Vitamin B6 occurs in 3 forms–pyridoxine, pyridoxamine, and pyridoxal. B6 is absorbed inside the large intestine. The muscle stores approximately 75 80 % of the vitamin even though the live stores approximately 5-10 %.
B6 is necessary for transaminations, ammonia release,, side chain cleavage reactions, dehydratases and decarboxylations. Its aldehyde class acts as a Schiff base to react with the amino groups of amino acids. It essentially acts to shuttle nitrogen between compounds.
Functions- The three sorts of B6 can all be switched into to the coenzyme PLP which aids in transamination and protein metabolism. PLP is essential for glycogen degradation; it also will help with the development of the neurotransmitter, serotonin, the nonprotein part of hemoglobin (heme), nucleic acids, and lecithin. Vitamin B6 is essential for the metabolism of tryptophan to niacin.
· Transaminations These responses are needed to recycle as well as reuse nitrogen in the entire body. They’re the first phase in amino acid catabolism as well as the last step in the synthesis of nonessential amino acids. Example: a-ketoglutarate + asparate glutamate + oxaloacetate
· Serine/ Threonine Deamination (Dehydratases) This response supplies the production of the a keto acids of serine as well as threonine through oxidative removal of N as ammonia Example: Serine a-keto-serine + NH4+
· Decarboxylation These reactions often appear on the neuroactive amines of seratonin, tyramine, histamine, and GABA. They are undoubtedly crucial in porphyrin synthesis, intermediates inside the synthesis of sphingomyelin, lecithin and taurine, as well as for the breakdown and desulfuration of cysteine.
· Glycogen meal service delivery of all B6 in the body is sure to glycogen phosphorylase though the importance is unknown. The response is vital for recycling of folate and is as follows:
Serine glycine + 5,10-methylene-THF
Deficiency Deficiencies of vitamin B6 are pretty rare. Individuals with a diet deficient in vitamin B6 will first show signs of weakness, nervousness, insomnia, irritability, and hydrated skin lesions. More advanced symptoms consist of growth failure, impaired motor function, hypochromic microcytic anemia, sleek tongue, as well as convulsions.
The impaired motor performance as well as other psychological problems may be linked to a reduction in amino acid-based neurotransmitters (serotonin, GABA, tyramine, epinephrine). You see a rise in urea excretion because of a decline synthesis of nonessential amino acids. The nitrogen from these amino acids is not reused by transamination and instead is excreted and lost. You see a rise in urinary excretion particularly within the following amino acids: metabolites of glycine, methionine, and tryptophan. The hypochromic microcytic anemia is mainly because that there is a lowered synthesis of the B6 dependent porphyrin ring of hemoglobin.
Those who are at most risk would be the older folk with poor vitamin intake, hemodialysis patients, alcoholics, and all those who are on drug therapy. Overall, individuals with an impressive metabolic stress.
Sources Foods richest in vitamin B6 include:
o whole grains o legumes o nuts o navy beans o walnuts o meat (sirloin plus chicken) o fish (salmon plus shellfish) o bananas as well as apples o broccoli and spinach
Therapeutics Vitamin B6 may provide therapeutic advantages for the next syndromes: carpal tunnel syndrome, glucose intolerance, sideroblastic anemia, neurologic problems, hyperoxaluria, convulsive seizures, monosodium glutarate (MSG) intolerance, premenstral syndrome (Immune function and pms). Furthermore, vitamin B6 may help reduce homocysteine levels and thus the risk of developing cardiovascular disease.