrosis Factor- with Insulin Resistance

Department of Medicine (M.-F.H., J.B.M.), Harvard Medical School and the General Medicine Division, and Harvard Medical School and the Diabetes Center, Department of Medicine (D.M.N., J.B.M.), Massachusetts General Hospital, Boston, Massachusetts 02114; The National Heart, Lung, and Blood Institute’s Framingham Heart Study, Department of Endocrinology and Metabolism (C.S.F.), Harvard Medical School and the Brigham and Women’s Hospital, and Department of Biostatistics (L.M.S.), and Department of Mathematics and Statistics/Consulting Unit (R.B.D.), Boston University School of Public Health, Boston, Massachusetts; Boston University, Boston, Massachusetts 02215; and Department of Medicine (P.W.F.W.), Cardiology Division, Emory University School of Medicine, Atlanta, Georgia 30306

Address all correspondence and requests for reprints to: James B. Meigs, M.D., M.P.H., General Medicine Division, Massachusetts General Hospital, 50 Staniford Street, 9th Floor, Boston, Massachusetts 02114. E-mail: hjmeigs{at}partners.org.

Context: Adipose tissue-derived adipokines may contribute to insulin resistance.

Objective: We tested the hypothesis that adipokines are associated with insulin resistance in a community-based cohort and that associations are maintained in people with and without the metabolic syndrome (high vs. low risk of diabetes).

Design, Setting, and Participants: We studied a cross-sectional sample of 2356 individuals attending the seventh examination (1998–2001) of the Framingham Offspring Study. We measured levels of glucose, insulin, adiponectin, resistin, and TNF in fasting blood samples and defined metabolic syndrome by updated National Cholesterol Education Program criteria. We used ANOVA to test associations of adipokines with insulin resistance and multivariable logistic regression models to assess joint associations of adipokines and metabolic syndrome with insulin resistance.

Main Outcome Measure: Homeostasis model (HOMA-IR), with insulin resistance defined by HOMA-IR greater than the 75th percentile, was measured.

Results: Age- and sex-adjusted HOMA-IR levels were inversely related to adiponectin (r = –0.40, P < 0.0001) and positively related to resistin (r = 0.13, P < 0.0001) and TNF (r = 0.12, P < 0.0001). The prevalence of insulin resistance increased with decreasing tertiles of adiponectin (from 10.9% in the third to 42.5% in the first tertile; P < 0.0001) and increasing tertiles of resistin (from 19.3 to 30.9%; P < 0.0001) and TNF (from 18.8 to 32.0%; P < 0.0001). Results were similar after adjustment for body mass index. These associations were present in individuals with or without the metabolic syndrome. In multivariable regression models, metabolic syndrome and adipokines individually and jointly were significantly associated with insulin resistance.

Conclusion: Adverse levels of adipokines are associated with insulin resistance in individuals at low or high diabetes risk.

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