Plasma osteopontin is not associated with vascular markers of subclinical atherosclerosis in a population of young adults without symptoms of cardiovascular disease. The Cardiovascular Risk in Young Finns Study

Abstract

Objective: Osteopontin is used as a biomarker for measuring the severity of atherosclerosis, but the role of osteopontin in the pathogenesis of atherosclerosis is not clear. Methods: The distribution and determinants of osteopontin were studied in a randomized cohort of 1,817 young adults (aged 30–45 years) without clinical symptoms of atherosclerosis. Results: The mean ± SD osteopontin concentration was 60.7 ± 15.6 μg/mL in men and 51.7 ± 16.0 μg/mL in women. In multivariable models the correlates of osteopontin explained 6.9% (Model R²) of the total variation in osteopontin in men, including CRP (β = 3.02, p < 0.0001), SHBG (β = 0.21, p < 0.0001), total cholesterol (β = − 1.78, p = 0.002), age (β = − 0.26, p = 0.02) and alcohol use (β = 0.57, p = 0.04) and of these CRP had the greatest influence (Partial R² = 2.1%). In women, multivariable correlates of osteopontin included CRP (β = 2.90, p < 0.0001), total cholesterol (β = − 1.99, p = 0.002), insulin (β = − 1.76, p = 0.001), physical activity (β = 0.66, p = 0.03), adiponectin (β = 0.25, p = 0.008) and diastolic blood pressure (β = 0.14, p = 0.003). These five variables explained 6.7% (Model R²) of the total variation in osteopontin, with CRP (Partial R² = 2.7%) having the greatest influence. Osteopontin was not associated with carotid intima-media thickness, carotid elasticity, brachial endothelial function or the presence of a carotid plaque in either sex. Conclusion: We found no evidence of association between osteopontin levels and early vascular markers of atherosclerosis in asymptomatic young adults, suggesting that osteopontin is not implicated in the preclinical atherosclerotic changes in vascular structure and function.

Key Words::

• Epidemiology
• osteopontin
• cohort study
• inflammation
• risk factors

Acknowledgements

The Young Finns Study has been financially supported by the Academy of Finland: grants 126925, 121584, 124282, 129378 (Salve), 117787 (Gendi), and 41071 (Skidi), the Social Insurance Institution of Finland, Kuopio, Tampere and Turku University Hospital Medical Funds, Juho Vainio Foundation, Paavo Nurmi Foundation, Finnish Foundation of Cardiovascular Research and Finnish Cultural Foundation. The expert technical assistance in the statistical analyses by Irina Lisinen and Ville Aalto is gratefully acknowledged.

Declaration of interest: The authors report no conflict of interest. The authors alone are responsible for the content and writing of the paper.