γ-Tocopherol Accelerated Sodium Excretion in a Dose-Dependent Manner in Rats with a High Sodium Intake

Uto‐Kondo, Harumi; Tani, Makoto; Kiyose, Chikako; Usuda, Mika; Taguchi, Chie; Hasegawa, Maiko; Machida, Naoko; Kishimoto, Yoshimi; Saito, Hisako; Ueda, Tadahiko; Igarashi, Osamu; Kondo, Kazuo

doi:10.3164/jcbn.2007030

Cited by 2 publications

(1 citation statement)

References 15 publications

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“…An antioxidant effect of α-tocopherol was reported in a murine liver model where rats fed with supplemental vitamin E had higher liver α-tocopherol levels and decreased lipid peroxidation after the introduction of an oxidizing agent 1 . Beyond antioxidant effects, γ-tocopherol increased sodium excretion in a dose-dependent manner in rats fed an NaCl-rich diet 16 , suggesting that dietary γ-tocopherol may prevent vascular dementia associated with hypertension. Furthermore, triple transgenic mice for Alzheimer disease showed lower natural killer cell activity than that of the controls before the onset of Alzheimer disease 17 , whilst dietary supplementation of vitamin E is known to enhance natural killer cell proliferation in older adults 18 .…”

Section: Discussionmentioning

confidence: 99%

Dietary intake of tocopherols and risk of incident disabling dementia

Aoki

Yamagishi

Maruyama

et al. 2021

Sci Rep

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Tocopherols, strong antioxidants, may be useful in preventing dementia, but the epidemiological evidence is insufficient. We performed a community-based follow-up study of Japanese, the Circulatory Risk in Community Study, involving 3739 people aged 40–64 years at baseline (1985–1999). Incident disabling dementia was followed up from 1999 through 2020. For subtype analysis, we classified disabling dementia into that with and that without a history of stroke. Dietary intake of tocopherols (total, α, β, γ, and δ) were estimated using 24-h recall surveys. During a median follow-up of 19.7 years, 670 cases of disabling dementia developed. Total tocopherol intake was inversely associated with risk of disabling dementia with multivariable hazard ratios (95% confidence intervals) of 0.79 (0.63–1.00) for the highest versus lowest quartiles of total tocopherol intake (P for trend = 0.05). However, the association was strengthened when further adjusted for α-linolenic acid intake (Spearman correlation with total tocopherol intake = 0.93), with multivariable hazard ratios of 0.50 (0.34–0.74) (P for trend = 0.001) but was weakened and nonsignificant when further adjusted for linoleic acid intake (Spearman correlation with total tocopherol intake = 0.92), with multivariable hazard ratios of 0.69 (0.47–1.01) (P for trend = 0.05). Similar but nonsignificant inverse associations were observed for α-, γ-, and δ-tocopherols but not for β-tocopherol. These results were similar regardless of the presence of a history of stroke. Dietary tocopherol intake was inversely associated with risk of disabling dementia, but its independent effect was uncertain owing to a high intercorrelation of α-linolenic linoleic acids with total tocopherol intake. Even with such confounding, a diet high in tocopherols may help prevent the onset of dementia.

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Section: Discussionmentioning

confidence: 99%

Dietary intake of tocopherols and risk of incident disabling dementia

Aoki

Yamagishi

Maruyama

et al. 2021

Sci Rep

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Changes in the concentrations of vitamin E analogs and their metabolites in rat liver and kidney after oral administration

Kiyose

Saito

Yachi

et al. 2015

J. Clin. Biochem. Nutr.

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Vitamin E analog, such as α- and γ-tocopherol, can undergo ω-oxidation without cleavage of the chroman ring, and this pathway is responsible for generation of the major urinary vitamin E metabolite, carboxyethyl hydroxychroman. However, it is still unclear how carboxyethyl hydroxychroman is changed in various tissues after vitamin E intake. We therefore investigated changes in the concentrations of α- and γ-tocopherol and their metabolites in rat liver and kidney. The concentration of α-tocopherol in rat liver increased until 6 h after oral administration, and then decreased. The change in the concentration of α-carboxyethyl hydroxychroman in rat liver in the α-Toc group slowly increased until 12 h after oral administration. Cytochrome P450 3A1 mRNA expression significantly increased from 12 h after the start of α-tocopherol administration. The change in the concentration of γ-carboxyethyl hydroxychroman in rat liver in the γ-Toc group markedly increased until 12 h after oral administration. On the other hand, γ-carboxyethyl hydroxychroman in rat kidney showed greater accumulation than α-carboxyethyl hydroxychroman from 3 h to 24 h after oral administration. From these results, we considered that γ-carboxyethyl hydroxychroman formed in the liver continues to be released into the bloodstream and is transported to the kidney rapidly.

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γ-Tocopherol Accelerated Sodium Excretion in a Dose-Dependent Manner in Rats with a High Sodium Intake

Cited by 2 publications

References 15 publications

Dietary intake of tocopherols and risk of incident disabling dementia

Dietary intake of tocopherols and risk of incident disabling dementia

Changes in the concentrations of vitamin E analogs and their metabolites in rat liver and kidney after oral administration

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