Fetuin-A (AHSG) and its usefulness in clinical practice. Review of the literature

Anna Maria Dabrowska, Jerzy Stanislaw Tarach, Beata Wojtysiak-Duma, Dariusz Duma, Anna Maria Dabrowska, Jerzy Stanislaw Tarach, Beata Wojtysiak-Duma, Dariusz Duma

Abstract

Background: Fetuin-A, also called Alpha 2-Heremans Schmid Glycoprotein, is a multifunctional plasma agent what has been proven in animal and human studies. It plays a role as a physiological inhibitor of insulin receptor tyrosine kinase associated with insulin resistance and a negative acute phase reactant. It also regulates bone remodeling and calcium metabolism being an important inhibitor of calcium salt precipitation and vascular calcifications.

Methods: PubMed database was searched for articles from 2002 up to December 2014 to identify the role of fetuin-A in the pathogenesis of selected internal diseases.

Results: Due to secretion of fetuin-A mainly by the liver, it may be a marker of liver function and predictor of mortality in patients with cirrhosis and hepatocellular cancer. The associations between high fetuin-A and metabolic syndrome as well as its hepatic manifestation- nonalcoholic fatty liver disease and atherogenic lipid profile have been well proven. However, fetuin-A relation with BMI is not so clear. Contrary to few reports, many authors suggest that fetuin-A may be an independent risk factor for type 2 diabetes and marker of diabetic complications. Close associations of high and low fetuin-A concentrations with cardiovascular diseases and mortality risk have been reported which is explained by differences in analyzed populations, stages of atherosclerosis and calcifications, coexistence of type 2 diabetes or kidney dysfunction and different main pathways of fetuin-A actions in various diseases.

Conclusions: Fetuin-A has a diagnostic potential as a biomarker for liver dysfunction, cardiovascular diseases and disorders associated with metabolic syndrome.

Keywords: atherosclerosis; cardiovascular disease; diabetes; fetuin-A; obesity.

Source: PubMed

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