Evidence map›Paper›PMID 22969154›Full record

ArticleJournal of lipid research2012

Disruption of P450-mediated vitamin E hydroxylase activities alters vitamin E status in tocopherol supplemented mice and reveals extra-hepatic vitamin E metabolism.

Sabrina A Bardowell, Xinxin Ding, Robert S Parker

Open access · hybridAbstract read
In one paragraph

Article in Journal of lipid research, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.

0numbers the graph read from it
0cells of the map it votes in
27citing papers in PubMed
1.4field-weighted citation impact, top 22% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

27 citing papers in PubMed, 56 citations in OpenAlex.

  1. Trial
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  4. Article
  5. Review
  6. Scientific opinion on the tolerable upper intake level for vitamin E.EFSA journal. European Food Safety Authority · 2024
    Article
  7. Review
  8. Review
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  10. Article
  11. Article
  12. Article
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  17. Article
  18. Article
  19. Complexity of vitamin E metabolism.World journal of biological chemistry · 2016
    Review
  20. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

3 authors at 2 institutions in 1 country.

Sabrina A BardowellDivision of Nutritional Sciences, Cornell University, Ithaca, NY, USA.
Xinxin Ding
Robert S Parker
Cornell University · USState University of New York · US

Funding

INTERVENTIONS FOR PREVENTING &MANAGING CHRONIC ILLNESST32NR007091 · NINR · UNIV OF NORTH CAROLINA CHAPEL HILL · PI Cheryl L Giscombe, Cathi Barbra Propper · 1996 to 2026
$11.8M
NUTRITION TRAININGT32DK007158 · NIDDK · CORNELL UNIVERSITY ITHACA · PI PATRICIA A CASSANO, Julia L. Finkelstein · 1986 to 2026
$7.4M
Functions of Tocopherol Transfer TroteinR01DK067494 · NIDDK · CORNELL UNIVERSITY ITHACA · PI MANOR, DANNY · 2004 to 2012
$2.8M
NIDDK NIH HHS DK-007158NIDDK NIH HHS DK-067494NIDDK NIH HHS R01 DK067494NIDDK NIH HHS T32 DK007158NINR NIH HHS T32 NR007091
6 · The paper itself

Abstract

The widely conserved preferential accumulation of α-tocopherol (α-TOH) in tissues occurs, in part, from selective postabsorptive catabolism of non-α-TOH forms via the vitamin E-ω-oxidation pathway. We previously showed that global disruption of CYP4F14, the major but not the only mouse TOH-ω-hydroxylase, resulted in hyper-accumulation of γ-TOH in mice fed a soybean oil diet. In the current study, supplementation of Cyp4f14(-/-) mice with high levels of δ- and γ-TOH exacerbated tissue enrichment of these forms of vitamin E. However, at high dietary levels of TOH, mechanisms other than ω-hydroxylation dominate in resisting diet-induced accumulation of non-α-TOH. These include TOH metabolism via ω-1/ω-2 oxidation and fecal elimination of unmetabolized TOH. The ω-1 and ω-2 fecal metabolites of γ- and α-TOH were observed in human fecal material. Mice lacking all liver microsomal CYP activity due to disruption of cytochrome P450 reductase revealed the presence of extra-hepatic ω-, ω-1, and ω-2 TOH hydroxylase activities. TOH-ω-hydroxylase activity was exhibited by microsomes from mouse and human small intestine; murine activity was entirely due to CYP4F14. These findings shed new light on the role of TOH-ω-hydroxylase activity and other mechanisms in resisting diet-induced accumulation of tissue TOH and further characterize vitamin E metabolism in mice and humans.

Indexed as

Dietary SupplementsAnimalsCytochrome P-450 Enzyme SystemCytochrome P450 Family 4LiverMiceMice, KnockoutVitamin ECyp4f14 protein, mouseCytochrome P-450 Enzyme SystemCytochrome P450 Family 4Vitamin E

Identifiers

PMID22969154
PMCPMC3494260
OpenAlexW2145155912

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.