| Intended use |
Fetuin-A synthesized in the liver is secreted into the blood stream and it is deposited, accumulated as a noncollagenous protein in mineralized bones and teeth. Fetuin-A acts as an important circulating inhibitor of ectopic calcification, a frequently seen complication in degenerative diseases. Low Fetuin-A level may be associated with higher cardiovascular mortality in chronic renal failure, liver cancer and liver cirrhosis patients on long-term dialysis.
Human Fetuin-A represents a natural inhibitor of tyrosine kinase activity of the insulin receptor. Fetuin-A may play a significant role in regulating post-prandial glucose disposition, insulin sensitivity, weight gain, and fat accumulation and may be a novel therapeutic target in the treatment of type 2 diabetes, obesity, and other insulin-resistant conditions.
• Fetuin-A level (< 0.35 g/l) indicates a higher risk of cardiovascular calcification and increase mortality in ESRD-patients.
• Fetuin-A level (> 1.00 g/l) in elderly population, an independent risk factor of type II diabetes.
• Fetuin-A is an important predictor of death in acute myocardial infarction.
• Involved with the regulation of calcium metabolism and osteogenesis. |
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Human Fetuin-A
