Excess α‐tocopherol decreases extrahepatic phylloquinone in phylloquinone‐fed rats but not menaquinone‐4 in menaquinone‐4‐fed rats

Hanzawa, Fumiaki; Sakuma, Eri; Nomura, Saki; Uchida, Tomono; Oda, Hiroaki; Ikeda, Shoichiro

doi:10.1002/mnfr.201300710

Cited by 11 publications

(17 citation statements)

References 31 publications

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“…This result could at least partially explain the excessive bleeding observed in patients supplemented with vitamin E (11). This result seems in disagreement with previous data obtained in rats and showing a non-significant decrease of phylloquinone serum concentration 6 h after gavage with 0.2 mg of phylloquinone and 10 mg of ␣-tocopherol (12). However, our data suggest that the phylloquinone absorption peak is probably earlier, around 3-4 h (Fig.…”

Section: Discussioncontrasting

confidence: 99%

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Intestinal Scavenger Receptors Are Involved in Vitamin K1 Absorption

Goncalves

Margier

Roi

et al. 2014

Journal of Biological Chemistry

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Vitamin K1 (phylloquinone) intestinal absorption is thought to be mediated by a carrier protein that still remains to be identified. Apical transport of vitamin K1 was examined using Caco-2 TC-7 cell monolayers as a model of human intestinal epithelium and in transfected HEK cells. Phylloquinone uptake was then measured ex vivo using mouse intestinal explants. Finally, vitamin K1 absorption was compared between wild-type mice and mice overexpressing scavenger receptor class B type I (SR-BI) in the intestine and mice deficient in cluster determinant 36 (CD36). Phylloquinone uptake by Caco-2 cells was saturable and was significantly impaired by co-incubation with α-tocopherol (and vice versa). Anti-human SR-BI antibodies and BLT1 (a chemical inhibitor of lipid transport via SR-BI) blocked up to 85% of vitamin K1 uptake. BLT1 also decreased phylloquinone apical efflux by ∼80%. Transfection of HEK cells with SR-BI and CD36 significantly enhanced vitamin K1 uptake, which was subsequently decreased by the addition of BLT1 or sulfo-N-succinimidyl oleate (CD36 inhibitor), respectively. Similar results were obtained in mouse intestinal explants. In vivo, the phylloquinone postprandial response was significantly higher, and the proximal intestine mucosa phylloquinone content 4 h after gavage was increased in mice overexpressing SR-BI compared with controls. Phylloquinone postprandial response was also significantly increased in CD36-deficient mice compared with wild-type mice, but their vitamin K1 intestinal content remained unchanged. Overall, the present data demonstrate for the first time that intestinal scavenger receptors participate in the absorption of dietary phylloquinone.

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Section: Discussioncontrasting

confidence: 99%

“…Although it has been confirmed that excess of ␣-tocopherol could affect phylloquinone metabolism, the mechanisms of this phenomenon have not been fully elucidated (12). We suggest that a competition with vitamin E could also take place with uptake transporters in the intestine and would thus lead to decreased vitamin K absorption.…”

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confidence: 79%

Intestinal Scavenger Receptors Are Involved in Vitamin K1 Absorption

Goncalves

Margier

Roi

et al. 2014

Journal of Biological Chemistry

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“…In their most recent study, Farley et al [235] concluded that α-TOH, or even α-CEHC, interferes with an intermediate step in the formation of tissue-specific menaquinone-4 from phylloquinone, such as alterations in the transport via chylomicrons or other lipoproteins or reductions of the cellular uptake of phylloquinone or menadione, an intermediate product of phylloquinone in the menaquinone formation pathway. This hypothesis is supported by findings of Hanzawa et al [236] who found that rats fed a diet with 0.75 mg/kg phylloquinone for six weeks have decreased phylloquinone tissue concentrations with supplementation of 100 mg α-TOH while in rats fed with 0.75 mg/kg menaquinone diet the tissue concentrations of menaquinone remained unchanged with an increased application of α-TOH.…”

Section: Interaction With Vitamin K Metabolismsupporting

confidence: 67%

“…Finally, the form of vitamin E also contributes to the interference with vitamin K metabolism, as γ-TOH is not as potent as α-TOH in decreasing extrahepatic phylloquinone concentrations [236] . Taken together, vitamin K metabolism is disturbed by vitamin E at the level of extrahepatic synthesis of menaquinone from phylloquinone or menadione and the different vitamin E forms also lead to differing effects on the metabolic interactions.…”

Section: Interaction With Vitamin K Metabolismmentioning

confidence: 99%

Complexity of vitamin E metabolism

Schmölz¹,

Birringer²,

Lorkowski³

et al. 2016

WJBC

183

138

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Bioavailability of vitamin E is influenced by several factors, most are highlighted in this review. While gender, age and genetic constitution influence vitamin E bioavailability but cannot be modified, life-style and intake of vitamin E can be. Numerous factors must be taken into account however, i.e. , when vitamin E is orally administrated, the food matrix may contain competing nutrients. The complex metabolic processes comprise intestinal absorption, vascular transport, hepatic sorting by intracellular binding proteins, such as the significant α-tocopherol-transfer protein, and hepatic metabolism. The coordinated changes involved in the hepatic metabolism of vitamin E provide an effective physiological pathway to protect tissues against the excessive accumulation of, in particular, non-α-tocopherol forms. Metabolism of vitamin E begins with one cycle of CYP4F2/CYP3A4-dependent ω-hydroxylation followed by five cycles of subsequent β-oxidation, and forms the water-soluble end-product carboxyethylhydroxychroman. All known hepatic metabolites can be conjugated and are excreted, depending on the length of their sidechain, either via urine or feces. The physiological handling of vitamin E underlies kinetics which vary between the different vitamin E forms. Here, saturation of the side-chain and also substitution of the chromanol ring system are important. Most of the metabolic reactions and processes that are involved with vitamin E are also shared by other fat soluble vitamins. Influencing interactions with other nutrients such as vitamin K or pharmaceuticals are also covered by this review. All these processes modulate the formation of vitamin E metabolites and their concentrations in tissues and body fluids. Differences in metabolism might be responsible for the discrepancies that have been observed in studies performed in vivo and in vitro using vitamin E as a REVIEW

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“…Among the vitamin K types, PK is added to the AIN93-rodent diet (16), which is widely used in animal experiments as a standard rodent diet. We have revealed that PK concentration in the extrahepatic tissues of rats fed the AIN93-rodent diet decreases as the vitamin E content in the diet increases (17). Consumption of a diet containing a 75 IU a-tocopherol/kg diet, a basal content of vitamin E in the AIN93-rodent diet, significantly lowered PK concentration in the various tissues except for the liver of rats, although consumption of a diet containing an excess amount of g-tocopherol lowered PK concentration in some tissues.…”

mentioning

confidence: 99%

Tissue Distribution of Menaquinone-7 and the Effect of α-Tocopherol Intake on Menaquinone-7 Concentration in Rats

Ikeda¹,

Hanzawa²,

Takahashi³

et al. 2018

Journal of Nutritional Science and Vitaminology

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We have reported that vitamin E intake lowers phylloquinone (PK) concentration in extrahepatic tissues of rats. In this study, we aimed to clarify the characteristic of the distribution of menaquinone-7 (MK-7), a vitamin K contained in fermented foods, by comparison with other vitamin K distributions and to clarify the effect of vitamin E intake on MK-7 concentration in rats. Rats were fed a vitamin K-free diet (Free group), a diet containing 0.75 mg PK/kg (PK group), a 0.74 mg menaquinone-4 (MK-4)/kg diet (MK-4 group), a 1.08 mg MK-7/kg diet (MK-7 group), or a 0.29 mg menadione (MD)/kg diet (MD group) for 16 wk. MK-7 mainly accumulated in the liver, spleen, and adrenal gland of the MK-7 group, although PK accumulated in the serum and all tissues of the PK group. Conversely, MK-4 was present in all tissues of the PK, MK-4, MK-7, and MD groups. MK-4 concentration in the serum, liver, adipose tissue, and spleen was higher in the MK-4 group than in the other groups; however, MK-4 concentration in the kidney, testis, tibia, and brain was lower in the MK-4 group than in the PK, MK-7, and MD groups. Next, vitamin E-and K-deficient rats were orally administered MK-7 with or without a-tocopherol. a-Tocopherol did not affect MK-7 or MK-4 concentration in the serum and various tissues. These results suggested that MK-7 is particularly liable to accumulate in the liver, and MK-7 concentration is not affected by vitamin E intake.

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Excess α‐tocopherol decreases extrahepatic phylloquinone in phylloquinone‐fed rats but not menaquinone‐4 in menaquinone‐4‐fed rats

Abstract: Excess α-tocopherol decreased extrahepatic PK in rats fed PK but not MK-4 in rats fed MK-4.

Cited by 11 publications

References 31 publications

Intestinal Scavenger Receptors Are Involved in Vitamin K1 Absorption

Intestinal Scavenger Receptors Are Involved in Vitamin K1 Absorption

Complexity of vitamin E metabolism

Tissue Distribution of Menaquinone-7 and the Effect of α-Tocopherol Intake on Menaquinone-7 Concentration in Rats

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