Evidence map›Paper›PMID 24606904›Full record

ArticleCell metabolism2014

RBP4 activates antigen-presenting cells, leading to adipose tissue inflammation and systemic insulin resistance.

Pedro M Moraes-Vieira, Mark M Yore, Peter M Dwyer, Ismail Syed, Pratik Aryal, Barbara B Kahn

Open access · bronzeAbstract read
In one paragraph

Article in Cell metabolism, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 162 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
162citing papers in PubMed, 1 pooled it
10.8field-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

162 citing papers in PubMed, 1 synthesis or guideline pooled it, 281 citations in OpenAlex.

  1. Pooled it
  2. Fetuin-b Mediates Lipid Overload-Induced Hepatic Lipid Accumulation in Large Yellow Croaker (Larimichthys crocea).FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2026
    Article
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  15. Adipokines: masterminds of metabolic inflammation.Nature reviews. Immunology · 2025
    Review
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  17. Article
  18. Article
  19. Review
  20. Ucp1 Ablation Improves Skeletal Muscle Glycolytic Function in Aging Mice.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025
    Article

102 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 2 institutions in 1 country.

Pedro M Moraes-VieiraDivision of Endocrinology, Diabetes, and Metabolism, Department of Medicine, Beth Israel Deaconess Medical Center and Harvard Medical School, 330 Brookline Avenue, Boston, MA 02215, USA.
Mark M YoreDivision of Endocrinology, Diabetes, and Metabolism, Department of Medicine, Beth Israel Deaconess Medical Center and Harvard Medical School, 330 Brookline Avenue, Boston, MA 02215, USA.
Peter M DwyerDivision of Endocrinology, Diabetes, and Metabolism, Department of Medicine, Beth Israel Deaconess Medical Center and Harvard Medical School, 330 Brookline Avenue, Boston, MA 02215, USA.
Ismail SyedDivision of Endocrinology, Diabetes, and Metabolism, Department of Medicine, Beth Israel Deaconess Medical Center and Harvard Medical School, 330 Brookline Avenue, Boston, MA 02215, USA.
Pratik AryalDivision of Endocrinology, Diabetes, and Metabolism, Department of Medicine, Beth Israel Deaconess Medical Center and Harvard Medical School, 330 Brookline Avenue, Boston, MA 02215, USA.
Barbara B KahnDivision of Endocrinology, Diabetes, and Metabolism, Department of Medicine, Beth Israel Deaconess Medical Center and Harvard Medical School, 330 Brookline Avenue, Boston, MA 02215, USA. Electronic address: bkahn@bidmc.harvard.edu.
Beth Israel Deaconess Medical Center · USHarvard University · US

Funding

Transgenic CoreP30DK057521 · NIDDK · MASSACHUSETTS GENERAL HOSPITAL · PI FLOREZ, JOSE CARLOS · 2000 to 2019
$31.4M
INTEGRATED ENDOCRINE &METABOLIC RESEARCH TRAININGT32DK007516 · NIDDK · BETH ISRAEL DEACONESS MEDICAL CENTER · PI BARBARA B. KAHN · 1986 to 2026
$6.8M
Glucose Transporter Regulation in Obesity and DiabetesR37DK043051 · NIDDK · BETH ISRAEL DEACONESS MEDICAL CENTER · PI KAHN, BARBARA B. · 2006 to 2015
$5.0M
GLUCOSE TRANSPORTER REGULATION IN OBESITY AND DIABETESR01DK043051 · NIDDK · BETH ISRAEL DEACONESS MEDICAL CENTER · PI KAHN, BARBARA B. · 1992 to 2020
$4.4M
Training Program in Nutrition and MetabolismT32HD052961 · NICHD · MASSACHUSETTS GENERAL HOSPITAL · PI GRINSPOON, STEVEN K. · 2005 to 2016
$1.3M
NICHD NIH HHS 2T32HD052961-06A1NICHD NIH HHS T32 HD052961NIDDK NIH HHS 5T32DK07516-29NIDDK NIH HHS P30 DK057521NIDDK NIH HHS P30 DK57521NIDDK NIH HHS R01 DK043051NIDDK NIH HHS R37 DK043051NIDDK NIH HHS R37 DK43051NIDDK NIH HHS T32 DK007516
6 · The paper itself

Abstract

Insulin resistance is a major cause of diabetes and is highly associated with adipose tissue (AT) inflammation in obesity. RBP4, a retinol transporter, is elevated in insulin resistance and contributes to increased diabetes risk. We aimed to determine the mechanisms for RBP4-induced insulin resistance. Here we show that RBP4 elevation causes AT inflammation by activating innate immunity that elicits an adaptive immune response. RBP4-overexpressing mice (RBP4-Ox) are insulin resistant and glucose intolerant and have increased AT macrophage and CD4 T cell infiltration. In RBP4-Ox, AT CD206(+) macrophages express proinflammatory markers and activate CD4 T cells while maintaining alternatively activated macrophage markers. These effects result from direct activation of AT antigen-presenting cells (APCs) by RBP4 through a JNK-dependent pathway. Transfer of RBP4-activated APCs into normal mice is sufficient to induce AT inflammation, insulin resistance, and glucose intolerance. Thus, RBP4 causes insulin resistance, at least partly, by activating AT APCs that induce CD4 T cell Th1 polarization and AT inflammation.

Indexed as

Adipose TissueAnimalsAntigen-Presenting CellsBone Marrow CellsCD4-Positive T-LymphocytesCell ProliferationGlucose IntoleranceHumansInsulin ResistanceJNK Mitogen-Activated Protein KinasesLectins, C-TypeLiverMacrophagesMaleMannose-Binding LectinsMannose ReceptorJNK Mitogen-Activated Protein KinasesLectins, C-TypeMannose-Binding LectinsMannose ReceptorRBP4 protein, humanReceptors, Cell SurfaceRecombinant ProteinsRetinol-Binding Proteins, Plasma

Identifiers

PMID24606904
PMCPMC4078000
OpenAlexW2079691056

What OpenQuestion holds

Textmetadata
LicenceTDM
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.