Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “PANTOTHENIC ACID”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 109 records · Page 6Linked to original sources
PubMed1981

Pantothenic acid nutritional status in the elderly--institutionalized and noninstitutionalized.

Pantothenic acid nutritional status was evaluated in 37 men (32 noninstitutionalized and five institutionalized) and 54 women (33 noninstitutionalized and 21 institutionalized) 65 yr of age or older. A fasting blood sample, a 24-h urine specimen and a food consumption record for 1 wk were obtained from each subject. Hematological, anthropometric, and dietary parameters indicated these 91 subjects were similar to elderly populations evaluated in other studies. Pantothenic acid was analyzed by both radioimmunoassay and microbiological assay. By combining methods it was possible to differentiate various forms and derivatives of pantothenic acid. Free pantothenic acid, but not the phosphoderivatives, was observed in urine. Microbiological and radioimmunoassay estimations of pantothenic acid showed good correlation (r = 0.91). Pantothenic acid excretion in the institutionalized subjects (7.5 +/- 1.3 (x +/- SEM) mg/g creatinine) was comparable to the excretion levels in the noninstitutionalized subjects (5.9 +/- 0.6 mg/g creatinine). Those consuming pantothenic acid supplements had significantly higher excretion levels. Blood pantothenic acid values between the groups, noninstitutionalized (537 +/- 27.4 ng/ml) and institutionalized (615 +/- 47.3 ng/ml), were comparable. The average dietary intake of pantothenic acid for the elderly population studied was 5.9 +/- 0.1 mg/day with the institutionalized and noninstitutionalized subjects having a similar intake of 2.9 mg/1000 kcal. Institutionalized elderly males and females were consuming 2237 and 1962 kcal, respectively, while their noninstitutionalized counterparts were consuming 2201 and 1887 kcal.

Aged↗
PubMed1987

Regulation of pantothenic acid transport in the heart. Involvement of a Na+-cotransport system.

Pantothenic acid transport was studied in the isolated perfused rat heart and isolated sheep cardiac sarcolemmal vesicles. In the perfused heart, pantothenic acid transport was significantly greater if hearts were perfused as working hearts rather than Langendorff hearts, but was unaffected by the perfusion substrates used (11 mM glucose or 1.2 mM palmitate). Uptake rates of pantothenic acid in working hearts are dependent on perfusate concentrations of pantothenic acid (a Vmax of 418 nmol/g dry weight/30 min and a Km for pantothenic acid of 10.7 mircoM were obtained). Reduction in perfusate Na+ concentration from 145 to 105 mM (the Na+ was replaced with 40 mM choline) resulted in a small but significant decrease in pantothenic acid uptake. At 145 mM Na+, addition of a mixture of amino acids, whose uptake is Na+-dependent, resulted in a significant decrease in pantothenic acid uptake by the heart (173 +/- 5 to 132 +/- 12 nmol/g dry weight). If an inward Na+ gradient in isolated, purified sarcolemmal vesicles, was imposed, a rapid uptake of pantothenic acid was observed. Uptake rates are markedly reduced if Na+ was replaced by equimolar concentrations of K+ or if external Na+ was reduced below 40 mM. In the presence of Na+, increasing pantothenic acid concentrations resulted in an increase in pantothenic acid uptake by the vesicles. Combined, these data demonstrate that pantothenic acid is transported across the myocardial sarcolemmal membrane by a Na+-dependent mechanism, which may be common to a number of small molecules.

Animals↗
PubMed1976

Metabolic response to a pantothenic acid deficient diet in humans.

The responses of human subjects to a low pantothenic acid test diet and to the same diet supplemented with 10 mg pantothenic acid daily for 63 days were observed. Pantothenic acid in urine and blood and also nitrogen balance were used as criteria for nutritional evaluation. The mean daily urinary pantothenic acid excretion decreased from 3.05 to 0.79 mg in male adult subjects fed a pantothenic acid deficient diet and increased from 3.95 to 5.84 mg in 4 subjects fed a 10 mg supplemented diet from the beginning to the end of 63-day study. Subsequently, a test dose of 100 mg of pantothenic acid was given to both groups for a 7-day period. Subjects previously deprived of pantothenic acid retained 63% of the test dose on the first day of the test period in contrast to 48% retained by supplemented subjects. On the 7th day, both groups retained approximately 40% of the dose. While in general, blood pantothenic acid levels decreased in unsupplemented subjects and remained constant in supplemented subjects, blood pantothenic acid responded less readily to intake than urinary pantothenic acid. Nitrogen retention tended to be higher in supplemented subjects than in those deprived of dietary pantothenic acid.

Adult↗
PubMed1988

Insulin effects on pantothenic acid uptake in isolated perfused working hearts from diabetic rats.

Pantothenic acid uptake was studied in isolated working hearts from spontaneously diabetic BB Wistar and streptozocin-induced diabetic (STZ-D) rats. If insulin treatment was stopped for a 24-h period from spontaneously diabetic rats, a significant decrease in the rate of pantothenic uptake was noted (from 147.3 +/- 5.0 to 110.8 +/- 10.6 nmol.g-1 dry wt.30 min-1). Pantothenic acid uptake rates were also reduced in 48-h STZ-D rats (118.0 +/- 6.1 nmol.g-1 dry wt.30 min-1, compared to 158.2 +/- 5.3 in control rats). The decrease in pantothenic acid uptake in all diabetic animals occurred whether hearts were perfused with 1.2 mM palmitate or 1.2 mM palmitate and 11 mM glucose. If insulin (500 microU/ml) was added to the perfusion medium of hearts from spontaneously diabetic rats perfused with palmitate and glucose, a significant increase in pantothenic acid uptake was noted (from 110.8 +/- 10.6 to 167.0 +/- 9.4 nmol.g-1 dry wt.30 min-1). Insulin had no significant effect on pantothenic acid uptake in hearts from spontaneously diabetic rats perfused with palmitate alone. In STZ-D rats, insulin added to hearts perfused with palmitate and glucose resulted in a small but significant increase in pantothenic acid uptake (from 118.0 +/- 6.1 to 130.6 +/- 4.0 nmol.g-1 dry wt.30 min-1). Insulin had no effect on pantothenic acid uptake in control hearts perfused either in the presence or absence of glucose. These data suggest that insulin, in the presence of glucose, can increase pantothenic acid uptake in diabetic rats.

Animals↗
PubMed2001

Saccharomyces cerevisiae is capable of de Novo pantothenic acid biosynthesis involving a novel pathway of beta-alanine production from spermine.

Pantothenic acid and beta-alanine are metabolic intermediates in coenzyme A biosynthesis. Using a functional screen in the yeast Saccharomyces cerevisiae, a putative amine oxidase, encoded by FMS1, was found to be rate-limiting for beta-alanine and pantothenic acid biosynthesis. Overexpression of FMS1 caused excess pantothenic acid to be excreted into the medium, whereas deletion mutants required beta-alanine or pantothenic acid for growth. Furthermore, yeast genes ECM31 and YIL145c, which both have structural homology to genes of the bacterial pantothenic acid pathway, were also required for pantothenic acid biosynthesis. The homology of FMS1 to FAD-containing amine oxidases and its role in beta-alanine biosynthesis suggested that its substrates are polyamines. Indeed, we found that all the enzymes of the polyamine pathway in yeast are necessary for beta-alanine biosynthesis; spe1Delta, spe2Delta, spe3Delta, and spe4Delta are all beta-alanine auxotrophs. Thus, contrary to previous reports, yeast is naturally capable of pantothenic acid biosynthesis, and the beta-alanine is derived from methionine via a pathway involving spermine. These findings should facilitate the identification of further enzymes and biochemical pathways involved in polyamine degradation and pantothenic acid biosynthesis in S. cerevisiae and raise questions about these pathways in other organisms.

Pantothenic Acid↗
PubMed2003

Fermentative activity and production of volatile compounds by Saccharomyces grown in synthetic grape juice media deficient in assimilable nitrogen and/or pantothenic acid.

AIMS: To understand the impact of assimilable nitrogen and pantothenic acid on fermentation rate and synthesis of volatile compounds by Saccharomyces under fermentative conditions. METHODS AND RESULTS: A 2 x 3 factorial experimental design was employed with the concentrations of yeast assimilable nitrogen (YAN) (60 and 250 mg l(-1)) and pantothenic acid (10, 50 and 250 microg l(-1)) as variables. In media containing 250 microg l(-1) pantothenic acid, H2S production by two different species of Saccharomyces decreased when YAN was increased from 60 to 250 mg l(-1). Conversely, H2S production was significantly higher when the concentration of assimilable nitrogen was increased if pantothenic acid was deficient (10 or 50 microg l(-1)). Yeast synthesis of other volatile compounds were impacted by both assimilable nitrogen and pantothenic acid. CONCLUSIONS: While growth and fermentative rate of Saccharomyces was more influenced by nitrogen than by pantothenic acid, complicated interactions exist between these nutrients that affect the synthesis of volatile compounds including H2S. SIGNIFICANCE AND IMPACT OF THE STUDY: This study has important implications for the winemaking industry where a better understanding of the nutritional requirements of Saccharomyces is necessary to reduce fermentation problems and to improve final product quality.

Alcohols↗
PubMed1986

Development and characterization of pantothenic acid transport in brain.

In vitro, the transport of [3H]pantothenic acid into and from rabbit brain slices was studied. In newborn rabbits and throughout development, forebrain and cerebellar slices were able to accumulate and phosphorylate [3H]pantothenic acid comparably to slices from adults. The accumulation and phosphorylation of [3H]pantothenic acid by adult forebrain slices were not decreased by substitution of LiCl for NaCl in the artificial CSF or by addition of short-chain fuels (e.g., 5 mM pyruvate or acetoacetate) to the medium. However, probenecid and ouabain (both 1 mM) and medium-chain fatty acids (e.g., 0.1 mM octanoate, nonanoate, and decanoate) profoundly inhibited [3H]pantothenic acid accumulation by forebrain slices but not intracellular phosphorylation and conversion to [3H]CoA. There in vitro results suggest that brain slices accumulate pantothenic acid by a saturable system (probably facilitated diffusion) that is sensitive to inhibition by probenecid and medium-chain fatty acids.

Animals↗
PubMed1999

Human peripheral blood mononuclear cells: ; Inhibition of biotin transport by reversible competition with pantothenic acid is quantitatively minor.

A transporter present in intestinal cells and in choriocarcinoma cells has been shown to transport both pantothenic acid and biotin at similar transporter affinities. However, the concentration of pantothenic acid in most foods and biological fluids is approximately 200 times the concentration of biotin; theoretically, pantothenic acid might substantially reduce biotin transport via competition. In the present study, we sought to determine whether pantothenic acid reduces biotin transport by the biotin transporter in peripheral blood mononuclear cells (PBMC). PBMC were isolated from human blood by gradient centrifugation. Incubations with [(3)H]biotin and pantothenic acid were conducted at physiologic concentrations. Intracellular [(3)H]biotin was quantified after washing by liquid scintillation counting. Pantothenic acid at 10 to 1,000 nmol/L reduced biotin (475 pmol/L) uptake by less than 12% (P < 0.05). Based on Lineweaver-Burk plots, the competition was reversible. Several structural analogs of pantothenic acid at 1,000 nmol/L reduced biotin transport by only 7 to 15% (P = 0.13). No pattern of molecular structure required for recognition by the transporter was apparent. Extracellular pantothenic acid did not affect biotin efflux from [(3)H]biotin-loaded PBMC (P > 0.05), suggesting that countertransport of extracellular pantothenic acid and intracellular biotin does not increase biotin efflux from PBMC. We conclude that the physiologic effects of pantothenic acid on the transport of biotin in PBMC are likely to be quantitatively minor.

Journal Article↗
PubMed1975

[Influencing of acetylation and corticosterone biosynthesis through long-term pantothenic acid deficiency in rats].

The effect of different dietary intake of pantothenic acid (150;100;25 and 0% of the requirement) on the metabolism of rats was studied during 15 months. The ability of the adrenals for synthesis of corticosterone and the rate of acetylation of a sulfonamid (Sulfisomidin) were taken as parameters. The above mentioned parameters were influenced significantly already after two weeks and a pantothenic acid free diet containing the antagonist omega-methyl-pantothenic acid. With a 25% supply of pantothenic acid and without omega-methyl-pantothenic acid it lasted half a year until significant alterations of acetylation could be demonstrated. The synthetic ability of the adrenals for corticosteroids was significantly increased after a year in the 25% group. After the end of the study, this hyperfunctional state was followed by hypofunction, resulting in a significantly reduced ability of synthesis of the glands. Studies of this type were conducted to obrain basic informations for later experiments in human beings.

Acetylation↗
PubMed1984

Accumulation of pantothenic acid by the isolated choroid plexus and brain slices in vitro.

In vitro, the transport of [14C]pantothenic acid into and from the isolated rabbit choroid plexus, an anatomical locus of the blood-CSF barrier, and brain slices was studied. The choroid plexus accumulated [14C]pantothenic acid from the medium against a concentration gradient, although at low concentrations (less than 1 microM) there was substantial intracellular phosphorylation and binding of the [14C]pantothenic acid. The saturable accumulation process in choroid plexus was inhibited by probenecid and caproic acid but not by nicotinic acid or by weak bases. The accumulation process was markedly inhibited by N-ethylmaleimide, poly-L-lysine (which blocks sodium transport), and low temperatures. [14C]Pantothenic acid was readily released from choroid plexus by a temperature-dependent process. Brain slices also accumulated and, at low concentrations, phosphorylated [14C]pantothenic acid from the medium by a temperature-, probenecid-, and N-ethylmaleimide-sensitive saturable process. However, unlike choroid plexus, brain slices did not concentrate free pantothenic acid and [14C]pantothenic acid accumulation was not sensitive to poly-L-lysine. [14C]Pantothenic acid was readily released from brain slices by a temperature-sensitive process. These results are consistent with the view that [14C]pantothenic acid enters the isolated choroid plexus and brain slices by active transport and facilitated diffusion, respectively.

Animals↗