As a multifunctional protein, fetuin-A has positive effects on health such as calcification, cardiovascular diseases and tumor development processes with various mechanisms, whereas it plays a negative role in the processes of obesity, diabetes and fatty liver disease.
Lower plasma fetuin-A levels were associated with an increased risk of all-cause and CVD mortality in patients with coronary artery disease independently of traditional CVD risk factors.
Therefore, we examined the effects of 6-month AEX+WL on plasma fetuin-A levels (36-48 hours after the last bout of exercise), aerobic capacity (VO<sub>2max</sub>), body composition, glucose tolerance, and insulin sensitivity (M) in 16 sedentary, overweight-obese older men (age = 60 ± 2 years, BMI = 31 ± 1 kg/m<sup>2</sup>) with no history of cardiovascular disease or diabetes.
Fetuin-A is an inhibitor of vascular calcification, and pentraxin 3 (PTX3) is produced at the site of inflammation, which is associated with cardiovascular disease (CVD).
Genetic variation and fetuin-A levels were assessed in 3299 community-living individuals (2733 Caucasians and 566 African Americans) 65 years of age or older, free of previous cardiovascular disease, who participated in the Cardiovascular Health Study (CHS) in 1992-1993.
These data provide evidence for the causal nature of the recently reported association between fetuin-A plasma levels and MI risk, thereby suggesting an involvement of fetuin-A in the pathogenesis of cardiovascular disease.
Fetuin A is an important mineralization inhibitor, and polymorphisms in the corresponding alpha2-Heremans-Schmid glycoprotein (AHSG) gene have been shown to be associated with serum fetuin A levels and free phosphate levels, as well as cardiovascular disease death.
In a logistic regression model (N= 101), fetuin-A was significantly (P < 0.05) associated with the presence of carotid plaques independently of age, CVD, diabetes, S-albumin, gender, and inflammation.