Vitamin B12
Cobalamin (Vitamin B12) is required for development of red blood cells and is used to make the protective coating surrounding nerves. Vitamin B12 is an essential nutrient in our diet. Cobalamin (Vitamin B12) exists in a number of different chemical forms. All have a cobalt atom at the center of a corrin ring. In nature, the Vitamin B12 is mainly in the 2-deoxyadenosyl (ado) form, which is located in mitochondria. It is the cofactor for the enzyme methylmalonyl CoA mutase. The other major natural Vitamin B12 is methylcobalamin, the form in human plasma and in cell cytoplasm. It is the cofactor for methionine synthase. There are also minor amounts of hydroxocobalamin to which methyl- and adocobalamin are rapidly converted by exposure to light.
Dietary Sources and Requirements
Vitamin B12 is synthesized solely by microorganisms. Ruminants obtain Vitamin B12 from the foregut, but the only source for humans is food of animal origin, e.g., meat, fish, and dairy products. Vegetables, fruits, and other foods of non-animal origin are free from Vitamin B12 unless they are contaminated by bacteria. A normal Western diet contains between 5 and 30µg of Vitamin B12 daily. Adult daily losses (mainly in the urine and feces) are between 1 and 3µg (~0.1% of body stores) and, as the body does not have the ability to degrade Vitamin B12, daily requirements are also about 1–3µg. Body stores are of the order of 2–3 mg, sufficient for 3–4 years if supplies are completely cut off.
Absorption
Two mechanisms exist for absorption of Vitamin B12. One is passive, occurring equally through buccal, duodenal, and ileal mucosa; it is rapid but extremely inefficient, <1% of an oral dose being absorbed by this process. The normal physiologic mechanism is active; it occurs through the ileum and is efficient for small (a few micrograms) oral doses of cobalamin and is mediated by gastric intrinsic factor (IF). Dietary Vitamin B12 is released from protein complexes by enzymes in the stomach, duodenum, and jejunum; it combines rapidly with a salivary glycoprotein that belongs to the family of cobalamin-binding proteins known as haptocorrins (HCs). In the intestine, the haptocorrin is digested by pancreatic trypsin and the Vitamin B12 transferred to Intrinsic Factor.
Intrinsic Factor is produced in the gastric parietal cells of the fundus and body of the stomach, and its secretion parallels that of hydrochloric acid. The IF-cobalamin (Vitamin B12) complex passes to the ileum, where IF attaches to a specific receptor (cubilin) on the microvillus membrane of the enterocytes. Cubilin is also present in yolk sac and renal proximal tubular epithelium. Cubulin appears to traffic by means of amnionless (AMN), an endocytic receptor protein that directs sublocalization and endocytosis of cubulin with its ligand IF-cobalamin complex (Vitamin B12). The cobalamin (Vitamin B12)-IF complex enters the ileal cell where IF is destroyed. After a delay of about 6 h, the Vitamin B12 appears in portal blood attached to transcobalamin (TC) II.
Vitamin B12 is a vitamin. It can be found in foods such as meat, fish, and dairy products. It can also be made in a laboratory.
Vitamin B12 is used for treating and preventing vitamin B12 deficiency, a condition in which vitamin B12 levels in the blood are too low. It is also used to treat pernicious anemia, a serious type of anemia that is due to vitamin B12 deficiency and is found mostly in older people.
Vitamin B12 is also used for memory loss; Alzheimer’s disease; boosting mood, energy, concentration and the immune system; and slowing aging. It is also used for heart disease, lowering high homocysteine levels (which may contribute to heart disease), male infertility, diabetes, sleep disorders, depression, mental disorders, weak bones (osteoporosis), swollen tendons, AIDS, inflammatory bowel disease, asthma, allergies, a skin disease called vitiligo, preventing cervical and other cancers, and skin infections.
Medicines for the control of overweight and weight loss with the use of vitamin B12 shots are gaining importance. The Vitamin B12 in human beings is maintained as two active coenzymes in the cells: methylcobalamin and deoxyadenosylcobalamin. Deoxyadenosylcobalamin (deoxyadenosyl b12) is a cofactor for the mitochondrial mutase enzyme, of the kerb’s cycle that catalyzes the isomerization of L-methylmalonyl CoA to succinyl CoA. This step may be the reason for the usage of B12 shots for weight loss because this step is an important reaction in carbohydrate, protein and lipid metabolism. This is a destructive process (catabolism) of the fats, carbohydrates and amino acids, which could help in weight loss.
The vitamin B12 and B6 intake alone does not help in weight loss. The weight loss obtained with vitamin B12 is a combination of efforts to lose weight. Controlled and adequate Diet and daily exercise are also inevitable for weight loss, along with Vitamin B12+b6. Nevertheless there is always a possibility that Vitamin B12 + B6 shots may be used for weight loss. Vitamin B12 has extremely low toxicity and even taking it in enormous doses appears not to be harmful to healthy individuals.
Treatment of vitamin B12 deficiency can unmask polycythemia Vera, which is characterized by an increase in blood volume and the number of red blood cells. The correction of megalobic anemia with vitamin B12 can result in fatal hypokalemia and gout in susceptible individuals, and it can obscure folate deficiency in megaloblastic anemia.
Vitamin B12 in the form of cyanocobalamin is contradicted in early Leber’s disease, which is hereditary optic nerve atropathy. Cyanocobalamin can cause severe and swift optic atrophy, but other forms of vitamin B12 are available. However, the sources of this statement are not clear, while an opposing view] concludes that "The clinical picture of optic neuropathy associated with vitamin B12 deficiency shows similarity to that of Leber’s disease, optic neuropathy. Both involve the nerve fibres of the papillomacular bundle. The present case reports suggest that optic neuropathy in patients carrying a primary LHON mtDNA mutation may be precipitated by vitamin B12 deficiency. Therefore, known carriers should take care to have an adequate dietary intake of vitamin B12 and malabsorption syndromes like those occurring in familial pernicious anemia or after gastric surgery should be excluded."
