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Chronic inflammation role in the obesity-diabetes association: a case-cohort study

Vivian C Luft1*, Maria I Schmidt12, James S Pankow3, David Couper4, Christie M Ballantyne5, J Hunter Young6 and Bruce B Duncan12

Author Affiliations

1 Graduate Studies Program in Epidemiology, School of Medicine, Federal University of Rio Grande do Sul, Porto Alegre, RS, Brazil

2 Department of Epidemiology, Gillings School of Global Public Health, University of North Carolina, Chapel Hill, NC, United States of America

3 Division of Epidemiology & Community Health, School of Public Health, University of Minnesota, Minneapolis, MN, United States of America

4 Department of Biostatistics, Gillings School of Global Public Health, University of North Carolina, Chapel Hill, NC, United States of America

5 Department of Medicine, Baylor College of Medicine, Houston, TX, United States of America

6 Departments of Medicine and Epidemiology, The Johns Hopkins University, Baltimore, MD, United States of America

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Diabetology & Metabolic Syndrome 2013, 5:31  doi:10.1186/1758-5996-5-31

Published: 27 June 2013



Chronic inflammation is related to both obesity and diabetes. Our aim was to investigate to what extent this inflammation contributes to the association between obesity and diabetes.


Using a case-cohort design, we followed 567 middle-aged individuals who developed diabetes and 554 who did not over 9 years within the ARIC Study. Weighted Cox proportional hazards analyses permitted statistical inference to the entire cohort.


Obese individuals (BMI≥30 kg/m2), compared to those with BMI<25 kg/m2, presented a large increased risk of developing diabetes (HR[obesity]=6.4, 95%CI 4.5–9.2), as did those in the highest (compared to the lowest) quartile of waist circumference (HR[waist]=8.3, 95%CI 5.6–12.3), in analyses adjusted for age, gender, ethnicity, study center, and parental history of diabetes. Notably, further adjustment for adiponectin and inflammation markers halved the magnitude of these associations (HR[obesity]=3.2, 95%CI 2.1–4.7; and HR[waist]=4.2, 95%CI 2.8–6.5). In similar modeling, attenuation obtained by adding fasting insulin, instead of these markers, was only slightly more pronounced HR[obesity]=2.7, 95%CI 1.7–4.1; and HR[waist]=3.6, 95%CI 2.3–5.8).


The marked decrease in the obesity-diabetes association after taking into account inflammation markers and adipokines indicates their major role in the pathways leading to adult onset of diabetes in obese individuals.

Diabetes; Obesity; Inflammation; Adipokines; Humans; Epidemiologic studies