Evidence map›Paper›PMID 26650570›Full record

ArticleEndocrinology2016

Hepatocyte-Specific Disruption of CD36 Attenuates Fatty Liver and Improves Insulin Sensitivity in HFD-Fed Mice.

Camella G Wilson, Jennifer L Tran, Derek M Erion, Nicholas B Vera, Maria Febbraio, Ethan J Weiss

Open access · bronzeAbstract read
In one paragraph

Article in Endocrinology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 249 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
249citing papers in PubMed, 1 pooled it
14.4field-weighted citation impact, top 1% 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

249 citing papers in PubMed, 1 synthesis or guideline pooled it, 456 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Review
  4. Review
  5. Article
  6. Review
  7. Article
  8. Article
  9. Review
  10. Article
  11. Article
  12. Article
  13. Circulating Liver-Derived and CD36Journal of extracellular vesicles · 2026
    Article
  14. CD36 and Its Role in Obesity.Obesity reviews : an official journal of the International Association for the Study of Obesity · 2026
    Review
  15. Protective role of hydroalcoholic extract ofResearch in pharmaceutical sciences · 2026
    Article
  16. Article
  17. Article
  18. Article
  19. Integrative Omics Reveal Female-Specific Benefits of p16Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026
    Article
  20. Macrophage Plg-RJournal of thrombosis and haemostasis : JTH · 2026
    Article

189 more citing papers are in PubMed but not listed here.

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

6 authors at 3 institutions in 2 countries.

Camella G WilsonCardiovascular Research Institute (C.G.W., J.L.T., E.J.W.), University of California, San Francisco, San Francisco, California 94158-9001; Pfizer Pharmaceuticals (D.M.E., N.B.V.), Cambridge, Massachusetts 02139; and School of Dentistry (M.F.), University of Alberta, Edmonton AB, Canada T6G 2E1.
Jennifer L TranCardiovascular Research Institute (C.G.W., J.L.T., E.J.W.), University of California, San Francisco, San Francisco, California 94158-9001; Pfizer Pharmaceuticals (D.M.E., N.B.V.), Cambridge, Massachusetts 02139; and School of Dentistry (M.F.), University of Alberta, Edmonton AB, Canada T6G 2E1.
Derek M ErionCardiovascular Research Institute (C.G.W., J.L.T., E.J.W.), University of California, San Francisco, San Francisco, California 94158-9001; Pfizer Pharmaceuticals (D.M.E., N.B.V.), Cambridge, Massachusetts 02139; and School of Dentistry (M.F.), University of Alberta, Edmonton AB, Canada T6G 2E1.
Nicholas B VeraCardiovascular Research Institute (C.G.W., J.L.T., E.J.W.), University of California, San Francisco, San Francisco, California 94158-9001; Pfizer Pharmaceuticals (D.M.E., N.B.V.), Cambridge, Massachusetts 02139; and School of Dentistry (M.F.), University of Alberta, Edmonton AB, Canada T6G 2E1.
Maria FebbraioCardiovascular Research Institute (C.G.W., J.L.T., E.J.W.), University of California, San Francisco, San Francisco, California 94158-9001; Pfizer Pharmaceuticals (D.M.E., N.B.V.), Cambridge, Massachusetts 02139; and School of Dentistry (M.F.), University of Alberta, Edmonton AB, Canada T6G 2E1.
Ethan J WeissCardiovascular Research Institute (C.G.W., J.L.T., E.J.W.), University of California, San Francisco, San Francisco, California 94158-9001; Pfizer Pharmaceuticals (D.M.E., N.B.V.), Cambridge, Massachusetts 02139; and School of Dentistry (M.F.), University of Alberta, Edmonton AB, Canada T6G 2E1.
University of California, San Francisco · USPfizer (United States) · USUniversity of Alberta · CA

Funding

UCSF Liver Core CenterP30DK026743 · NIDDK · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI Holger Willenbring · 1986 to 2026
$30.7M
Research BaseP30DK063720 · NIDDK · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI KRUMMEL, MATTHEW F · 2003 to 2019
$21.8M
UCSF Nutrition Obesity Research CenterP30DK098722 · NIDDK · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI CHRISTIAN VAISSE · 2015 to 2026
$14.6M
Growth hormone signaling and lipid metabolism in fatty liver diseaseR01DK091276 · NIDDK · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI WEISS, ETHAN · 2011 to 2015
$1.7M
NIDDK NIH HHS 1R01DK091276NIDDK NIH HHS P30 DK026743NIDDK NIH HHS P30 DK063720NIDDK NIH HHS P30 DK098722NIDDK NIH HHS R01 DK091276
6 · The paper itself

Abstract

CD36/FAT (fatty acid translocase) is associated with human and murine nonalcoholic fatty liver disease, but it has been unclear whether it is simply a marker or whether it directly contributes to disease pathogenesis. Mice with hepatocyte-specific deletion of Janus kinase 2 (JAK2L mice) have increased circulating free fatty acids (FAs), dramatically increased hepatic CD36 expression and profound fatty liver. To investigate the role of elevated CD36 in the development of fatty liver, we studied two models of hepatic steatosis, a genetic model (JAK2L mice) and a high-fat diet (HFD)-induced steatosis model. We deleted Cd36 specifically in hepatocytes of JAK2L mice to generate double knockouts and from wild-type mice to generate CD36L single-knockout mice. Hepatic Cd36 disruption in JAK2L livers significantly improved steatosis by lowering triglyceride, diacylglycerol, and cholesterol ester content. The largest differences in liver triglycerides were in species comprised of oleic acid (C18:1). Reduction in liver lipids correlated with an improvement in the inflammatory markers that were elevated in JAK2L mice, namely aspartate aminotransferase and alanine transaminase. Cd36 deletion in mice on HFD (CD36L-HFD) reduced liver lipid content and decreased hepatic 4,4-difluoro-4-bora-3a,4a-diaza-s-indacene-FA uptake as compared with CON-HFD. Additionally, CD36L-HFD mice had improved whole-body insulin sensitivity and reduced liver and serum inflammatory markers. Therefore, CD36 directly contributes to development of fatty liver under conditions of elevated free FAs by modulating the rate of FA uptake by hepatocytes. In HFD-fed animals, disruption of hepatic Cd36 protects against associated systemic inflammation and insulin resistance.

Indexed as

Diet, High-FatAnimalsCD36 AntigensFatty Acids, NonesterifiedHepatocytesInsulin ResistanceLiverMaleMiceMice, KnockoutNon-alcoholic Fatty Liver DiseaseOrgan SpecificityTriglyceridesCD36 AntigensFatty Acids, NonesterifiedTriglycerides

Identifiers

PMID26650570
PMCPMC4733118
OpenAlexW2193344030

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.