Vitamin B12

Vitamin B12(cobalamin) is the collective name for several compounds that are in the center of porphyrin skeletal cobalt. Vitamin B12 has a number of biological functions - plays an important role in hematopoiesis, is essential for the development of the central nervous system in children, contributes to the formation of nucleic acids, transmetylation marches and has anabolic effect. Deficiency of vitamin B12 in adults causes macrocytic anemia, impaired rear and lateral spinal cords, peripheral nerves and dementia or depression. Lack of vitamin B12 also affects secondary folate cycle resulting in impaired synthesis of purines and pyrimidines necessary for the formation of DNA and RNA.

Source
In nutritionally significant quantities occurs only in animal foods. Rich sources are liver, kidney, meat warm-blooded animals (1-2 ìg/100 g), fish, egg yolk and dairy products (milk ìg/100, 0.3 ml cheese ìg/100 0.2 to 0.6g). Plant foods contain trace amounts of vitamin B12 only if it has been processed by bacterial fermentation (e.g beer). Absorbed in the small intestine only if the stomach creates a complex with an internal factor .Therefore it is necessary to properly functioning stomach and large amounts of vitamin B12 are formed by the intestinal flora in humans unusable. Cobalamine with an internal factor in the distal ileum bind to specific receptor cubilin and this complex then enters by endocytosis into enterocytes. Inside the enterocyte cobalamin binds to other carriers and excreted into the plasma. 75-80% is bound to haptocorrin and goes to hepatocytes. The cells of other organs enter only vitamin B12 bound to transcobalamin II (the holotranskobalamin) after binding to specific receptors through endocytosis. The cell cobalamin is converted to active metabolites and adenosylcobalamine methylcobalamin, which serve as cofactors of enzymes. The daily recommended dose for adults : 3 mg. Minimal in infants: approximately 0.1 to 0.3 mg.

Function
Haemopoiesis; development of the central nervous system in childhood; cofactor of two metabolic reactions: conversion of homocysteine to methionine by methionine synthase (failure of this reaction leads to the accumulation of homocysteine); conversion metylmalonyl-CoA to succinyl-CoA action metylmalonyl-CoA mutase (failure of this reaction leads to an accumulation of methylmalonic acid and its increased urinary excretion).

Deficit
Its deficiency is clinically manifested failure to thrive, macrocytic anemia and neurological symptoms. An adult is a stock (2-5 mg) of vitamin B12 in the liver, which cover the need for a period of 5-10 years. Stocks, which creates the infant in utero (approximately 25 micrograms), will be exhausted as early as 3-5 months. Among laboratory manifestations include mostly macrocytic anemia, elevated aminotransferases, hyperhomocysteinemia and increased acid secretion metylmalonic acid plasma concentrations of homocysteine and methylmalonic acid excretion increased in the urine. Metabolic changes precede clinical manifestations. Pernicious anemia is an autoimmune disease that leads to atrophy of the gastric mucosa and by the lack of intrinsic factor.

Surplus
Signs of excess were reported even after a high intake (5 mg) of the supplement.

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