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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

Abstract

Background

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.

Methods

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.

Results

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).

Conclusions

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.

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