Fructosamine 3 Kinase

Fructosamine 3 Kinase

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About Fructosamine 3 Kinase \ FN3K:

Fructosamine 3-kinase (FN3K) is an enzyme that catalyzes the phosphorylation of fructosamines. A process which in turn leads to the gradual shedding from proteins and destabilization. Phosphorylation refers to the introduction of a phosphate group into a molecule. FN3K phosphorylates protein-bound or low-molecular-mass fructosmaines on the third carbon. Protein-bound fructoselysine becomes fructoselysine-3-phosphate. The condensation of lysine and glucose is an inevitable process.The deglycation system arbitrated by FN3K is a crucial contributing factor to protect cells from the adverse effects of nonenzymatic glycation.
Fructosamines form due to a spontaneous reaction between a primary amine and glucose; preceded by an Amadori rearrangement. This activity is known as glycation, and it affects low-molecular-mass compounds and proteins.

FN3K Mechanism
FN3K leads to the formation of fructose 3-phosphate (F3P). A spontaneous decomposition of F3P results in a formation of 3-deoxyglucosone (3DG). This process can bring about diabetic complications. FN3K is present in all types of mammalian tissues and was primarily discovered in rat lenses. Studies were initially conducted to determine if diabetic rat lenses were able to inhibit the activity of FN3K and gain enhanced glycation. Such studies concluded that removing 3DG, by inhibition of Fructosamine 3-kinase, was a feasible option to treat diabetes and similar diseases. FN3K appears able to protect proteins from nonenzymatic glycation processes. It has long been established that control of blood sugar levels can minimize the effects of diabetes. Elevated blood glucose concentration is accountable for the longer-term complications.
Non-enzymatic glycation occurs when sugars and glucose react with amine-containing molecules spontaneously. In the study of the diabetic rat lenses, fructose-3-phosphate was discovered. The study data determined that the Fru-3p was present due to the phosphorylation occurring from a fructose-3-phosphokinase. The same activity was found in other tissues, including the pancreas, kidneys and sciatic nerves. This enzyme was found to phosphorylate a wide variety of fructosamines.

Fructosamine 3 Kinase Interaction
There is said to be an association between Chronic Obstructive Pulmonary Disease (COPD) and diabetes. Increased carbonyl stress is linked to the worsening of COPD. In diabetes cases, heightened levels of reactive carbonyls lead to the forming of AGEs (Advanced Glycation End Products). As stated previously, this process can be prevented by FN3K. One study investigated FN3K in COPD, in the belief that this enzyme may be a factor in controlling carbonyl stress. A Metformin treatment of AECOPD patients was shown to increase FN3K and thought to potentially reduce the severity of the disease.
FN3K enzyme activity has also been studied in relation to human colorectal cancer; one study used thirty patients undergoing surgery of the colon. FN3K activity and gene expression were monitored and analyzed. Results concluded that the levels of FN3K were lower in the cancer tissue than in the normal colorectal mucosa. FN3K gene expression was concluded to possibly be a factor in the progression of this type of cancer.