Evidence map›Paper›PMID 25030662›Full record

ArticleJournal of lipid research2014

Lxr-driven enterocyte lipid droplet formation delays transport of ingested lipids.

Lourdes Cruz-Garcia, Amnon Schlegel

Open access · hybridAbstract read
In one paragraph

Article in Journal of lipid research, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.

0numbers the graph read from it
0cells of the map it votes in
30citing papers in PubMed
4.1field-weighted citation impact, top 7% 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

30 citing papers in PubMed, 46 citations in OpenAlex.

  1. Review
  2. Review
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  5. Review
  6. Coenzyme Q10 Metabolism: A Review of Unresolved Issues.International journal of molecular sciences · 2023
    Review
  7. Review
  8. Review
  9. Article
  10. Article
  11. Review
  12. Recent Application of Zebrafish Models in Atherosclerosis Research.Frontiers in cell and developmental biology · 2021
    Review
  13. A novel system to quantify intestinal lipid digestion and transport.Biochimica et biophysica acta. Molecular and cell biology of lipids · 2018
    Article
  14. [Establishment of zebrafish model for non-alcoholic steatohepatitis].Zhonghua gan zang bing za zhi = Zhonghua ganzangbing zazhi = Chinese journal of hepatology · 2018
    Article
  15. Article
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  19. Review
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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

2 authors at 1 institution in 1 country.

Lourdes Cruz-GarciaUniversity of Utah Molecular Medicine (U2M2) Program,University of Utah, Salt Lake City, UT 84112 Department of Internal Medicine, Division of Endocrinology, Metabolism, and Diabetes,University of Utah, Salt Lake City, UT 84112.
Amnon SchlegelUniversity of Utah Molecular Medicine (U2M2) Program,University of Utah, Salt Lake City, UT 84112 Department of Internal Medicine, Division of Endocrinology, Metabolism, and Diabetes,University of Utah, Salt Lake City, UT 84112 Department of Biochemistry, School of Medicine, University of Utah, Salt Lake City, UT 84112.
University of Utah · US

Funding

WU P&FP30DK020579 · NIDDK · WASHINGTON UNIVERSITY · PI Jennifer Lynn Powers Carson · 2013 to 2026
$27.1M
NIDDK NIH HHS P30 DK020579NIDDK NIH HHS P30-DK020579
6 · The paper itself

Abstract

Liver X receptors (Lxrs) are master regulators of cholesterol catabolism, driving the elimination of cholesterol from the periphery to the lumen of the intestine. Development of pharmacological agents to activate Lxrs has been hindered by synthetic Lxr agonists' induction of hepatic lipogenesis and hypertriglyceridemia. Elucidating the function of Lxrs in regulating enterocyte lipid handling might identify novel aspects of lipid metabolism that are pharmacologically amenable. We took a genetic approach centered on the single Lxr gene nr1h3 in zebrafish to study the role of Lxr in enterocyte lipid metabolism. Loss of nr1h3 function causes anticipated gene regulatory changes and cholesterol intolerance, collectively reflecting high evolutionary conservation of zebrafish Lxra function. Intestinal nr1h3 activation delays transport of absorbed neutral lipids, with accumulation of neutral lipids in enterocyte cytoplasmic droplets. This delay in transport of ingested neutral lipids protects animals from hypercholesterolemia and hepatic steatosis induced by a high-fat diet. On a gene regulatory level, Lxra induces expression of acsl3a, which encodes acyl-CoA synthetase long-chain family member 3a, a lipid droplet-anchored protein that directs fatty acyl chains into lipids. Forced overexpression of acls3a in enterocytes delays, in part, the appearance of neutral lipids in the vasculature of zebrafish larvae. Activation of Lxr in the intestine cell-autonomously regulates the rate of delivery of absorbed lipids by inducting a temporary lipid intestinal droplet storage depot.

Indexed as

Amino Acid SequenceAnimalsBase SequenceBiological TransportCaco-2 CellsCoenzyme A LigasesDiet, High-FatEnterocytesFatty AcidsFatty LiverFemaleGene ExpressionHumansHypercholesterolemiaIntestinal AbsorptionLipid DropletsCoenzyme A LigasesFatty AcidsLiver X ReceptorsLong-Chain-Fatty-Acid-CoA LigaseNR1H3 protein, humanOrphan Nuclear Receptorsacyl-CoA synthetase long-chain family member 3diet and dietary lipidselectron microscopyfatty acid/transportintestinenuclear receptors/liver X receptornutritiontranscription activator-like effector nucleasezebrafish

Identifiers

PMID25030662
PMCPMC4617358
OpenAlexW2322492973

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.