Evidence map›Paper›PMID 21808061›Full record

ArticleThe Journal of biological chemistry2011

Adipocyte-specific inactivation of Acyl-CoA synthetase fatty acid transport protein 4 (Fatp4) in mice causes adipose hypertrophy and alterations in metabolism of complex lipids under high fat diet.

Lena-Solveig Lenz, Jana Marx, Walee Chamulitrat, Iris Kaiser, Hermann-Josef Gröne, Gerhard Liebisch, Gerd Schmitz, Christoph Elsing, Beate K Straub, Joachim Füllekrug and 2 more

Open access · hybridAbstract read
In one paragraph

Article in The Journal of biological chemistry, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed
1.5field-weighted citation impact, top 19% 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

24 citing papers in PubMed, 51 citations in OpenAlex.

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  20. Acyl-CoA metabolism and partitioning.Annual review of nutrition · 2014
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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

12 authors at 4 institutions in 2 countries.

Lena-Solveig LenzDepartment of Internal Medicine IV, University of Heidelberg, 69120 Heidelberg.
Jana MarxDepartment of Internal Medicine IV, University of Heidelberg, 69120 Heidelberg.
Walee ChamulitratDepartment of Internal Medicine IV, University of Heidelberg, 69120 Heidelberg.
Iris KaiserDepartment of Internal Medicine IV, University of Heidelberg, 69120 Heidelberg.
Hermann-Josef GröneDepartment of Cellular and Molecular Pathology, German Cancer Research Center, 69120 Heidelberg.
Gerhard LiebischInstitute of Clinical Chemistry, University of Regensburg, 93042 Regensburg.
Gerd SchmitzInstitute of Clinical Chemistry, University of Regensburg, 93042 Regensburg.
Christoph ElsingDepartment of Internal Medicine, St. Elisabeth Hospital, 46225 Dorsten.
Beate K StraubDepartment of General Pathology, Institute of Pathology, 69120 Heidelberg.
Joachim FüllekrugDepartment of Internal Medicine IV, University of Heidelberg, 69120 Heidelberg.
Wolfgang StremmelDepartment of Internal Medicine IV, University of Heidelberg, 69120 Heidelberg.
Thomas HerrmannDepartment of Internal Medicine IV, University of Heidelberg, 69120 Heidelberg; Department of Internal Medicine I, Klinikum Idar-Oberstein, 55743 Idar-Oberstein, Germany. Electronic address: dr._thomas_herrmann@email.de.
Heidelberg University · DEUniversity of Regensburg · DEGerman Cancer Research Center · DESt. Elisabeth Hospital · CW

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Fatp4 exhibits acyl-CoA synthetase activity and is thereby able to catalyze the activation of fatty acids for further metabolism. However, its actual function in most tissues remains unresolved, and its role in cellular fatty acid uptake is still controversial. To characterize Fatp4 functions in adipocytes in vivo, we generated a mouse line with adipocyte-specific inactivation of the Fatp4 gene (Fatp4(A-/-)). Under standard conditions mutant mice showed no phenotypical aberrance. Uptake of radiolabeled palmitic and lignoceric acid into adipose tissue of Fatp4(A-/-) mice was unchanged. When exposed to a diet enriched in long chain fatty acids, Fatp4(A-/-) mice gained more body weight compared with control mice, although they were not consuming more food. Pronounced obesity was accompanied by a thicker layer of subcutaneous fat and greater adipocyte circumference, although expression of genes involved in de novo lipogenesis was not changed. However, the increase in total fat mass was contrasted by a significant decrease in various phospholipids, sphingomyelin, and cholesteryl esters in adipocytes. Livers of Fatp4-deficient animals under a high fat diet exhibited a higher degree of fatty degeneration. Nonetheless, no evidence for changes in insulin sensitivity and adipose inflammation was found. In summary, the results of this study confirm that Fatp4 is not crucial for fatty acid uptake into adipocytes. Instead, under the condition of a diet enriched in long chain fatty acids, adipocyte-specific Fatp4 deficiency results in adipose hypertrophy and profound alterations in the metabolism of complex lipids.

Indexed as

AdipocytesAdipose TissueAnimalsDietary FatsFatty AcidsFatty Acid Transport ProteinsHypertrophyLipid MetabolismLiverLiver DiseasesMiceMice, KnockoutDietary FatsFatty AcidsFatty Acid Transport ProteinsSlc27a4 protein, mouse

Identifiers

PMID21808061
PMCPMC3195640
OpenAlexW2017176768

What OpenQuestion holds

Textmetadata
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Registered trials

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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.