JOURNAL ARTICLE
RESEARCH SUPPORT, NON-U.S. GOV'T
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Circulating hepcidin is independently associated with systolic blood pressure in apparently healthy individuals.

BACKGROUND AND AIMS: Few studies have described the association between hepcidin levels and cardiometabolic risk in the general population and more so by considering robust adjustment for confounding factors. Therefore, the aim of the present study was to investigate the associations between circulating hepcidin and anthropometric, biochemical and vascular variables related to cardiometabolic risk in healthy individuals adjusting for relevant covariates.

METHODS: Two-hundred thirty nine individuals (20-65 years old) were included in this cross-sectional study. Outcome variables were fasting glucose, triglycerides, LDL cholesterol, HDL cholesterol, total cholesterol, waist circumference, systolic and diastolic blood pressures, and the Framingham risk score. Multivariate linear regression and ANCOVA analyses including covariates of body mass index (BMI), menopausal status, physical inactivity, alcohol intake, insulin resistance, subclinical/chronic inflammation, ferritin and soluble transferrin receptors were used to describe the associations between hepcidin and cardiometabolic risk markers.

RESULTS: In adjusted linear regression analyses, there was no significant association in men. In women, a relationship between hepcidin and triglycerides became significant after adjustments (p <0.05). By comparing quartiles of hepcidin levels, systolic blood pressure values in men were significantly higher in the upper quartile of hepcidin vs. the rest of quartiles independently of BMI, chronic inflammation, insulin resistance and other iron markers (ANCOVA, p <0.05). There were no significant independent associations with the Framingham risk score (total points).

CONCLUSION: We found a threshold effect of hepcidin levels on systolic blood pressure specifically in men. Further larger studies and experimental research are required to investigate possible mechanisms for the relationship between hepcidin metabolism and vascular function.

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