Functions of Pantothenic acid
Pantothenic acid is a part of coenzyme A (CoA), which plays a basic role in metabolism in the release of energy from carbohydrates, fats, and proteins, and also in the synthesis of fatty acids, sterols, and steroid hormones. Acetyl CoA or active acetate is formed in the oxidative decarboxylation of pyruvic acid, {3-oxidation of fatty acids, and degradation of some amino acids. It can then be oxidized completely in the citric acid cycle, or it can transfer the acetyl-group to various acceptors in the synthesis of the substances mentioned above. Pantothenic acid is also essential for the formation of porphyrin (for heme synthesis) and acetylcholine (a neurotransmitter) and in the acetylation of certain drugs before excretion (sulfonamides). Other important thioesters of CoA that participate in the intermediary metabolism include succinyl CoA, propionyl CoA, and malonyl CoA. Coenzyme A also acts as a carrier of acyl groups that are intermediates in fatty acid oxidation and in the incorporation of fatty acids to triglycerides and other lipids.
In addition to CoA, pantothenic acid is found in the 4 phosphopantetheine of the acyl carrier protein (ACP), which serves as a cofactor in fatty acid synthesis by the fatty acid synthetase complex. Acyl carrier protein binds the growing acyl group during the stepwise addi tion of 2carbon units.
In contrast to other vitamins, pantothenic acid does not constitute the functional part of CoA or ACP; the sulfhydryl group of pantetheine participates in the thioester formation with the organic acid substrates.
Pantothenic acid deficiency has been produced experimentally in humans either by a combination of deficient diet and an antagonist,omega methyl pantothenic acid, or by feeding a semisynthetic diet almost free of pantothenic acid. Similar symptoms were reported in both studies, including vomiting and general malaise, abdominal soreness and cramps, weakness and cramping of the legs, tenderness in the heels, and insomnia.
In a recent studyof patients with ulcerative or granulomatous colitis, a markedly reduced coenzyme A activity was observed in the colonal mucosa. Impaired synthesis of CoA was suggested because the total concentration of pantothenic acid in affected mucosa was normal. Whether this biochemical defect is the resul t of or a causative factor in the disease is not knmvn.
