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Vitamin B5 is a vitamin which supports carbohydrate, protein and fat metabolism and hemoglobin synthesis. It helps release energy from protein, carbohydrates and fat. It is needed to support a variety of body functions including the maintenance of a healthy digestive system.
Vitamin B5 may be useful in acne, alcoholism, allergies, hairloss, asthma, attention deficit-hyperactivity disorder (ADHD), autism, candidiasis, heart disease, carpal tunnel syndrome, respiratory disorders, celiac disease, cystitis, dandruff, depression, diabetic neuropathy, enhancing immune function, improving athletic performance, grey hair, headache, hyperactivity, hypoglycemia, insomnia, irritability, low blood pressure, multiple sclerosis, muscular dystrophy, muscular cramps in the legs associated with pregnancy or alcoholism, neuralgia and obesity.
It may also be used orally for osteoarthritis, rheumatoid arthritis, Parkinson's disease, peripheral neuritis, premenstrual syndrome (PMS), prostatitis, protection against mental and physical stress and anxiety, reducing signs of aging, reducing susceptibility to colds and other infections, retarded growth, shingles, skin disorders, stimulating adrenal glands, mouth ulcers, chronic fatigue syndrome, vertigo and wound healing.
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Published Clinical Studiesclin
[Pantothenic acid]1
Shimizu S.
Division of Applied Life Sciences, Graduate School of Agriculture, Kyoto University.
Pantothenic acid is the antipellagra vitamin essential to many animals for growth and health. It is widely distributed in nature; appreciable amounts are found in liver and some microorganisms. Bound forms of pantothenic acid, such as coenzyme A and 4'-phosphopantetheine, play important roles in various metabolic processes, especially, in fatty acid synthesis and degradation.
Publication Types:
PMID: 10540865 [PubMed - indexed for MEDLINE]
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Pantothenic acid in health and disease.2
Tahiliani AG, Beinlich CJ.
Geisinger Clinic, Weis Center for Research, Danville, Pennsylvania 17822.
In summary, the vitamin pantothenic acid is an integral part of the acylation carriers, CoA and acyl carrier protein (ACP). The vitamin is readily available from diverse dietary sources, a fact which is underscored by the difficulty encountered in attempting to induce pantothenate deficiency. Although pantothenic acid deficiency has not been linked with any particular disease, deficiency of the vitamin results in generalized malaise clinically. In view of the fact that pantothenate is required for the synthesis of CoA, it is surprising that tissue CoA levels are not altered in pantothenate deficiency. This suggests that the cell is equipped to conserve its pantothenate content, possibly by a recycling mechanism for utilizing pantothenate obtained from degradation of pantothenate-containing molecules. Although the steps involved in the conversion of pantothenate to CoA have been characterized, much remains to be done to understand the regulation of CoA synthesis. In particular, in view of what is known about the in vitro regulation of pantothenate kinase, it is surprising that the enzyme is active in vivo, since factors that are known to inhibit the enzyme are present in excess of the concentrations known to inhibit the enzyme. Thus, other physiological regulatory factors (which are largely unknown) must counteract the effects of these inhibitors, since the pantothenate-to-CoA conversion is operative in vivo. Another step in the biosynthetic pathway that may be rate limiting is the conversion of 4'-phosphopantetheine (4'-PP) to dephospho-CoA, a step catalyzed by 4'-phosphopantetheine adenylyl-transferase. In mammalian systems, this step may occur in the mitochondria or in the cytosol. The teleological significance of these two pathways remains to be established, particularly since mitochondria are capable of transporting CoA from the cytosol. Altered homeostasis of CoA has been observed in diverse disease states including starvation, diabetes, alcoholism, Reye syndrome (RS), medium-chain acyl CoA dehydrogenase deficiency, vitamin B12 deficiency, and certain tumors. Hormones, such as glucocorticoids, insulin, and glucagon, as well as drugs, such as clofibrate, also affect tissue CoA levels. It is not known whether the abnormal metabolism observed in these conditions is the result of altered CoA metabolism or whether CoA levels change in response to hormonal or nonhormonal perturbations brought about in these conditions. In other words, a cause-effect relation remains to be elucidated. It is also not known whether the altered CoA metabolism (be it cause or result of abnormal metabolism) can be implicated in the manifestations of a disease. Besides CoA, pantothenic acid is also an integral part of the ACP molecule.(ABSTRACT TRUNCATED AT 400 WORDS)
PMID: 1746161 [PubMed - indexed for MEDLINE]
Pantothenic acid status of pregnant and lactating women.3
Song WO, Wyse BW, Hansen RG.
Pantothenic acid nutritional status was evaluated longitudinally in 26 pregnant women (experimental group) during their third trimester of pregnancy and at 2 weeks and 3 months postpartum. Seventeen nonpregnant and nonlactating women (control group) participated at the same time intervals. All the women were assessed by the intake calculated from a reported 2-day dietary record and by fasted blood, plasma, and 24-hour urinary levels of pantothenate determined by a radioimmunoassay. Estimated daily mean dietary pantothenate intake and the vitamin density for the experimental group were not statistically different from those for the control group. The dietary pantothenate intake averaged 2.75 mg/1,000 kcal. Average pantothenate blood level of the experimental group was lower than that of the control group. No significant difference was found between the two groups in the pantothenate levels of fasting plasma and urinary excretion. When they did not take pantothenic acid supplements, members of the experimental group had intakes less than the Estimated Safe and Adequate Daily Dietary Intake and lower mean blood values than the members of the control group. This suggests that pregnant and lactating women need to consume more pantothenate to maintain a blood vitamin level similar to that of nonpregnant women. This may be achieved by an increased caloric intake, if desirable, or by more careful selection of foods high in the nutrient.
PMID: 3968356 [PubMed - indexed for MEDLINE]
Pantothenic acid decreases valproic acid-induced neural tube defects in mice (I).4
Sato M, Shirota M, Nagao T.
Laboratory of Reproductive and Developmental Toxicology, Hatano Research Institute, Food and Drug Safety Center, Kanagawa, Japan.
The effect of the administration of pantothenic acid (PTA) on valproic acid (VPA)-induced teratogenesis was examined in ICR mice. VPA (300, 400, and 500 mg/kg, s.c.) or PTA (3 x 10, 3 x 100, and 3 x 300 mg/kg, i.p.) was injected on day 8.5 of gestation (plug day = day 0.5). Exencephaly was induced dose dependently by single injections of VPA. Three administrations of PTA alone at any dose levels showed neither embryocidal nor teratogenic effects. In combined treatment experiments, PTA (3 x 300 mg/kg) was injected 1 hr before, immediately before, and 1 hr after VPA administration. PTA significantly reduced VPA-induced exencephaly, while none of the other external malformations such as open eyelid or skeletal malformations such as fused, absent, or bifurcated ribs and fused thoracic vertebrae and fused sternebrae were reduced. The results suggest that PTA reduces the incidence of neural tube defect induced by VPA in mice.
PMID: 8638254 [PubMed - indexed for MEDLINE]
Pantothenic acid deficiency as the pathogenesis of acne vulgaris.5
Leung LH.
Department of General Surgery, Hong Kong Central Hospital, Hong Kong.
For years, the pathogenesis of acne vulgaris has been known to be strongly influenced by hormonal factors. However, the exact role of and the interrelationship among the various hormones in question have not been well elucidated. Here, I wish to suggest a radically different theory for its pathogenesis and relate its basic pathology to a deficiency in pantothenic acid, a vitamin hitherto not known to cause any deficiency syndrome in humans. Hence, the effect of hormonal factors in this disease entity becomes secondary to that of the availability of pantothenic acid. A complete cure of this condition is effected by a very liberal replacement therapy with the vitamin.
PMID: 7476595 [PubMed - indexed for MEDLINE]
Pantothenic acid as a weight-reducing agent: fasting without hunger, weakness and ketosis.6
Department of General Surgery, Hong Kong Central Hospital.
With the conventional method of fasting or aggressive dieting to reduce excess body fat, hunger, weakness, ketogenesis and ketosis are the sequential events that follow. It is not fully understood why, under conditions of negative calorie balance where complete energy release from storage fat is critical, ketosis should arise with a concomitant wastage of energy. Here, I wish to propose a theory that relates the formation of ketone bodies under such conditions to a deficiency in dietary pantothenic acid. Supplementation of this vitamin would facilitate complete catabolism of fatty acids and thus the formation of ketone bodies could be circumvented. As a result, a sufficient amount of energy would be released from storage fat to relieve dieters of the sensation of hunger and weakness which otherwise would be difficult to endure. Hence, using this method for weight reduction together with a careful observation of calorie intake, I have great success in treating overweight-to-obese patients to lose weight.
PMID: 8583972 [PubMed - indexed for MEDLINE]
[The use of pantothenic acid preparations in treating patients with viral hepatitis A]7
Komar VI.
Calcium pantothemate in the daily dose 300 mg and 600 mg and pantetheine in the dose 90 mg and 180 mg per os were applied for 3-4 weeks in combined therapy of 156 patients with viral hepatitis A. In addition to the positive clinico-biochemical effect, these drugs produced an immunomodulatory action and a beneficial effect on the level of blood serum immunoglobulins and the phagocytic activity of peripheral blood neutrophils. Pantetheine provided the most pronounced therapeutic effect.
PMID: 1810066 [PubMed - indexed for MEDLINE]
8 Hypolipidemic effect of pantothenic acid derivatives in mice with hypothalamic obesity induced by aurothioglucose.
Naruta E, Buko V.
Department of Experimental Hepathology, Institute of Biochemistry, National Academy of Sciences, Grodno, Belarus.
The hypolipidemic effects of pantothenic acid derivatives (phosphopantothenate, panthenol and pantethine) were studied in mice with hypothalamic obesity. Hypothalamic obesity in mice was induced by single injection of aurothioglucose (300 mg/kg body wt, i.p.). All the tested substances were administered during the last 10 days before decapitation (i.m., of dosage equivalent to 150 mg/kg body wt of phosphopantothenate). The studied substances inhibited the weight gain of the animals with hypothalamic obesity over the last 10 days of the experiment. The treatment with aurothioglucose increased food intake and mean body weight, blood glucose level; insulin, serum total cholesterol, triglyceride, the sum of LDL + VLDL and LDL-cholesterol concentration; triglyceride and cholesterol fractions in the liver; triglyceride and FFA content as well as lipoprotein lipase activity in adipose tissue of experimental mice. The administration of the assay compounds lowered food intake and mean body weight, insulin and glucose levels and decreased the content of triglycerides, total cholesterol and cholesterol esters in serum and adipose tissue as well as raised the activity of lipoprotein lipase in adipose tissue and serum lipolytic activity in obese mice. Among the compounds studied the reverse effect of panthenol was especially pronounced. The mechanism of hypolipidemic effects of pantothenic acid derivatives can be related to the reduced resistance to insulin and activation of lipolysis in serum and adipose tissue.
PMID: 11817109 [PubMed - indexed for MEDLINE]
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