Post by possiblehelp on Sept 1, 2011 15:53:44 GMT
I found something very interesting today. It says that b12 helps with the metabolism of choline. If you don't want to read all of it, the information on this is in the third paragraph. It gives me something to think about. Also sleep affects metabolism too (Just throwing that in there), if you don't get good sleep every night it will begin to affect you and your digestion will become bad, the same with a vitamin b12 deficiency; it also affects digestion and a lot of people with body odor have BAD digestion.
Info on the b12 metabolizing choline is in the third paragraph.
------------------------------------------------------------------------------------
The primary role of vitamin B12 is as an essential cofactor for the enzymes methionine synthase and methylmalonyl-CoA mutase (McDowell, 2000). Methionine synthase effects the transfer of a methyl group from folic acid (N5-methyl-tetrahydrofolate) to homocysteine, forming methionine. Therefore, a vitamin B12 deficiency reduces methionine supply and metabolic recycling of methyl groups. The latter effect interrupts the normal metabolism of folic acid and blocks its utilization. Thus, a vitamin B12 deficiency produces a secondary deficiency of folic acid, and a characteristic anemia (McDowell, 2000).
Methylmalonyl-CoA mutase, the second enzyme requiring vitamin B12 as a cofactor, catalyzes an essential step in the conversion of propionic acid to glucose via its entry into the Krebs cycle. Methylmalonyl-CoA also arises from the metabolism of odd-chained fatty acids and certain amino acids (valine, isoleucine, methionine and threonine) (Girard, 1998a). The propionic acid pathway is of particular importance in ruminants because of their dependence on propionic acid as the primary glucose precursor, and the production of propionic acid in the rumen fermentation of dietary carbohydrates. As a result of the blockage in utilization of propionic acid, a vitamin B12 or cobalt deficiency in ruminants results in the accumulation of succinic acid in the rumen and methylmalonic acid in blood and urine (Kennedy et al., 1995).
The availability of vitamin B12 for methyl group transfer affects the supply and transfer rate of methyl groups in intermediary metabolism. Thus, vitamin B12 status affects the metabolism of choline and its derivatives, and the synthesis of the purines and pyrimidines, components of DNA and RNA. As a result, rapidly dividing cells, in particular the red blood cells, are sensitive to vitamin B12 status. The nervous system is also quite sensitive to the availability of vitamin B12 , possibly due to its high rate of metabolism. Reduction in the rate of protein synthesis is thought to be a principal cause of the growth depression frequently observed in vitamin B12-deficient animals (Friesecke, 1980).
Info on the b12 metabolizing choline is in the third paragraph.
------------------------------------------------------------------------------------
The primary role of vitamin B12 is as an essential cofactor for the enzymes methionine synthase and methylmalonyl-CoA mutase (McDowell, 2000). Methionine synthase effects the transfer of a methyl group from folic acid (N5-methyl-tetrahydrofolate) to homocysteine, forming methionine. Therefore, a vitamin B12 deficiency reduces methionine supply and metabolic recycling of methyl groups. The latter effect interrupts the normal metabolism of folic acid and blocks its utilization. Thus, a vitamin B12 deficiency produces a secondary deficiency of folic acid, and a characteristic anemia (McDowell, 2000).
Methylmalonyl-CoA mutase, the second enzyme requiring vitamin B12 as a cofactor, catalyzes an essential step in the conversion of propionic acid to glucose via its entry into the Krebs cycle. Methylmalonyl-CoA also arises from the metabolism of odd-chained fatty acids and certain amino acids (valine, isoleucine, methionine and threonine) (Girard, 1998a). The propionic acid pathway is of particular importance in ruminants because of their dependence on propionic acid as the primary glucose precursor, and the production of propionic acid in the rumen fermentation of dietary carbohydrates. As a result of the blockage in utilization of propionic acid, a vitamin B12 or cobalt deficiency in ruminants results in the accumulation of succinic acid in the rumen and methylmalonic acid in blood and urine (Kennedy et al., 1995).
The availability of vitamin B12 for methyl group transfer affects the supply and transfer rate of methyl groups in intermediary metabolism. Thus, vitamin B12 status affects the metabolism of choline and its derivatives, and the synthesis of the purines and pyrimidines, components of DNA and RNA. As a result, rapidly dividing cells, in particular the red blood cells, are sensitive to vitamin B12 status. The nervous system is also quite sensitive to the availability of vitamin B12 , possibly due to its high rate of metabolism. Reduction in the rate of protein synthesis is thought to be a principal cause of the growth depression frequently observed in vitamin B12-deficient animals (Friesecke, 1980).