Chronic inflammation role in the obesity-diabetes association: a case-cohort study
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...
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Published in: | Diabetology and metabolic syndrome Vol. 5; no. 1; p. 31 |
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Main Authors: | , , , , , , |
Format: | Journal Article |
Language: | English |
Published: |
England
BioMed Central Ltd
27-06-2013
BioMed Central |
Subjects: | |
Online Access: | Get full text |
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Summary: | 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. |
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Bibliography: | ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 23 |
ISSN: | 1758-5996 1758-5996 |
DOI: | 10.1186/1758-5996-5-31 |