Effect Of Vitamin B6 Deficiency Research Articles

Effects of Vitamin B6 Deficiency on the Composition and Functional Potential of T Cell Populations.

The immune system is critical in preventing infection and cancer, and malnutrition can weaken different aspects of the immune system to undermine immunity. Previous studies suggested that vitamin B6 deficiency could decrease serum antibody production with concomitant increase in IL4 expression. However, evidence on whether vitamin B6 deficiency would impair immune cell differentiation, cytokines secretion, and signal molecule expression involved in JAK/STAT signaling pathway to regulate immune response remains largely unknown. The aim of this study is to investigate the effects of vitamin B6 deficiency on the immune system through analysis of T lymphocyte differentiation, IL-2, IL-4, and INF-γ secretion, and SOCS-1 and T-bet gene transcription. We generated a vitamin B6-deficient mouse model via vitamin B6-depletion diet. The results showed that vitamin B6 deficiency retards growth, inhibits lymphocyte proliferation, and interferes with its differentiation. After ConA stimulation, vitamin B6 deficiency led to decrease in IL-2 and increase in IL-4 but had no influence on IFN-γ. Real-time PCR analysis showed that vitamin B6 deficiency downregulated T-bet and upregulated SOCS-1 transcription. This study suggested that vitamin B6 deficiency influenced the immunity in organisms. Meanwhile, the appropriate supplement of vitamin B6 could benefit immunity of the organism.

The Effects of Vitamin B6 Deficiency or Supplementation on Cutaneous Sensitivity in Diabetic and Non-Diabetic Mice

The Journal of Alternative and Complementary MedicineVol. 20, No. 5 Education ResearchThe Effects of Vitamin B6 Deficiency or Supplementation on Cutaneous Sensitivity in Diabetic and Non-Diabetic MiceJeanne Drisko, Sarah Tague, Ourania Stephanopoulos, Michelle Winter, Ken McCarson, and Peter SmithJeanne DriskoSearch for more papers by this author, Sarah TagueSearch for more papers by this author, Ourania StephanopoulosSearch for more papers by this author, Michelle WinterSearch for more papers by this author, Ken McCarsonSearch for more papers by this author, and Peter SmithSearch for more papers by this authorPublished Online:7 May 2014https://doi.org/10.1089/acm.2014.5275.abstractAboutSectionsView articleView Full TextPDF/EPUB Permissions & CitationsPermissionsDownload CitationsTrack CitationsAdd to favorites Back To Publication ShareShare onFacebookTwitterLinked InRedditEmail View article"The Effects of Vitamin B6 Deficiency or Supplementation on Cutaneous Sensitivity in Diabetic and Non-Diabetic Mice." The Journal of Alternative and Complementary Medicine, 20(5), p. A104FiguresReferencesRelatedDetails Volume 20Issue 5May 2014 InformationCopyright 2014, Mary Ann Liebert, Inc.To cite this article:Jeanne Drisko, Sarah Tague, Ourania Stephanopoulos, Michelle Winter, Ken McCarson, and Peter Smith.The Effects of Vitamin B6 Deficiency or Supplementation on Cutaneous Sensitivity in Diabetic and Non-Diabetic Mice.The Journal of Alternative and Complementary Medicine.May 2014.A104-A104.http://doi.org/10.1089/acm.2014.5275.abstractPublished in Volume: 20 Issue 5: May 7, 2014PDF download

Effects of Vitamin B6 Deficiency on Lipid Metabolism in HepG2 Cells

We previously observed a decrease of plasma arachidonate (C20:4 n‐6) and an increase of erythrocyte oleate (C18:1 n‐9) in human volunteers with marginal vitamin B6 (VB6) deficiency. The objective of our current study was to investigate whether VB6 deficiency affects lipid metabolism in HepG2 cells and mechanisms involved. HepG2 cells were cultured for 6 wk in regular minimal essential medium (RMEM) containing 2.2 μM pyridoxal (PL) or VB6 – free MEM containing 10 nM, 20 nM, and 50 nM PL. After 6 wk, the intracellular pyridoxal 5′ – phosphate was 73 % lower for cells cultured in MEM containing 10 nM PL versus 2.2 μM PL. Total fatty acids increased 21%, the proportion of total arachidonate decreased from 4.3% to 3.6% (p < 0.05), and that of total oleate increased from 32% to 35% (p < 0.05) in VB6 –deficient cells cultured in medium with 10 nM PL compared to cells cultured in RMEM. Moreover, membrane lipid analysis showed that the proportion of arachidonate and dihomo‐γ‐linoleate (C20:3 n‐6) decreased respectively from 5.1% to 4.5% (p = 0.01) and from 0.9% to 0.6% (p < 0.001) in cells cultured in 10nM – PL medium compared to cells in RMEM. Our study demonstrated that VB6 deficiency moderately affects fatty acid profiles in HepG2 cells. Further investigation will focus on fatty acid metabolic kinetics in HepG2 cells with VB6 deficiency. Supported by NIH grant DK072398.Grant Funding Source: NIH grant DK072398

Effect of vitamin B6 deficiency on antioxidative status in rats with exercise-induced oxidative stress

This study investigated the effect of vitamin B6 deficiency on antioxidant enzyme activities and lipid profile in rats with exercise-induced oxidative stress. Forty eight rats were fed either a vitamin B6 deficient diet (B6-) or a control diet (control) for 4 weeks and then subdivided into 3 groups: pre-exercise (PreE); post-exercise (PostE); recess after exercise (recessE). Compared to those of control group, plasma catalase and hepatic cytosol superoxide dismutase (SOD, EC 1.15.1.1) activities of B6- group were lower regardless of exercise. The ratio of reduced glutathione/oxidized glutathione (GSH/GSSG) of B6- group was lower in PreE and there was no difference between PostE and recessE. The level of malondialdehyde (MDA) of B6- was significantly higher in PreE and PostE. High-density lipoprotein-cholesterol (HDL-C) level of B6- group was lower regardless of exercise. Atherosclerotic index of B6- group was higher in PreE and there was no difference between PostE and recessE. It is suggested that a reduction in antioxidative status caused by vitamin B6 deficiency may be aggravated under exercise-induced oxidative stress.

Vitamin B6 Deficiency can Reduce Fuel Storage and Utilization in Physically Trained Rats

This study investigated the effect of vitamin B6 deficiency on the utilization and recuperation of stored fuel in physically trained rats. 48 rats were given either vitamin B6-deficient (B6-) diet or control (B6) diet for 4 weeks and were trained on treadmill for 30 minutes daily. All animals were then subdivided into 3 groups: before-exercise (BE); during-exercise (DE); after-exercise (AE). The DE group was exercised on treadmill for 1 hour just before being sacrificed. Animals in the AE group were allowed to take a rest for 2 hours after being exercised like the DE group. Glucose and free fatty acids were compared in plasma. Glycogen and triglyceride were compared in liver and skeletal muscle. Protein levels were compared in plasma, liver, and skeletal muscle. Compared with the B6+ group, plasma glucose levels of the B6- group were significantly lower before and after exercise. Muscle glycogen levels of the B6- group were significantly lower than those of the B6+ group regardless of exercise. The liver glycogen level of the B6- group was also significantly lower than that of B6+ group during and after exercise. Before exercise, plasma free fatty acid levels were not significantly different between the B6+ and B6- groups, and plasma free fatty acid levels of the B6- group were significantly lower during and after exercise. The muscle triglyceride level of the B6- group was significantly lower than that of the B6+ group before exercise, and there were no differences between B6+ and B6- groups during and after exercise. Liver triglyceride levels were not significantly different between B6+ and B6- groups. Plasma protein levels of the B6- group were lower than those of B6+ before and after exercise. Muscle protein levels of the B6- group were not significantly different from those of the B6 group. Liver protein levels of the B6- group were significantly lower than that of the B6+ group after exercise. Liver protein levels of both B6+ and B6- groups were not significantly changed, regardless of exercise. Thus, it is suggested that vitamin B6 deficiency may reduce fuel storage and utilization with exercise in physically trained rats.

PD-04.04: Vitamin B6 deficiency causes hypocitraturia within one week in rats

Citrate is an effective inhibitor of the nucleation, growth, and aggregation of calcium oxalate crystals. Several citrate-containing compounds have been used in the treatment and management of urolithiasis. Changes of the acid-base balance are known to induce marked changes in the urinary citrate level, e.g., hypocitraturia is associated with acidosis, potassium depletion, and starvation. We have previously shown that vitamin B6 deficiency causes hypocitraturia as well as hyperoxaluria in rats. Here we investigated the effects of vitamin B6 deficiency on urinary citrate and oxalate excretion in rats over time.

Effect of vitamin B6 deficiency on the utilization of fuel with exercise in rats

Forty eight rats were fed either a control diet (+B6) or vitamin B6 deficient diet (-B6) diet for 4 weeks and were subdivided into 3 groups: before exercise (BE); during exercise (DE); after exercise (AE). DE group were exercised on treadmill for 1 hours just before sacrifice at the end of 4th week of respective diet and AE group were recuperated 1 hour after exercised like DE group. The levels of glucose (GLU), glycogen (GLY), protein (PRO), free fatty acid (FFA) and triglyceride (TG) were compared in plasma, liver and skeletal muscle. There were no differences between +B6 and -B6 in muscle and liver GLY before and during exercise but liver GLY was not recovered and 40% lower after exercise in –B6 group. Muscle TG was decreased with exercise in +B6 group(15% in DE, 28% in AE) but was not changed with exercise in –B6 group. Liver TG was decreased with exercise in -B6 group(26% in AE) but was not changed with exercise in +B6 group. Plasma FFA was increased with exercise in +B6 group(18% in DE, 16% in AE) while was decreased with exercise in –B6 group(35% in DE, 38% in AE). There were no changes in plasma, liver and muscle PRO of both +B6 and –B6 group with exercise. These results suggest that vitamin B6 deficiency may influence the utilization of fuel stores.

Effect of vitamin B6 deficiency on glyoxylate metabolism in rats with or without glyoxylate overload

We examined the effect of vitamin B6 deficiency on glyoxylate metabolism and hepatic alanine: glyoxylate aminotransferase (AGT) activity in rats with normal or high glyoxylate intake. Male rats were divided into four groups: a control group, a vitamin B6-free diet group, a glyoxylate water group, and a vitamin B6-free diet + glyoxylate water group. Each group was given special diet (control or vitamin B6-deficient diet) and drinking water (plain or 0.5% glyoxylate water) for 4 weeks, after which biochemical parameters and hepatic AGT mRNA level were measured. Compared with control rats, the urinary oxalate/creatinine ratio was higher in each of the other 3 groups. The urinary glycolate/creatinine ratio was also higher in the vitamin B6-free diet group and the vitamin B6-free diet + glyoxylate water group than the control group, while the urinary glycine/creatinine and citrate/creatinine ratio was lower in both groups. The hepatic AGT mRNA level was reduced in the vitamin B6-free diet group, but was increased in the glyoxylate water group than the control group. These results suggest that vitamin B6 is necessary for glyoxylate metabolism as a coenzyme of AGT. Especially in the presence of a high glyoxylate intake, vitamin B6 deficiency leads to severe hyperoxaluria and hypocituria.

Effect of Vitamin B6 Deficiency on S-Adenosylhomocysteine Hydrolase Activity as a Target Point for Methionine Metabolic Regulation

The objective of this study was to clarify the relationship between the accumulation of S-adenosylhomocysteine (SAH) and the change in the SAH hydrolase activity in vitamin B6 (B6). Male Wistar rats were fed a control diet (control and pair-fed groups) or B6-free diet (B6-deficient group) for 5 wk. Although the SAH-synthetic activity of SAH hydrolase significantly increased in the B6-deficient group, SAH-hydrolytic activity of SAH hydrolase showed no significant difference in the liver among the three groups. On the other hand, SAH hydrolase mRNA in the liver did not show any significant change. Thus, the accumulation of SAH would be due to the increased SAH-synthetic activity of SAH hydrolase. The disturbed methionine metabolism by B6-deficiency, such as a significant increase of plasma homocysteine, might induce the activation of SAH hydrolase in the direction of SAH synthesis.

Effect of vitamin B6 deficiency on urinary oxalate excretion in rats

Effect of vitamin B6 deficiency on urinary oxalate excretion in rats

Hepatic Alanine-glyoxylate Aminotransferase Activity and Oxalate Metabolism in Vitamin B6 Deficient Rats

Hepatic Alanine-glyoxylate Aminotransferase Activity and Oxalate Metabolism in Vitamin B6 Deficient Rats

Effect of vitamin B6 deficiency on the synthesis and accumulation of S-adenosylhomocysteine and S-adenosylmethionine in rat tissues.

The effect of vitamin B6-deficiency on the B6-vitamer concentrations, level of S-adenosylhomocysteine (SAH) and S-adenosylmethionine (SAM) were studied in rat tissues. The plasma pyridoxal 5'-phosphate (PLP) and, pyridoxal (PL) levels were lower in the B6-deficient group compared to the control group. After 5 weeks of feeding the experimental diets, tissue PLP, pyridoxamine 5'-phosphate (PMP) and PL concentrations were significantly lower in the B6-deficient group compared to the control and the pair-fed control groups. Thymus PLP and PL levels were lower in the B6-deficient group. The concentration of SAM in the B6-deficient group decreased to approximately 50% and 25% in liver and thymus, respectively. However SAH concentration was 3.5 and 2 fold higher compared to the control and the pair-fed control groups. Thus, the ratio of SAM/SAH was significantly decreased in the B6-deficient group compared to the control or the pair fed-control group. In addition, the S-adenosylhomocysteine hydrolase (EC 3.3.1.1) activity increased by 45% and 15% in liver and thymus, respectively, in the B6-deficient group compared to the pair-fed control and the control groups. However, the activity of L-methionine S-adenosyltransferase (EC 2.5.1.6) was also unaffected. Concentrations of SAH and SAM, SAM/SAH ratio and activities of S-adenosylhomocysteine hydrolase and L-methionine S-adenosyltrasferase in rat brain were not affected by the B6-deficiency. We infer that the alteration of B6 metabolism, especially the reduction of PLP contents in liver and thymus, caused by the B6 deficiency, resulted in accumulation of SAH as well as reduction of SAM and the SAM/SAH ratio. The reduction of the SAM/SAH ratio was due to a block in the catabolism of methionine via the trans-sulfuration pathway. These may lead to inhibition of transmethylation reaction of DNA, RNA and protein, the synthesis and function of thymic lymphocyte and result in damage to tissues.

Influence of dietary n-3 polyunsaturated fatty acids on plasma lipemic effect of vitamin B6 deficiency.

Since many connections exist between vitamin B6 and lipid metabolism, we aim to investigate the lipemic effect of different dietary intakes of polyunsaturated fatty acids in rats fed a vitamin B6 deficient diet. Diets were either vitamin B6 deficient (-B6) or vitamin B6 sufficient, pair-fed to the deficient group (PF) and ad libitum (N). The diets were combined with normal lipid (LC: soya bean-coconut-palm oils) and fish oil (FO: soya bean-fish oil). The fish oil diet with sufficient vitamin B6 content caused an increase in n-3 long chain polyunsaturated fatty acids and a decrease in arachidonic acid. In the -B6 group fed a normal lipid diet, the arachidonic acid percentage decreased and the linoleic acid percentage increased; in the -B6 group fed fish oil these changes in fatty acid composition, already consequent upon dietary intake of n-3 long chain polyunsaturated fatty acids, did not show further variations. In the dietary condition of vitamin B6 deficiency, plasma cholesterol content increased in rats fed a lipid control diet, whereas no hypocholesterolemic effect was observed in those fed a fish oil diet. Plasma triglyceride contents were not influenced by dietary lipid quality because, in all conditions, the lower food intake of the PF groups caused a decrease and vitamin B6 deficiency caused an elevation in triglyceride contents which reached those of the ad libitum groups. The study highlights the interaction between vitamin B6 and polyunsaturated fatty acids and the opportunity of dietary intake of fish oil to counterbalance some effects of vitamin B6 deficiency.

Effect of vitamin B6 deficiency on an antibody production in mice.

To investigate the effects of vitamin B6 (B6) deficiency on an antibody production in BALB/c mice, the production of specific immunoglobulin (Ig) E antibody against dinitrophenylated ovalbumin (DNP-OVA) were measured by the methods of enzyme linked immunosorbent assay. The mice fed on on a B6 deficient diet for 4 weeks were immunized intraperitoneally with DNP-OVA absorbed to aluminum hydroxide gel. The contents of anti DNP-IgE antibodies in sera of B6 deficient mice significantly increased compared to that of control mice fed on a diet containing B6. In addition, Interleukin-4, which was known to induce IgE production in allergic reactions from splenocytes of B6 deficient mice, was approximately four-fold higher than that in control mice. According to the recovery test to the B6 deficient mice, that is feeding the control diet for 21 days, all values in terms of the body, thymus, and spleen weight, total serum protein, IgG, and anti DNP-IgE content, regained almost the same levels as those of control. These results suggest that B6 deficiency in mice would have relation to the stimulation of specific IgE antibody production against DNP-OVA.

Effects of vitamin B6 deficiency on the conversion ratio of tryptophan to niacin.

To investigate how vitamin B6 (B6) deficiency affects the whole metabolism of tryptophan-niacin, rats were fed for 19 days with each of the following four kinds of diets; a complete 20% casein diet (control diet), the control diet without B6, the control diet without nicotinic acid, and the control diet without nicotinic acid and B6, and the urinary excretion of such tryptophan metabolites as kynurenic acid, xanthurenic acid, nicotinamide, N1-methylnicotinamide, N1-methyl-2-pyridone-5-carboxamide, and N1-methyl-4-pyridone-3-carboxamide each and the enzyme activities involved in tryptophan-niacin pathway were measured. The urinary excretion of kynurenic acid decreased while that of xanthurenic acid increased drastically in the two B6-deficient groups, when compared with the B6-containing groups. These results indicate that the rats fed with the B6-free diets were in the vitamin-deficient state. The conversion ratio was calculated from the ratio of the urinary excretion of sum of nicotinamide, N1-methylnicotinamide, N1-methyl-2-pyridone-5-carboxamide, and N1-methyl-4-pyridone-3-carboxamide, to the Trp intake. The ratio was statistically lower in the B6-free diet than in the B6-containing diet under the niacin-free conditions.

A Simple HPLC Method for the Determination of S-Adenosylmethionine and S-Adenosylhomocysteine in Rat Tissues: The Effect of Vitamin B6 Deficiency on These Concentrations in Rat Liver

A simple method using isocratic HPLC with ultraviolet detection was established for the simultaneous measurement of S-adenosylmethionine (SAM) and S-adenosylhomocysteine (SAH) in rat tissues. The method provides rapid resolution of both compounds in a single run by direct injection of the perchloric acid extract of tissue, so that sampling procedures and analytical errors can be reduced in. determining the SAM/SAH ratio, a measure of transmethylation reactions. The assay has a detection limit of 25 pmol and is linear in the range 50-2000 pmol. This procedure was applied to determine the change of SAM/SAH ratio in liver caused by vitamin B6 deficiency. The marked reduction of the SAM/SAH ratios in vitamin B6-deficient rats were due to a drastic rise in SAH concentration with a concurrent striking decrease in SAM concentration.

Effect of vitamin B6 deficiency on the expression of glycogen phosphorylase mRNA in rat liver and skeletal muscle.

The effect of vitamin B6 deficiency on the expression of glycogen phosphorylase mRNA in rat liver and skeletal muscle was investigated. The level of phosphorylase mRNA in the muscle of vitamin B6-deficient rats was reduced to 40% of that in the control rats. By contrast, the phosphorylase mRNA level was increased 5-fold in the liver of the deficient animals. It was also found that the expression of the beta-actin gene, generally regarded as a 'housekeeping' gene, was unaffected by B6 deficiency in the muscle but was enhanced in the liver of the deficient animals. These observations suggest that vitamin B6 may modulate the transcriptional activation of the phosphorylase gene in a tissue-specific manner.

Effect of Vitamin B6Deficiency on Linoleic Acid Desaturation in the Arachidonic Acid Biosynthesis of Rat Liver Microsomes

The effect of vitamin B6 deficiency on the desaturation of linoleic acid (18:2n-6) to γ-linolenic acid (18:3n-6) in rat liver microsomes was studied. Rats fed with a vitamin B6-deficient 70% casein diet for 5 weeks displayed a striking decrease mainly in the activity of terminal Δ6-desaturase in the 18:2n-6 desaturation system, although the activity of the electron-transport enzyme, NADH-cytochrome b5 reductase, was also significantly decreased. The 18:2n-6 desaturation index, the arachidonic acid (20:4n-6)/ 18:2n-6 ratio in the liver microsomal total lipids and in their phosphatidylcholine (PC) fraction, decreased together with the microsomal Δ6-desaturase activity, these changes being quite faithfully reflected in the plasma lipid. Among the microsomal lipid components, the PC content significantly decreased. In addition, a highly positive correlation was found between the PC content and Δ6-desaturase activity in liver microsomes. In an in vitro experiment, the Δ6-desaturase activity decreased linearly with increasing rate of PC hydrolysis by phospholipase C. These results suggest that the altered PC content in microsomes induced by vitamin B6 deficiency in vivo may affect the 18:2n-6 desaturation and thus decrease the biosynthesis of 20:4n-6

Interaction between vitamin B6 deficiency and low EFA dietary intake on kidney phospholipids and PGE 2 in the rat

Vitamin B6 is involved in the metabolism of long chain polyunsaturated fatty acids and phospholipids. We have studied the interaction between pyridoxine deficiency and low amounts of dietary essential fatty acids (EFA) in the rat. The fatty acid composition of kidney phospholipids of pyridoxine deficient animals shows a decrease of 20:3 n9 and an increase of 20:4 n6 in comparison with control and pair fed animals. This variation of fatty acid composition could be due to the simultaneous effect of vitamin B6 deficiency, which reduces the oxidation of linolenate, and of a low intake of EFAs which stimulates delta-6-desaturase. The dietary treatment also influences kidney Prostaglandin E 2 (PGE 2) levels which are higher in vitamin B6 deficient animals. This effect could be correlated with a higher response to sympathic stimulation caused by the simultaneous presence of vitamin B6 deficiency and low EFA availability. Also the higher level of arachidonate could be involved in promoting PGE 2 synthesis.

Effect of Vitamin B6 Deficiency on Glycogen Metabolism in the Skeletal Muscle, Heart, and Liver of Rats.

The effect of vitamin B6 deficiency was studied on glycogen metabolism in the gastrocnemius muscle, heart, and liver of rats. The glycogen phosphorylase activities in the gastrocnemius muscle and heart but not in the liver of vitamin B6-deficient rats were significantly decreased. The decrease in the enzyme activity in the gastrocnemius muscle was due to decrease in the amount of enzyme. The glycogen content of the muscle of vitamin B6-deficient rats was higher than that of the controls, but the glycogen content of the liver was similar in the two groups. These data suggest that glycogen degradation was impaired in the muscle but not the liver of vitamin B6-deficient rats.