Evidence map›Paper›PMID 34314388›Full record

ArticleJCI insight2021

Fatty acid mobilization from adipose tissue is mediated by CD36 posttranslational modifications and intracellular trafficking.

Alexes C Daquinag, Zhanguo Gao, Cale Fussell, Linnet Immaraj, Renata Pasqualini, Wadih Arap, Askar M Akimzhanov, Maria Febbraio, Mikhail G Kolonin

Open access · goldAbstract read
In one paragraph

Article in JCI insight, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 54 papers.

0numbers the graph read from it
0cells of the map it votes in
54citing papers in PubMed
4.9field-weighted citation impact, top 3% 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

54 citing papers in PubMed, 74 citations in OpenAlex.

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  9. Observational
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  19. Regulation of lipid storage and inflammation in the liver by CEACAM1.European journal of clinical investigation · 2024
    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

9 authors at 4 institutions in 2 countries.

Alexes C DaquinagThe Brown Foundation Institute of Molecular Medicine, University of Texas Health Science Center, Houston, Texas, USA.
Zhanguo GaoThe Brown Foundation Institute of Molecular Medicine, University of Texas Health Science Center, Houston, Texas, USA.
Cale FussellThe Brown Foundation Institute of Molecular Medicine, University of Texas Health Science Center, Houston, Texas, USA.
Linnet ImmarajDepartment of Dentistry, University of Alberta, Edmonton, Alberta, Canada.
Renata PasqualiniRutgers Cancer Institute of New Jersey, Rutgers New Jersey Medical School, Newark, New Jersey, USA.
Wadih ArapRutgers Cancer Institute of New Jersey, Rutgers New Jersey Medical School, Newark, New Jersey, USA.
Askar M AkimzhanovDepartment of Biochemistry and Molecular Biology, University of Texas Health Science Center, Houston, Texas, USA.
Maria FebbraioDepartment of Dentistry, University of Alberta, Edmonton, Alberta, Canada.
Mikhail G KoloninThe Brown Foundation Institute of Molecular Medicine, University of Texas Health Science Center, Houston, Texas, USA.
Brown Foundation · USRutgers, The State University of New Jersey · USUniversity of Alberta · CAThe University of Texas Health Science Center at Houston · US

Funding

The Function of Prohibitin / Annexin 2 Interaction in White Adipose TissueR01DK088131 · NIDDK · UNIVERSITY OF TEXAS HLTH SCI CTR HOUSTON · PI KOLONIN, MIKHAIL G · 2010 to 2021
$3.1M
NIDDK NIH HHS R01 DK088131
6 · The paper itself

Abstract

The mechanism controlling long-chain fatty acid (LCFA) mobilization from adipose tissue is not well understood. Here, we investigated how the LCFA transporter CD36 regulates this process. By using tissue-specific KO mouse models, we showed that CD36 in adipocytes and endothelial cells mediated both LCFA deposition into and release from adipose tissue. We demonstrated the role of adipocytic and endothelial CD36 in promoting tumor growth and chemoresistance conferred by adipose tissue-derived LCFAs. We showed that dynamic cysteine S-acylation of CD36 in adipocytes, endothelial cells, and cancer cells mediated intercellular LCFA transport. We demonstrated that lipolysis induction in adipocytes triggered CD36 deacylation and deglycosylation, as well as its dissociation from interacting proteins, prohibitin-1 (PHB) and annexin 2 (ANX2). Our data indicate that lipolysis triggers caveolar endocytosis and translocation of CD36 from the cell membrane to lipid droplets. This study suggests a mechanism for both outside-in and inside-out cellular LCFA transport regulated by CD36 S-acylation and its interactions with PHB and ANX2.

Indexed as

Gene Expression RegulationProtein Processing, Post-TranslationalAdipocytesAdipose TissueAnimalsAnimals, Genetically ModifiedBiological TransportCD36 AntigensCell MembraneCells, CulturedDisease Models, AnimalDNAFatty AcidsLipolysisMetabolic DiseasesMiceCD36 AntigensDNAFatty AcidsAdipose tissueCancerCell BiologyMetabolismObesity

Identifiers

PMID34314388
PMCPMC8492349
OpenAlexW3184002526

What Socratic holds

Textmetadata
LicenceCC BY
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 Socratic graph.