Pantothenic acid is widely distributed in many foods. Therefore, problems of deficiency of the vitamin are rare. The vitamin has critical roles in metabolism, being an integral part of the acylation factors coenzyme-A (CoA) and acyl-carrier protein (ACP). In these forms, pantothenic acid is required for the normal metabolism of fatty acids, amino acids, and carbohydrates, and has important roles in the acylation of proteins. Pantothenic acid is widely distributed in nature. It occurs mainly in bound forms (CoA, CoA esters, ACP).
Because pantothenic acid occurs in most foods and feedstuffs as CoA and ACP, the utilization of the vitamin in foods depends on the hydrolytic digestion of these protein complexes to release the free vitamin. Both CoA and ACP are degraded in the intestinal lumen by hydrolases and ultimately converted to pantothenic acid.
Pantothenic acid is transported in both the plasma and erythrocytes. Plasma contains the vitamin only in the free acid form, which erythrocytes take up by passive diffusion. Erythrocytes carry most of the vitamin in the blood. Pantothenic acid is taken into cells in its free acid form.
The greatest concentrations of CoA are found in the liver, adrenals, kidneys, brain, heart, and testes. Much of this (70% in liver, 95% in heart) is located in the mitochondria. The cerebrospinal fluid, because it is constantly renewed in the central nervous system, requires a constant supply of pantothenic acid, which, as CoA, is involved in the synthesis of the neurotransmitter acetylcholine in brain tissue.
All tissues have the ability to synthesize CoA from pantothenic acid of dietary origin. The concentration of non-acylated CoA determines the rate of oxidation-dependent mitochondrial energy production. CoA has been shown to enter mitochondria by non-specific membrane-binding as well as by an energy-dependent membrane transporter (1).
Pantothenic acid is excreted mainly in the urine as free pantothenic acid with urinary excretion of the vitamin correlating with dietary intake. An appreciable amount (~15% of daily intake) is oxidized completely, and is excreted across the lungs as CO2. Humans typically excrete, in the urine, 0.8–8.4 mg of pantothenic acid per day.
Both CoA and ACP function in a large number of vital metabolic transformations, including the tricarboxylic acid (TCA) cycle and the metabolism of fatty acids (2). There is a clear distinction between the metabolic roles of CoA and ACP: CoA is involved in a broad array of reactions related to oxidative energy metabolism and catabolism, whereas ACP is involved in synthetic reactions. CoA serves as an essential cofactor for some 4% of known enzymes, including at least 100 enzymes involved in intermediary metabolism. Acetyl-CoA, the “active acetate,” group has many metabolic uses: synthesis of fatty acids, and isopranoids (e.g., cholesterol, steroid hormones) acetylations of alcohols, amines, and amino acids (e.g., choline, sulfonamides, p-aminobenzoate, proteins) oxidation of amino acids, involvement in carnitine to form energy-equivalent acylcarnitines capable of being transported into the mitochondria where β-oxidation occurs; production of the “ketone body” acetoacetate derived from fat metabolism when glucose is limiting. ACP is a component of the multi enzyme complex fatty acid synthase (3).
Deprivation of pantothenic acid results in metabolic impairments, including reduced lipid synthesis and energy production. Signs and symptoms of pantothenic acid deficiency most frequently involve the skin, liver, adrenals, and nervous system. Owing to the wide distribution of the vitamin in nature, dietary deficiencies of pantothenic acid are rare; they are more common in circumstances of inadequate intake of basic foods and vitamins, and are often associated with (and mistakenly diagnosed as) deficiencies of other vitamins.
Pantothenic acid deficiency in humans has been observed only in severely malnourished patients and in subjects treated with the antagonist ω-methylpantothenic acid. In cases of the former type, neurologic signs (paresthesia in the toes and soles of the feet) have been reported. Subjects made deficient in pantothenic acid through the use of ω-methylpantothenic acid also developed burning sensations of the feet; in addition, they showed depression, fatigue, insomnia, vomiting, muscular weakness, and sleep and gastrointestinal disturbances. Changes in glucose tolerance, increased sensitivity to insulin, and decreased antibody production have also been reported.
Some evidence suggests that pantothenic acid intakes may not be adequate for some individuals (4). Urinary pantothenic acid excretion has been found to be low for pregnant women, adolescents, and the elderly, compared with the general population. A polymorphism of PanK2 has been identified as the metabolic basis of an autosomal recessive neurodegenerative disorder, Hallervorden-Spatz syndrome. Affected subjects show dystonia and optic atrophy or retinopathy, with the deposition of iron in basal ganglia.
The toxicity of pantothenic acid is negligible. No adverse reactions have been reported in any species following the ingestion of large doses of the vitamin. Massive doses (e.g., 10 g/day) administered to humans have not produced reactions more severe than mild intestinal distress and diarrhoea.
Sources of Pantothenic acid
The most important food sources of pantothenic acid are meats (liver and heart are particularly rich). Mushrooms, avocados, broccoli, and some yeasts are also rich in the vitamin. Whole grains are also good sources; however, the vitamin is localized in the outer layers, thus it is largely (up to 50%) removed by milling.
Pantothenic acid in foods and feedstuffs is fairly stable to ordinary means of cooking and storage. It can, however, be unstable to heat and either too alkaline or acid conditions. Reports indicate losses of 15-50% from cooking meat, and of 37–78% from heat-processing vegetables. The alcohol derivative, pantothenol, is more stable; for this reason it is used as a source of the vitamin in multivitamin supplements.
The biologic availability of pantothenic acid from foods and feedstuffs is a function of the efficiency of the enteric hydrolysis of its food forms and the absorption of those products. One study indicated “average” bioavailability of the vitamin in the American diet in the range of 40–60%; similar results were obtained for maize meals in another study (5,6).
Functions of Pantothenic acid
Benefits have been reported for the use of supplements of pantothenic acid and/or metabolites (7,8).
Reduced Serum Cholesterol Level
High doses (500–1,200 mg/day) of pantothine-a pantothenic acid derivative have been shown to reduce serum concentrations of total and LDL cholesterol and triglycerides, with increases in HDL cholesterol. While the underlying mechanism is unclear, it is thought to involve roles of pantetheine as a cofactor in shunting groups away from steroid synthesis to oxidative metabolism, and/or in reducing triglyceride synthesis (9).
Rheumatoid Arthritis (RA)
Patients with RA have been found to show lower blood pantothenic acid levels than healthy controls. Nearly 50 years ago, an unblinded trial found relief of symptoms in 20 patients treated with pantothenic acid (10). A subsequent randomized, controlled trial showed that high doses (up to 2 g/day) of calcium pantothenate reduced the duration of morning stiffness, the degree of disability, and the severity of pain for rheumatoid arthritis patients (11).
While pantothenic acid deficiency is known to reduce exercise endurance in animal models, results of the few studies conducted in humans have been inconsistent. Some showed improved efficiency of oxygen utilization and reduced lactate acid accumulation in athletes (12); others showed no benefits (13).
Studies in animal models have found pantothenic acid, given orally or topically as pantothenol, to promote the closure of wounds of the skin. Studies with humans given high, combined doses of pantothenic acid and ascorbic acid have shown no benefits, although a derivative, dexapanthenol, has been found useful in reducing skin dehydration and irritation (14,15).
Administration of a pantothenic acid-based dietary supplement in healthy adults with facial acne lesions is safe, well tolerated and reduced total facial lesion count versus placebo after 12 weeks. Secondary analysis shows that the study agent significantly reduced area-specific and inflammatory blemishes (16).
It has been suggested that pantothenic acid may have value in treating the systemic autoimmune disease lupus erythromatosus, the argument being a theoretical one based on the observation that lupus can be caused by drugs that impair pantothenic acid metabolism. No relevant clinical data have been reported. It has also been proposed that pantothenic acid may have value in the prevention of greying hair.
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Keywords-pantothenic acid, cholesterol, arthritis, skin, wound healing, acne