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

Okada, Mitsuko; Ishikawa, K.; Watanabe, Kayo

doi:10.3177/jnsv.37.349

Cited by 13 publications

(10 citation statements)

References 27 publications

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“…Glycogen phosphorylase activity was not increased by the addition of PLP in any case, suggesting that no apo-enzyme is contained in the tissue. B6 deficiency results in a decrease in the enzyme protein of glycogen phosphorylase (10), and in this study, 20-0, 20-0.5, 70-0 and 70-1 groups were estimated as B6 deficient when judged from this enzyme activity.…”

Section: Discussionmentioning

confidence: 54%

Dietary Protein as a Factor Affecting Vitamin B6 Requirement.

Okada

Shibuya

Akazawa

et al. 1998

Journal of Nutritional Science and Vitaminology, J Nutr Sci Vit

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SummaryRats were fed 20 or 70% casein diets with varying amounts of vitamin B6 (B6), and the B6 content and B6-dependent enzymatic activity in their tissues were examined to determine the minimum re quirement of B6 for animals subjected to different levels of dietary protein (i.e., 20%: 0, 1.45, 2.90, 5.80mg pyridoxine (PN)/kg diet; 70%: 0, 2.90, 5.80, 8.70mg PN/kg diet). B6 requirements for the rats were almost met in the 1.45mg PN/kg 20% casein diet and the 2.90mg PN/kg 70% casein diet when judged from the hepatic B6 content. However, almost twice the PN was required in both 20 and 70% casein diets when judged from PLP-enzymatic activity. The content of B6 vitamers in plasma appeared to be most sensitive to B6 status, though the satisfactory level is not known. It was confirmed that, in any case tested, a high-protein diet increased the requirement of B6. Key Words vitamin B6 requirement, vitamin B6 content, aspartate aminotransferase, glycogen phosphorylase Vitamin B6 (B6) is found in biological tissues and fluids as pyridoxine (PN), pyridoxal (PL), pyridoxamine (PM) and their phosphorylated derivatives. The vitamers function as coenzymes of glycogen phosphorylase and many amino acid metabolic enzymes. A high-protein diet increases the requirement for B6 as follows: First, a high-protein diet containing a low B6 content increases the urinary excre tion of xanthrenic acid (an abnormal metabolite of tryptophan) and some other tryptophan metabolites such as kynurenine and hydroxykynurenine (1); second, in animals fed a B6-free, high-protein diet, growth is retarded and is accompanied by a severe decrease in the activity of pyridoxal enzymes compared to animals fed a B6-free, low-protein diet (2, 3); and third, an increase in B6 intake increases phosphorylated pyridoxal (PLP) concentration, whereas increased protein intake decreases plasma PLP concentration (4).The accurate determination of B6 in biological samples is essential for assessing nutritional and metabolic requirements. There have been many attempts to analyze

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Section: Discussionmentioning

confidence: 54%

Dietary Protein as a Factor Affecting Vitamin B6 Requirement.

Okada

Shibuya

Akazawa

et al. 1998

Journal of Nutritional Science and Vitaminology, J Nutr Sci Vit

Self Cite

View full text Add to dashboard Cite

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“…Upregulating erythrocyte affinity for oxygen may help to compensate for the hypoxic condition brought on by the TBI-induced reduction in CBF, thus preventing the remaining tissue from entering an anoxic state. Vitamin B 6 also aids in glycogenolysis, and vitamin B 6 deficiencies reduce glycogen phosphorylase (GPh) activity in the rodent (Okada et al, 1991;Oka, 2001). GPh converts stored glycogen into glucose-1-phosphate, which is phosphorylated by the enzyme phosphoglucomutase, resulting in glucose-6-phosphate (G6P).…”

Section: Vitamin B 6 and Traumatic Brain Injurymentioning

confidence: 99%

Pyridoxine Administration Improves Behavioral and Anatomical Outcome after Unilateral Contusion Injury in the Rat

Kuypers

Hoane²

2010

Journal of Neurotrauma

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The purpose of this project was to evaluate the preclinical efficacy of pyridoxine, or vitamin B 6 . Rats received a 3.0 mm unilateral controlled cortical impact (CCI) injury of the sensorimotor cortex or sham surgery. Treatment with vitamin B 6 (600 or 300 mg/kg IP) or vehicle was administered at 30 min and 24 h post-CCI. Somatosensory dysfunction was evaluated with the vibrissae-forelimb placing and bilateral tactile adhesive removal tests. Sensorimotor dysfunction was evaluated with the locomotor placing and the forelimb asymmetry tests. On the forelimb asymmetry test both treatment groups displayed no asymmetry bias on any of the testing days post-CCI and were statistically no different than the shams. Both vitamin B 6 groups displayed a significant improvement in behavioral performance on the locomotor placing test compared to the vehicle-treated group. Administration of 600 mg/kg also significantly reduced tactile adhesive removal latencies on days 2, 4, 6, and 12 post-CCI. Both treatment groups were improved in their rate of recovery post-CCI on the vibrissae-forelimb placing test, but only the recovery seen in the 600-mg/kg group was significantly improved compared to vehicle. Finally, the 600-mg/kg dose resulted in significant cortical sparing compared to the vehicle-treated group. In general, the effects of vitamin B 6 on recovery of function were dose-dependent, with the 600-mg/kg dose consistently showing greater recovery than the 300-mg/kg dose. More experimental analyses are warranted to evaluate the potential preclinical efficacy and mechanistic action of vitamin B 6 .

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“…Glycogen phosphorylase is the enzyme responsible for the release of glucose-1-phosphate from muscle glycogen, and PLP is a cofactor for this enzyme (2). Vitamin B6 deficiency has been reported to decrease the activity and amount of muscle phosphorylase (3). Rats fed high levels of vitamin B6 have previously exhibited elevated concentrations of muscle phosphorylase (4).…”

Section: Introductionmentioning

confidence: 99%

Dietary vitamin B6 modulates the gene expression of myokines, Nrf2-related factors, myogenin and HSP60 in the skeletal muscle of rats

Suidasari

Uragami

Yanaka

et al. 2017

Experimental and Therapeutic Medicine

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Abstract. Previous studies have suggested that vitamin B6 is an ergogenic factor. However, the role of dietary vitamin B6 in skeletal muscle has not been widely researched. The aim of the present study was to investigate the effects of dietary vitamin B6 on the gene expression of 19 myokines, 14 nuclear factor erythroid 2-related factor 2 (Nrf2)-regulated factors, 8 myogenesis-related factors and 4 heat shock proteins (HSPs), which may serve important roles in skeletal muscles. Rats were fed a diet containing 1 (marginal vitamin B6 deficiency), 7 (recommended dietary level) or 35 mg/kg of pyridoxine (PN) HCl/ for 6 weeks. Gene expressions were subsequently analysed using reverse transcription-quantitative polymerase chain reaction. Food intake and growth were unaffected by this dietary treatment. The rats in the 7 and 35 mg/kg PN HCl groups exhibited a significant increase in the concentration of pyridoxal 5'-phosphate in the gastrocnemius muscle compared with the 1 mg/kg PN HCl diet (P<0.01). The expressions of myokines, such as IL-7, IL-8, secreted protein acidic and rich in cysteine, IL-6, growth differentiation factor 11, myonectin, leukaemia inhibitory factor, apelin and retinoic acid receptor responder (tazarotene induced) 1, the expression of Nrf2 and its regulated factors, such as heme oxygenase 1, superoxide dismutase 2, glutathione peroxidase 1 and glutathione S-transferase, and the expression of myogenin and HSP60 were significantly elevated in the 7 mg/kg PN HCl group compared with the 1 mg/kg PN HCl diet (P<0.05). No significant differences in levels of these genes were observed between the 35 and 1 mg/kg PN HCl, with the exception of GDF11 and myonectin, whose expressions were significantly increased in the 35 mg/kg PN HCl (P<0.05). Notably, the majority of gene expressions that were affected responded to dietary supplemental vitamin B6 in a similar manner. The results suggest that compared with the marginal vitamin B6 deficiency, the recommended dietary intake of vitamin B6 upregulates the gene expression of a number of factors that promote the growth and repair of skeletal muscle. IntroductionPyridoxal 5'-phosphate (PLP), the active form of vitamin B6, is known to modulate important metabolisms in the body (1). Skeletal muscle is the major source of PLP in the body (1). Some biological functions of vitamin B6 have been reported to be associated with fuel metabolism during exercise (2). It has been suggested that the exercise-related function of vitamin B6 is at least in part associated with the breakdown of muscle glycogen (2). Glycogen phosphorylase is the enzyme responsible for the release of glucose-1-phosphate from muscle glycogen, and PLP is a cofactor for this enzyme (2). Vitamin B6 deficiency has been reported to decrease the activity and amount of muscle phosphorylase (3). Rats fed high levels of vitamin B6 have previously exhibited elevated concentrations of muscle phosphorylase (4

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

Abstract: School of Medicine,for a gift of antirat muscle phosphorylase antiserum.

Cited by 13 publications

References 27 publications

Dietary Protein as a Factor Affecting Vitamin B6 Requirement.

Dietary Protein as a Factor Affecting Vitamin B6 Requirement.

Pyridoxine Administration Improves Behavioral and Anatomical Outcome after Unilateral Contusion Injury in the Rat

Dietary vitamin B6 modulates the gene expression of myokines, Nrf2-related factors, myogenin and HSP60 in the skeletal muscle of rats

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