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This version published online on May 20, 2008
Journal of Clinical Endocrinology & Metabolism, doi:10.1210/jc.2008-0425
A more recent version of this article appeared on August 1, 2008
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Submitted on February 22, 2008
Accepted on May 7, 2008

Associations of Adiponectin, Resistin, and TNF{alpha} with Insulin Resistance

Marie-France Hivert MD, Lisa M Sullivan PhD, Caroline S Fox MD MPH, David M. Nathan MD, Ralph B. D'Agostino Sr. PhD, Peter WF Wilson MD, and James B Meigs MD MPH*

Harvard Medical School and the General Medicine Division, Department of Medicine, Massachusetts General Hospital, Boston, MA (MFH, JBM); The National Heart, Lung, and Blood Institute's Framingham Heart Study, Harvard Medical School and the Department of Endocrinology and Metabolism, Brigham and Women's Hospital, Boston, MA (CSF); Department of Biostatistics, Boston University School of Public Health, Boston, MA (LMS); Harvard Medical School and the Diabetes Center, Department of Medicine, Massachusetts General Hospital, Boston, MA (DMN, JBM); Department of Mathematics and Statistics/Consulting Unit, Boston University, Boston, MA (RBD); Emory University School of Medicine, Atlanta, GA (PWFW)

* To whom correspondence should be addressed. E-mail: jmeigs{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 versus low risk of diabetes).

Design, Setting, and Participants: We studied a cross-sectional sample of 2,356 individuals attending the seventh examination (1998–2001) of the Framingham Offspring Study. We measured levels of glucose, insulin, adiponectin, resistin, and TNF{alpha} in fasting blood samples, and defined metabolic syndrome by updated NCEP 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.

Results: Age-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{alpha} (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 with increasing tertiles of resistin (from 19.3% to 30.9%; p<0.0001), and TNF{alpha} (from 18.8% to 32.0%; p<0.0001). Results were similar after adjustment for BMI. 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.
Key words: Insulin resistance • pre-diabetes • adipokines • adiponectin • resistin • TNF{alpha}




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