Dietary vitamin B-6 restriction does not alter rates of homocysteine remethylation or synthesis in healthy young women and men1–4

Davis, Steven R.; Scheer, Jennifer B.; Quinlivan, Eoin P.; Coats, Bonnie S.; Stacpoole, Peter W.; Gregory, Jesse F.

doi:10.1093/ajcn/81.3.648

Cited by 43 publications

(96 citation statements)

References 29 publications

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“…Additionally, decrease in plasma PLP may not have paralleled decrease in hepatic PLP stores, offering an additional potential explanation for the observed delay. The hyperhomocysteinemia induced by vitamin B 6 deficiency in this study is consistent with other reports in pigs (Smolin et al, 1983) and rats (Smolin and Benevenga, 1982;Smolin and Benevenga, 1984;Martinez et al, 2000), but not in healthy humans (Davis et al, 2005) with vitamin B 6 restriction treatment. The discrepancy with the latter observation likely reflects the severity of vitamin B 6 restriction; pigs with depressed plasma PLP concentrations are able to maintain plasma homocysteine concentrations within normal limits, however, this is limited to the first 2 weeks of depletion.…”

Section: Discussionsupporting

confidence: 93%

“…Previous research has shown that hepatic methionine concentration in rats and plasma methionine concentration in humans (Davis et al, 2005) are not affected by vitamin B 6 restriction. In the current study, increases in fasting plasma methionine concentrations in vitamin B 6 -deficient pigs were observed at the end of 6 weeks, relative to those of the control pigs.…”

Section: Discussionmentioning

confidence: 90%

“…Further reductions in plasma PLP concentrations were observed during subsequent weeks, with a nadir of 4-6 nmol/l reached by the end of the third week. Reduced plasma PLP concentrations induced by vitamin B 6 restriction have been reported in humans (Davis et al, 2005) and rats (Martinez et al, 2000;Scheer et al, 2005) but data in pigs are limited. In the experiment examining vitamin B 6 repletion, plasma PLP at the beginning of the depletion phase was 24.9 nmol/l and declined to 3.2 nmol/l, consistent with observations from Experiment 1.…”

Section: Discussionmentioning

confidence: 99%

“…Pyridoxal-5 0 -phosphate (PLP), a major biological form of vitamin B 6 in animal tissues, is a well established co-factor for the three enzymes directly involved in homocysteine disposition: cystathionine-bsynthase (CBS) and cystathionine-g-lyase (CGL) are key PLP-dependent enzymes in the transsulphuration pathway, and serine hydroxymethyltransferase (SHMT) is a PLPdependent enzyme important for the folate cycle and one carbon metabolism (House et al, 1999). Vitamin B 6 status and, therefore, nutritional supply are thus implicated in the regulation of homocysteine flux and overall sulphur amino acid metabolism (Smolin and Benevenga, 1982;Davis et al, 2005;Lima et al, 2006).…”

Section: Introductionmentioning

confidence: 99%

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Impairments in pyridoxine-dependent sulphur amino acid metabolism are highly sensitive to the degree of vitamin B6 deficiency and repletion in the pig

Zhang

Kebreab

Jing

et al. 2009

Animal

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The objectives of the current study included the characterization of the temporal changes in indices of sulphur amino acid metabolism in piglets in response to vitamin B 6 deficiency and repletion with graded levels of pyridoxine hydrochloride. In Experiment 1, 12 piglets (average initial weight 5 5.3 kg; n 5 6 per group) were fed a semi-purified diet containing either 0 (deficiency group) or 3 mg (control group) pyridoxine Á HCl/kg diet, using a pair-feeding design, for 6 weeks. Piglets consuming vitamin B 6 -deficient diets exhibited decreased average daily gains on the 4th week and feed conversion efficiency from the 4th week until the end of the trial ( P , 0.05). Plasma pyridoxal-5 0 -phosphate (PLP), in pigs consuming vitamin B 6 -deficient diets, was significantly lower than controls throughout the experiment ( P , 0.01), reaching a nadir of 14% of the control animals' value by the end of the trial. Indices of sulphur amino acid metabolism, including activities of hepatic cystathionine-b-synthase (CBS), cystathionine-g-lyase (CGL) and serine hydroxymethyltransferase, as well as hepatic-free cysteine concentrations were markedly decreased after 6 weeks of B 6 deficiency ( P , 0.05). Total hepatic mRNA expressions for CBS and CGL were not affected. Concurrently, hepatic-free homocysteine concentrations increased by more than eight-fold ( P , 0.01) at the end of the trial. An examination of plasma total homocysteine and cysteine concentrations revealed significant ( P , 0.05) differences between treatments, with evidence of an abrupt shift in concentrations at 3 weeks post-initiation of dietary treatments (.25-fold increase in homocysteine; halving of cysteine values). At the end of Experiment 1, vitamin B 6 deficiency significantly increased plasma methionine and serine levels, but decreased plasma glycine concentrations ( P , 0.05). In Experiment 2, 20 pigs of 14 days old (initial BW 5 5.0 kg) were subjected to a 4-week vitamin B 6 depletion protocol, based on results obtained in Experiment 1. After the depletion period and assessment of baseline status (four pigs), remaining pigs were allocated to one of four dietary vitamin B 6 repletion treatments: 0.75, 1.5, 2.25 and 3 mg/kg diet as pyridoxine Á HCl (n 5 4 per level) for 14 days. Significant dose-dependent increases in plasma PLP and cysteine, and decreases in homocysteine were observed, and these were sensitive to the duration of repletion. In conclusion, data from the current studies support the use of both plasma PLP and homocysteine as sensitive indices of vitamin B 6 status in the pig. Additionally, the observed patterns of responses in vitamin B 6 -sensitive metabolites are supportive of an inclusion level of 2.25 mg/kg diet, as pyridoxine Á HCl, in diets for young pigs.Keywords: cysteine, homocysteine, pig, sulphur amino acid, vitamin B 6 ImplicationsThe current study has provided a temporal characterization of the impact of B 6 deficiency and subsequent repletion on indices of sulphur amino acid metabolism in young pigs. The use of plasma and h...

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Section: Discussionsupporting

confidence: 93%

Section: Discussionmentioning

confidence: 90%

Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Impairments in pyridoxine-dependent sulphur amino acid metabolism are highly sensitive to the degree of vitamin B6 deficiency and repletion in the pig

Zhang

Kebreab

Jing

et al. 2009

Animal

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“…Vitamin B 6 , vitamin B 2 , cobalamin, and folate are involved in the Hcy pathway. Vitamin B 6 deficiency has only minor influence on fasting tHcy concentrations and is revealed only after methionine loading (29). Low vitamin B 2 levels in AED patients correlate weakly with tHcy concentrations, and this correlation disappears when folate is included into the regression model (30).…”

Section: Discussionmentioning

confidence: 99%

Hyperhomocysteinemia in Children Treated with Antiepileptic Drugs Is Normalized by Folic Acid Supplementation

Huemer

Ausserer

Graninger³

et al. 2005

Epilepsia

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Summary:Purpose: To assess the prevalence of hyperhomocysteinemia in pediatric patients treated with antiepileptic drugs (AEDs) and to evaluate the effect of folic acid supplementation on plasma total homocysteine (tHcy) concentrations in hyperhomocysteinemic patients.Methods: 123 patients from three regional hospitals participated in the study. Patients with hyperhomocysteinemia were included in a 3-month double-blind randomized trial testing oral folic acid supplementation (1 mg/day) versus placebo.Results: Hyperhomocysteinemia (tHcy >10.4 µmol/L) was present in 19 of 123 patients. Patients with hyperhomocysteinemia were older (13.7 ± 4 vs. 11.0 ± 3.9 years) and had significantly lower folate and cobalamin concentrations. Multidrug (two or more) AED treatment and duration of therapy correlated significantly with elevated total homocysteine (tHcy) and low folate. In contrast, polymorphisms in the methylene tetrahydrofolate reductase gene (MTHFR 677 C→T, 1298 A→C, 1793 G→A) had no significant impact on tHcy. Nine of 19 patients with hyperhomocysteinemia were randomized to placebo, whereas the remaining 10 patients received folic acid supplementation. Folic acid supplementation resulted in a significant increase of folate and decrease of tHcy, whereas both parameters remained unchanged in the placebo group.Conclusions: Hyperhomocysteinemia is present in 15.5% of children receiving long-term AED treatment. Multidrug treatment and long duration of therapy enhance the risk for hyperhomocysteinemia. Folic acid supplementation significantly reduces tHcy. We recommend assessment of serum folate and plasma tHcy in children receiving AEDs.

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Vitamin B ₆

Silva

Gregory

2012

Present Knowledge in Nutrition

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Dietary vitamin B-6 restriction does not alter rates of homocysteine remethylation or synthesis in healthy young women and men1–4

Abstract: Moderate vitamin B-6 deficiency does not significantly alter the rates of homocysteine remethylation or synthesis in healthy young adults in the absence of dietary methionine intake.

Cited by 43 publications

References 29 publications

Impairments in pyridoxine-dependent sulphur amino acid metabolism are highly sensitive to the degree of vitamin B6 deficiency and repletion in the pig

Impairments in pyridoxine-dependent sulphur amino acid metabolism are highly sensitive to the degree of vitamin B6 deficiency and repletion in the pig

Hyperhomocysteinemia in Children Treated with Antiepileptic Drugs Is Normalized by Folic Acid Supplementation

Vitamin B ₆

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