It is book among minerals for the reason that it includes a metal ion, cobalt
Vitamin Btwelve has the largest and most complex chemical structure of all the vitamins. For this reason cobalamin is the term used to refer to compounds having vitamin B12 activity. Methylcobalamin and 5-deoxyadenosylcobalamin are the forms of vitamin B12 used in the human body (1). The form of cobalamin used in most nutritional supplements and fortified foods, cyanocobalamin, is readily converted to 5-deoxyadenosylcobalamin and methylcobalamin in the body. In mammals, cobalamin is a cofactor for only two enzymes, methionine synthase and L-methylmalonyl-coenzyme A mutase (2).
Cofactor getting methionine synthase
Methylcobalamin becomes necessary to the intent behind new folate-centered chemical, methionine synthase. So it enzyme becomes necessary on the synthesis of amino acidic, methionine, from homocysteine. Methionine in turn is necessary into synthesis out of S-adenosylmethionine, a great methyl classification donor included in many physical methylation reactions, like the methylation of plenty of web sites inside DNA, RNA, and protein (3). Aberrant methylation out-of DNA and proteins, that triggers changes in chromatin construction and you may gene term, is actually a common element off malignant tumors tissues. Useless function of methionine synthase can lead to an accumulation of homocysteine, which has been of the improved threat of cardiovascular disease (Profile 1).
Cofactor to have L-methylmalonyl-coenzyme A good mutase
5-Deoxyadenosylcobalamin is required by the enzyme https://datingranking.net/escort-directory/davenport/ you to definitely catalyzes new transformation away from L-methylmalonyl-coenzyme A towards succinyl-coenzyme A good (succinyl-CoA), which in turn gets in the new citric acidic period (Profile 2). Succinyl-CoA takes on an important role from the creation of opportunity off lipids and healthy protein and is required for the synthesis of hemoglobin, the new outdoors-carrying pigment when you look at the red-colored bloodstream cells (3).
In healthy adults, vitamin B12 deficiency is uncommon, mainly because total body stores can exceed 2,500 ?g, daily turnover is slow, and dietary intake of only 2.4 ?g/day is sufficient to maintain adequate vitamin B12 status (see RDA) (4). In elderly individuals, vitamin B12 deficiency is more common mainly because of impaired intestinal absorption that can result in in B12 deficiency in this population.
Factors behind vitamin B12 insufficiency
Intestinal malabsorption, rather than inadequate dietary intake, can explain most cases of vitamin B12 deficiency (5). Absorption of vitamin B12 from food requires normal function of the stomach, pancreas, and small intestine. Stomach acid and enzymes free vitamin B12 from food, allowing it to bind to R-protein (also known as transcobalamin-1 or haptocorrin), found in saliva and gastric fluids. In the alkaline environment of the small intestine, R-proteins are degraded by pancreatic enzymes, freeing vitamin B12 to bind to intrinsic factor (IF), a protein secreted by specialized cells in the stomach. Receptors on the surface of the ileum (final part of the small intestine) take up the IF-B12 complex only in the presence of calcium, which is supplied by the pancreas (5). Vitamin B12 can also be absorbed by passive diffusion, but this process is very inefficient-only about 1% absorption of the vitamin B12 dose is absorbed passively (2). The prevalent causes of vitamin B12 deficiency are (1) an autoimmune condition known as pernicious anemia, and (2) a disorder called food-bound vitamin B12 malabsorption. Both conditions have been associated with a chronic inflammatory disease of the stomach known as atrophic gastritis.
Atrophic gastritis is thought to affect 10%-30% of people over 60 years of age (6). The condition is frequently associated with the presence of autoantibodies directed toward stomach cells (see Pernicious anemia) and/or infection by the bacteria, Helicobacter pylori (H. pylori) (7). H. pylori infection induces chronic inflammation of the stomach, which may progress to peptic ulcer disease, atrophic gastritis, and/or gastric cancer in some individuals. Diminished gastric function in individuals with atrophic gastritis can result in bacterial overgrowth in the small intestine and cause food-bound vitamin B12 malabsorption. Vitamin B12 levels in serum, plasma, and gastric fluids are significantly decreased in individuals with H. pylori infection, and eradication of the bacteria has been shown to significantly improve vitamin B12 serum concentrations (8).