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Osteocalcin as a potential risk biomarker for cardiovascular and metabolic diseases

  • Paolo Magni EMAIL logo , Chiara Macchi , Cesare R. Sirtori and Massimiliano Marco Corsi Romanelli
Published/Copyright: February 10, 2016

Abstract

Clear evidence supports a role for circulating and locally-produced osteocalcin (OC) in the pathophysiology of cardiovascular (CV) lesions and CV risk, also in combination with metabolic changes, including type 2 diabetes mellitus (T2DM). Reduced plasma OC levels are associated with greater incidence of pathological CV changes, like arterial and valvular calcification, coronary and carotid atherosclerosis and increased carotid intima-media thickness. The actual relationship between OC levels and incidence of major CV events is, however, still unclear. Moreover, reduced circulating OC levels have been mostly associated with insulin resistance, metabolic syndrome or T2DM, indicating relevant OC actions on pancreatic β-cells and insulin secretion and activity. Based on these observations, this review article will attempt to summarize the current evidence on the potential usefulness of circulating OC as a biomarker for CV and metabolic risk, also evaluating the currently open issues in this area of research.


Corresponding author: Paolo Magni, MD, PhD, Dipartimento di Scienze Farmacologiche e Biomolecolari, Università degli Studi di Milano, via G. Balzaretti, 9; 20133 Milan – Italy, Phone:+39-02-503-18229, Fax:+39-02-503-18204

  1. Author contributions: All the authors have accepted responsibility for the entire content of this submitted manuscript and approved submission.

  2. Research funding: None declared.

  3. Employment or leadership: None declared.

  4. Honorarium: None declared.

  5. Competing interests: The funding organization(s) played no role in the study design; in the collection, analysis, and interpretation of data; in the writing of the report; or in the decision to submit the report for publication.

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Received: 2015-9-30
Accepted: 2015-12-17
Published Online: 2016-2-10
Published in Print: 2016-10-1

©2016 Walter de Gruyter GmbH, Berlin/Boston

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