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Circulating cellular adhesion molecules and risk of diabetes: the Multi‐Ethnic Study of Atherosclerosis ( MESA )
Author(s) -
Pankow J. S.,
Decker P. A.,
Berardi C.,
Hanson N. Q.,
Sale M.,
Tang W.,
Kanaya A. M.,
Larson N. B.,
Tsai M. Y.,
Wassel C. L.,
Bielinski S. J.
Publication year - 2016
Publication title -
diabetic medicine
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.474
H-Index - 145
eISSN - 1464-5491
pISSN - 0742-3071
DOI - 10.1111/dme.13108
Subject(s) - medicine , diabetes mellitus , hazard ratio , quartile , cell adhesion molecule , endothelial activation , prospective cohort study , cohort study , endocrinology , immunology , inflammation , confidence interval
Aims To test the hypothesis that soluble cellular adhesion molecules would be positively and independently associated with risk of diabetes. Methods Soluble levels of six cellular adhesion molecules ( ICAM ‐1, E‐selectin, VCAM ‐1, E‐cadherin, L‐selectin and P‐selectin) were measured in participants in the Multi‐Ethnic Study of Atherosclerosis, a prospective cohort study. Participants were then followed for up to 10 years to ascertain incident diabetes. Results Sample sizes ranged from 826 to 2185. After adjusting for age, sex, race/ethnicity, BMI and fasting glucose or HbA 1c , four cellular adhesion molecules ( ICAM ‐1, E‐selectin, VCAM ‐1 and E‐cadherin) were positively associated with incident diabetes and there was a statistically significant trend across quartiles. Comparing the incidence of diabetes in the highest and lowest quartiles of each cellular adhesion molecule, the magnitude of association was largest for E‐selectin (hazard ratio 2.49; 95% CI 1.26–4.93) and ICAM ‐1 (hazard ratio 1.76; 95% CI 1.22–2.55) in fully adjusted models. Tests of effect modification by racial/ethnic group and sex were not statistically significant for any of the cellular adhesion molecules ( P > 0.05). Conclusions The finding of significant associations between multiple cellular adhesion molecules and incident diabetes may lend further support to the hypothesis that microvascular endothelial dysfunction contributes to risk of diabetes.