Fetuin

Fetuine are blood proteins that are synthesized in the liver and secreted into the blood. They belong to the large group of binding proteins in the blood, accomplish the transport and availability of substances of various kinds in the bloodstream. The best-known representatives of these transport proteins is the serum albumin, the most abundant protein in the blood serum of adult animals. Fetuin in fetal blood, however, comes in especially large amounts. Hence the name is derived fetuin (Latin fetus ). In fetal bovine serum fetuin, for example, contain more than albumin in the serum of adult animals, however, much more albumin than fetuin.

Fetuine are members of a family of proteins that emerged in evolution by gene duplication and exchange of gene segments from the smaller protein cystatin. Fetuine therefore belong to the so-called cystatin superfamily of proteins, which also include the histidine - rich glycoprotein ( HRG) and the kininogens ( KNG ) belong.

Human α2 -HS- glycoprotein (genetic symbol AHSG ) is synonymously known as α2 -HS, A2HS, AHS, HSGA and fetuin -A. Fetuin- A is present in one copy in the genome. 2000 was discovered in human, rat and mouse genome, the closely related fetuin -B. How fetuin -A is predominantly formed by the liver fetuin - B, but also a number of other secretory organs. Fetuine come in all previously investigated vertebrate genomes including fish and reptiles.

Representative

There are two different Fetuine known: fetuin -A and fetuin as

Fetuin -A

The function of fetuin - A in the body has been elucidated by gene knockout in mice. The feeding a mineral-rich diet elicited calcification of the lungs, heart and kidneys in these mice. Dramatic proportions reached calcification, fetuin -A than the knockout mice in the genetic background of DBA / 2 was crossed. This mouse strain naturally inclined to calcify injured tissue. The fetuin - A deficiency increased the calcification quite dramatically and it's totally without mineral-rich diet. Therefore, fetuin -A is considered to be a potent inhibitor of calcification in the blood. This type of calcification is extremely rare and can best be compared with the clinical picture of calciphylaxis. It has to do only indirectly related to the commonly known hardening of the arteries, arteriosclerosis.

Fetuin -A is increased in formation of a fatty degeneration liver. Fetuin-A inhibits adiponectin and increases the level of tumor necrosis factor -alpha ( TNF ), which has an inflammatory ( inflammatory ) effect on the blood vessels. Fetuin-A binds to insulin receptors in muscle and fat cells, and contributes to insulin resistance. People with high fetuin -A levels have first studies, an approximately 3 to 4 -fold increased stroke and heart attack risk. In developing an appropriate laboratory standards fetuin -A is thus potentially useful as an independent marker of cardiovascular risk.

Fetuin -B

Fetuin B has an important role in the regulation of the zona pellucida; the protein inhibits this Ovastacin, which can harden even before the penetration of a sperm, the zona pellucida. Female mice without fetuin -B are - despite normal development and function of the ovaries - barren.