Amazoniac
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INTERACTIONS OF THIAMIN, RIBOFLAVIN, AND OTHER B‐VITAMINS
"[W]hile lack of nicotinic acid dominates the picture, pellagra is in truth a disease of multiple deficiencies-nicotinic acid, protein, riboflavin, and perhaps haemopoietic factors."
"Excess leucine in the diet may antagonize the functions of vitamin B6 and impair the conversion of tryptophan to nicotinic acid."
"The formation of nicotinic acid from tryptophan requires not only the participation of pyridoxal phosphate but of niacin and riboflavin as well."
"Riboflavin deficiency was reported to decrease hepatic iron mobilization and probably impaired the absorption of dietary iron, but it did not appear to interfere with iron-induced biosynthesis of ferritin.24 The mechanism involved remains unclear."
"The ultrastructural changes in the myelinated peripheral nerves in riboflavin deprivation resemble those classically noted in vitamin B12 deficiency."
"Riboflavin deficiency did not produce an increase in the odd-chain fatty acids of neural lipids, a characteristic of vitamin B12 deficiency."
"Riboflavin deficiency has often been associated with oral lesions, like cheilosis, angular stomatitis, and glossitis. Patients with these lesions sometimes fail to respond to riboflavin treatment alone and require supplementation with vitamin B6 or other B-complex vitamins."
"[..]an interaction exists between vitamin B6 and vitamin C, but the precise interrelationship remains to be clarified."
"Vitamin B6 deficiency has been reported to cause an impairment in vitamin B12 absorption in the rat that results in a lowering of vitamin B12 levels in the serum and in reduced vitamin B12 stores in the liver."
"In the overall metabolic reactions involving biotin, participation of pantothenic acid in the form of coenzyme A is required. In the metabolism of leucine, valine, and isoleucine, in addition to biotin, pyridoxal phosphate, NAD, and FAD are required[.]"
"Leucine, valine, and isoleucine, following an initial transamination reaction with pyridoxal phosphate to form the corresponding a-keto acids, are oxidatively decarboxylated to form acetyl-CoA derivatives. The subsequent reactions are similar to the metabolism of fatty acids. The propionyl-CoA formed from valine and isoleucine requires biotin for its conversion to methylmalonyl-CoA. In the metabolism of leucine, the conversion of b-methylcrotonyl-CoA to b-methylglutaryl-CoA is a biotin-requiring reaction."
"Propionate metabolism in man requires pantothenic acid and biotin in its conversion to methylmalonic acid.44-46 As noted above, valine and isoleucine may serve as a source of propionate (FIGURE 10). Outward signs of an interaction between biotin and pantothenic acid appear to exist. Both biotin deficiency and pantothenic acid deficiency result in the depigmentation of the fur of black mice. Biotin deficiency may be aggravated by a simultaneous pantothenic acid deficiency. The addition of biotin to the diet not only protects the animals from a biotin deficiency, but also reduces the severity of the symptoms of a pantothenic acid deficiency. Biotin deficiency is associated with extensive fatty infiltration of the liver and kidney, which emphasizes its importance in the metabolism of fat.47"
"In mammals, vitamin B12 is required in the following reactions: (a) methylation of homocysteine and (b) the conversion of methylmalonyl-CoA to succinyl-CoA (FIGURES 3 and 4). The former also requires folic acid to complete the methylation reaction."
"The elevated levels of propionyl-CoA and methylmalonyl-CoA that occur in a vitamin B12 deficiency may inhibit the biosynthesis of malonyl-CoA, which is required for elongation processes, such as the conversion of linoleate to arachidonate.50 Vitamin B12 deficiency promotes a greater synthesis and accumulation of odd-number and branched-chain, 15- and 17-carbon, fatty acids. Elevated levels of these fatty acids were observed in the spinal cord phosphatidyl choline of a child with deranged vitamin B12 metabolism.51 Reports have suggested that the development of neurological lesions of pernicious anemia may be due in part to the progressive accumulation of branched-chain and odd-numbered saturated fatty acids into neural cerebrosides and phospholipids."
"Glycine may be metabolized via several pathways. One pathway, important in both plants and animals, involves four proteins and the interaction of pyridoxal phosphate, NAD, FAD, and tetrahydrofolic acid."
"Anemia is often observed in vitamin C-deficient patients. A normochromic, normocytic, or macrocytic type of anemia is generally observed, although megaloblastic anemia has been reported for some The presence of megaloblastic anemia in some scorbutic patients has given rise to the consideration that either a dietary deficiency of folk acid existed or that folate metabolism was impaired in vitamin C deficiency.53,59 In some instances, the megaloblastic anemia was effectively treated with ascorbic acid alone, while in other reports, supplements of folic acid were required.53,56"
"Pyruvate metabolism involves the essential paticipation of thiamin pyrophosphate in concert with the actions of lipoic acid, coenzyme A, NAD, and FAD (FIGURE 12). Although a vitamin B, deficiency can be produced readily in the human experimentally, the clinical signs and symptoms observed cannot be fully explained by known functions of the vitamin."
Questions should be addressed to burtlan, please.
"[W]hile lack of nicotinic acid dominates the picture, pellagra is in truth a disease of multiple deficiencies-nicotinic acid, protein, riboflavin, and perhaps haemopoietic factors."
"Excess leucine in the diet may antagonize the functions of vitamin B6 and impair the conversion of tryptophan to nicotinic acid."
"The formation of nicotinic acid from tryptophan requires not only the participation of pyridoxal phosphate but of niacin and riboflavin as well."
"Riboflavin deficiency was reported to decrease hepatic iron mobilization and probably impaired the absorption of dietary iron, but it did not appear to interfere with iron-induced biosynthesis of ferritin.24 The mechanism involved remains unclear."
"The ultrastructural changes in the myelinated peripheral nerves in riboflavin deprivation resemble those classically noted in vitamin B12 deficiency."
"Riboflavin deficiency did not produce an increase in the odd-chain fatty acids of neural lipids, a characteristic of vitamin B12 deficiency."
"Riboflavin deficiency has often been associated with oral lesions, like cheilosis, angular stomatitis, and glossitis. Patients with these lesions sometimes fail to respond to riboflavin treatment alone and require supplementation with vitamin B6 or other B-complex vitamins."
"[..]an interaction exists between vitamin B6 and vitamin C, but the precise interrelationship remains to be clarified."
"Vitamin B6 deficiency has been reported to cause an impairment in vitamin B12 absorption in the rat that results in a lowering of vitamin B12 levels in the serum and in reduced vitamin B12 stores in the liver."
"In the overall metabolic reactions involving biotin, participation of pantothenic acid in the form of coenzyme A is required. In the metabolism of leucine, valine, and isoleucine, in addition to biotin, pyridoxal phosphate, NAD, and FAD are required[.]"
"Leucine, valine, and isoleucine, following an initial transamination reaction with pyridoxal phosphate to form the corresponding a-keto acids, are oxidatively decarboxylated to form acetyl-CoA derivatives. The subsequent reactions are similar to the metabolism of fatty acids. The propionyl-CoA formed from valine and isoleucine requires biotin for its conversion to methylmalonyl-CoA. In the metabolism of leucine, the conversion of b-methylcrotonyl-CoA to b-methylglutaryl-CoA is a biotin-requiring reaction."
"Propionate metabolism in man requires pantothenic acid and biotin in its conversion to methylmalonic acid.44-46 As noted above, valine and isoleucine may serve as a source of propionate (FIGURE 10). Outward signs of an interaction between biotin and pantothenic acid appear to exist. Both biotin deficiency and pantothenic acid deficiency result in the depigmentation of the fur of black mice. Biotin deficiency may be aggravated by a simultaneous pantothenic acid deficiency. The addition of biotin to the diet not only protects the animals from a biotin deficiency, but also reduces the severity of the symptoms of a pantothenic acid deficiency. Biotin deficiency is associated with extensive fatty infiltration of the liver and kidney, which emphasizes its importance in the metabolism of fat.47"
"In mammals, vitamin B12 is required in the following reactions: (a) methylation of homocysteine and (b) the conversion of methylmalonyl-CoA to succinyl-CoA (FIGURES 3 and 4). The former also requires folic acid to complete the methylation reaction."
"The elevated levels of propionyl-CoA and methylmalonyl-CoA that occur in a vitamin B12 deficiency may inhibit the biosynthesis of malonyl-CoA, which is required for elongation processes, such as the conversion of linoleate to arachidonate.50 Vitamin B12 deficiency promotes a greater synthesis and accumulation of odd-number and branched-chain, 15- and 17-carbon, fatty acids. Elevated levels of these fatty acids were observed in the spinal cord phosphatidyl choline of a child with deranged vitamin B12 metabolism.51 Reports have suggested that the development of neurological lesions of pernicious anemia may be due in part to the progressive accumulation of branched-chain and odd-numbered saturated fatty acids into neural cerebrosides and phospholipids."
"Glycine may be metabolized via several pathways. One pathway, important in both plants and animals, involves four proteins and the interaction of pyridoxal phosphate, NAD, FAD, and tetrahydrofolic acid."
"Anemia is often observed in vitamin C-deficient patients. A normochromic, normocytic, or macrocytic type of anemia is generally observed, although megaloblastic anemia has been reported for some The presence of megaloblastic anemia in some scorbutic patients has given rise to the consideration that either a dietary deficiency of folk acid existed or that folate metabolism was impaired in vitamin C deficiency.53,59 In some instances, the megaloblastic anemia was effectively treated with ascorbic acid alone, while in other reports, supplements of folic acid were required.53,56"
"Pyruvate metabolism involves the essential paticipation of thiamin pyrophosphate in concert with the actions of lipoic acid, coenzyme A, NAD, and FAD (FIGURE 12). Although a vitamin B, deficiency can be produced readily in the human experimentally, the clinical signs and symptoms observed cannot be fully explained by known functions of the vitamin."
Questions should be addressed to burtlan, please.
