Evidence map›Paper›PMID 23964120›Full record

ArticleJournal of lipid research2013

CD36 deletion reduces VLDL secretion, modulates liver prostaglandins, and exacerbates hepatic steatosis in ob/ob mice.

Fatiha Nassir, Okunade L Adewole, Elizabeth M Brunt, Nada A Abumrad

Open access · hybridAbstract read
In one paragraph

Article in Journal of lipid research, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 53 papers.

0numbers the graph read from it
0cells of the map it votes in
53citing papers in PubMed
5.3field-weighted citation impact, top 4% 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

53 citing papers in PubMed, 103 citations in OpenAlex.

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  14. Current Therapeutical Approaches Targeting Lipid Metabolism in NAFLD.International journal of molecular sciences · 2023
    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

4 authors at 1 institution in 1 country.

Fatiha NassirDepartment of Medicine Washington University School of Medicine, St. Louis, MO 63110.
Okunade L Adewole
Elizabeth M Brunt
Nada A Abumrad
Washington University in St. Louis · US

Funding

Washington University Nutrition Obesity Research CenterP30DK056341 · NIDDK · WASHINGTON UNIVERSITY · PI Brian N Finck · 1999 to 2026
$30.2M
WU P&FP30DK020579 · NIDDK · WASHINGTON UNIVERSITY · PI Jennifer Lynn Powers Carson · 2013 to 2026
$27.1M
CD36 AND INTESTINAL FAT ABSORPTIONR01DK060022 · NIDDK · WASHINGTON UNIVERSITY · PI ABUMRAD, NADA A. · 2001 to 2021
$7.7M
FATTY ACID TRANSPORTER: REGULATION, IDENTIFICATIONR01DK033301 · NIDDK · WASHINGTON UNIVERSITY · PI ABUMRAD, NADA A. · 1986 to 2017
$5.2M
NIDDK NIH HHS DK-033301NIDDK NIH HHS DK-60022NIDDK NIH HHS P30 DK020579NIDDK NIH HHS P30 DK-056341NIDDK NIH HHS P30 DK056341NIDDK NIH HHS R01 DK033301NIDDK NIH HHS R01 DK060022
6 · The paper itself

Abstract

Recent findings described the role of CD36-mediated signaling in regulating cellular calcium and the release of various bioactive molecules, including the prostaglandins, neurotransmitters, cholecystokinin, and secretin. Here we document the role of CD36 in the secretion of hepatic VLDL. CD36 deletion resulted in 60% suppression of VLDL output in vivo, and VLDL secretion was reduced in vitro using incubated liver slices. The effect of CD36 deletion was mediated by enhancing formation of hepatic prostaglandins D2, F2, and E2. Treatment of CD36-deficient slices with inhibitors of cyclooxygenases reversed the reduction in triglyceride secretion. We also examined the effect of CD36 deletion on the obesity-associated spontaneous steatosis of the ob/ob mouse that is driven by enhanced de novo lipogenesis. Homozygous ob/ob mice lacking CD36 (ob-CD36⁻/⁻) were generated and studied for hepatic triglyceride accumulation and VLDL secretion. Livers of ob/ob mice were steatotic as expected and had 5-fold more CD36 on Kupffer cells and hepatocytes. CD36 deletion exacerbated the steatosis by impairing hepatic triglyceride and apoB secretion through increasing prostaglandin levels. These findings suggest an unappreciated role of CD36 in regulating VLDL secretion, which might have relevance to some forms of fatty liver. They provide insight into the association reported in humans between CD36 protein expression and serum levels of apoB and VLDL particle number.

Indexed as

Gene Knockout TechniquesAnimalsCD36 AntigensFatty LiverHumansLipoproteins, VLDLLiverMiceProstaglandinsCD36 AntigensLipoproteins, VLDLProstaglandinscyclooxygenaseKupffer cellstriglyceride

Identifiers

PMID23964120
PMCPMC3793603
OpenAlexW1977425580

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.