This report consists of a brief summary of experimental studies which emphasize (a) the dominant role played by vitamin B12 in the utilization of carbohydrates, (b) interrelationships between vitamin B12 absorption and endocrine function, and (c) some relationships of vitamin B12 to diabetes mellitus.
(1) Weanling rats fed a diet, rich in carbohydrate and low in fat require more vitamin B12 for growth.
(2) The fat content of the carcass of vitamin B12-deficient rats is abnormally low but can be elevated by injection of this vitamin.
(3) The administration of glucose to rats results in a decrease in the vitamin B12levels of plasma or liver.
(4) Deficiency of vitamin B12 causes hyperglycemia correctable with vitamin B12. In vitro experiments indicate that the red cells of vitamin B12-deficient animals are low in glutathione content as well as enzyme activity essential for the degradation of glucose. Other enzyme systems involved in carbohydrate metabolism such as coenzyme A in liver or DPN in liver are also deranged due to this deficiency.
(5) The effect of cortisone and thyroid on absorption of orally administered vitamin B12 and retention of injected vitamin B12 was re-emphasized. It was found that corticotropin (ACTH) or cortisone causes hyperglycemia, destruction of vitamin B12-binding substances in muscles as well as an elevation of the vitamin B12serum level. Thyroidectomy decreases absorption of vitamin B12.
(6) Some evidence of adrenal hyperactivity in diabetic patients with diabetic retinopathy, (as gathered by other investigators), has been reviewed. We caution against a premature interpretation that adrenal hyperactivity is causally or pathogenetically related to diabetic retinopathy; it may turn out to be a mere associated phenomenon.
(7) Diabetic patients without retinopathy excrete in their urines a significantly smaller amount of an orally administered radioactive vitamin B12-test dose than do non-diabetic subjects or diabetic patients with retinopathy. Fecal excretion tests confirm the above findings.
Vitamin B12, also called cobalamin, is a water-soluble vitamin that has a key role in the normal functioning of the brain and nervous system, and the formation of red blood cells. It is one of eight B vitamins. It is involved in the metabolism of every cell of the human body, especially affecting DNA synthesis, fatty acid and amino acid metabolism. No fungi, plants, or animals (including humans) are capable of producing vitamin B12. Only bacteria and archaea have the enzymes needed for its synthesis. Some substantial sources of B12 include animal products (shellfish, meat), fortified food products, and dietary supplements. B12 is the largest and most structurally complicated vitamin and can be produced industrially only through bacterial fermentation synthesis, typically used to manufacture B12 for fortified foods and supplements.
Vitamin B12 consists of a class of chemically related compounds (vitamers), all of which show pharmacological activity. It contains the biochemically rare element cobalt (chemical symbol Co) positioned in the center of a planar tetra-pyrrole ring called a corrin ring. The vitamer is produced by bacteria as hydroxocobalamin, but conversion between different forms of the vitamin occurs in the body after consumption.
Vitamin B12 was discovered as a result of its relationship to the disease pernicious anemia, an autoimmune disease in which parietal cells of the stomach responsible for secreting intrinsic factor are destroyed; these cells are also responsible for secreting acid in the stomach. Because intrinsic factor is crucial for the normal absorption of B12, its lack in the presence of pernicious anemia causes a vitamin B12 deficiency. Many other subtler kinds of vitamin B12 deficiency and their biochemical effects have since been elucidated. Due to impairment of vitamin B12 absorption during aging, people over age 60 are at risk of deficiency.
Vitamin B12 deficiency can potentially cause severe and irreversible damage, especially to the brain and nervous system. At levels only slightly lower than normal, a range of symptoms such as fatigue, lethargy, depression, poor memory, breathlessness, headaches, and pale skin, among others, may be experienced, especially in elderly people (over age 60) who produce less stomach acid as they age, thereby increasing their probability of B12deficiencies. Vitamin B12 deficiency can also cause symptoms of mania and psychosis.
Vitamin B12 deficiency is most commonly caused by low intakes, but can also result from malabsorption, certain intestinal disorders, low presence of binding proteins, and use of certain medications. Vitamin B12 is rare from plant sources, so vegetarians are most likely to suffer from vitamin B12 deficiency. Infants are at a higher risk of vitamin B12 deficiency if they were born to vegetarian mothers. The elderly who have diets with limited meat or animal products are vulnerable populations as well. Vitamin B12 deficiency may occur in between 40% to 80% of the vegetarian population. In Hong Kong and India, vitamin B12 deficiency has been found in roughly 80% of the vegan population as well.
Vitamin B12 is a co-substrate of various cell reactions involved in methylation synthesis of nucleic acid and neurotransmitters. Synthesis of the trimonoamine neurotransmitters can enhance the effects of a traditional antidepressant. The intracellular concentrations of vitamin B12 can be inferred through the total plasma concentration of homocysteine, which can be converted to methionine through an enzymatic reaction that uses 5-methyltetrahydrofolate as the methyl donor group. Consequently, the plasma concentration of homocysteine falls as the intracellular concentration of vitamin B12 rises. The active metabolite of vitamin B12 is required for the methylation of homocysteine in the production of methionine, which is involved in a number of biochemical processes including the monoamine neurotransmitters metabolism. Thus, a deficiency in vitamin B12 may impact the production and function of those neurotransmitters.