Evidence map›Paper›PMID 30553769›Full record

ArticleMolecular metabolism2019

Deletion of myeloid IRS2 enhances adipose tissue sympathetic nerve function and limits obesity.

Marie-Therese Rached, Steven J Millership, Silvia M A Pedroni, Agharul I Choudhury, Ana S H Costa, Darran G Hardy, Justyna A Glegola, Elaine E Irvine, Colin Selman, Megan C Woodberry and 6 more

Open access · goldAbstract read
In one paragraph

Article in Molecular metabolism, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
1.9field-weighted citation impact, top 14% 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

19 citing papers in PubMed, 28 citations in OpenAlex.

  1. Article
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  11. Review
  12. Review
  13. A Tale of Three Systems: Toward a Neuroimmunoendocrine Model of Obesity.Annual review of cell and developmental biology · 2021
    Review
  14. Article
  15. Article
  16. Review
  17. Review
  18. Article
  19. 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

16 authors at 4 institutions in 2 countries.

Marie-Therese RachedMRC London Institute of Medical Sciences, Du Cane Road, London, W12 0NN, UK; Institute of Clinical Sciences, Faculty of Medicine, Imperial College London, Du Cane Road, London, W12 0NN, UK.
Steven J MillershipMRC London Institute of Medical Sciences, Du Cane Road, London, W12 0NN, UK; Institute of Clinical Sciences, Faculty of Medicine, Imperial College London, Du Cane Road, London, W12 0NN, UK.
Silvia M A PedroniMRC London Institute of Medical Sciences, Du Cane Road, London, W12 0NN, UK; Institute of Clinical Sciences, Faculty of Medicine, Imperial College London, Du Cane Road, London, W12 0NN, UK.
Agharul I ChoudhuryMRC London Institute of Medical Sciences, Du Cane Road, London, W12 0NN, UK.
Ana S H CostaMRC Cancer Unit, University of Cambridge, Box 197, Cambridge Biomedical Campus, Cambridge, CB2 0XZ, UK.
Darran G HardyMRC London Institute of Medical Sciences, Du Cane Road, London, W12 0NN, UK; Institute of Clinical Sciences, Faculty of Medicine, Imperial College London, Du Cane Road, London, W12 0NN, UK.
Justyna A GlegolaMRC London Institute of Medical Sciences, Du Cane Road, London, W12 0NN, UK.
Elaine E IrvineMRC London Institute of Medical Sciences, Du Cane Road, London, W12 0NN, UK.
Colin SelmanInstitute of Biodiversity, Animal Health and Comparative Medicine, College of Medical, Veterinary and Life Sciences, University of Glasgow, Glasgow, G12 8QQ, UK.
Megan C WoodberryMRC London Institute of Medical Sciences, Du Cane Road, London, W12 0NN, UK.
Vijay K YadavWellcome Trust Sanger Institute, Hinxton, Cambridge, CB10 1SA, UK; Department of Genetics and Development, Columbia University, New York, 10032, USA.
Sanjay KhadayateMRC London Institute of Medical Sciences, Du Cane Road, London, W12 0NN, UK.
Antonio Vidal-PuigWellcome Trust Sanger Institute, Hinxton, Cambridge, CB10 1SA, UK; University of Cambridge Metabolic Research Laboratories, Wellcome Trust-MRC Institute of Metabolic Science, Cambridge, CB2 0QQ, UK.
Samuel VirtueUniversity of Cambridge Metabolic Research Laboratories, Wellcome Trust-MRC Institute of Metabolic Science, Cambridge, CB2 0QQ, UK.
Christian FrezzaMRC Cancer Unit, University of Cambridge, Box 197, Cambridge Biomedical Campus, Cambridge, CB2 0XZ, UK.
Dominic J WithersMRC London Institute of Medical Sciences, Du Cane Road, London, W12 0NN, UK; Institute of Clinical Sciences, Faculty of Medicine, Imperial College London, Du Cane Road, London, W12 0NN, UK. Electronic address: d.withers@imperial.ac.uk.
MRC London Institute of Medical Sciences · GBUniversity of Cambridge · GBUniversity of Glasgow · GBWellcome Sanger Institute · GB

Funding

Medical Research Council G0400192Medical Research Council G0600717Medical Research Council MC_U120097114Medical Research Council MC_UU_00014/2Medical Research Council MC_UU_00014/5Medical Research Council MC_UU_12012/2Medical Research Council MC_UU_12012/5Medical Research Council MC_UU_12022/6Wellcome Trust 098051
6 · The paper itself

Abstract

objectiveSympathetic nervous system and immune cell interactions play key roles in the regulation of metabolism. For example, recent convergent studies have shown that macrophages regulate obesity through brown adipose tissue (BAT) activation and beiging of white adipose tissue (WAT) via effects upon local catecholamine availability. However, these studies have raised issues about the underlying mechanisms involved including questions regarding the production of catecholamines by macrophages, the role of macrophage polarization state and the underlying intracellular signaling pathways in macrophages that might mediate these effects.

methodsTo address such issues we generated mice lacking Irs2, which mediates the effects of insulin and interleukin 4, specifically in LyzM expressing cells (Irs2

resultsThese animals displayed obesity resistance and preservation of glucose homeostasis on high fat diet feeding due to increased energy expenditure via enhanced BAT activity and WAT beiging. Macrophages per se did not produce catecholamines but Irs2

conclusionsOur studies identify a critical macrophage signaling pathway involved in the regulation of adipose tissue sympathetic nerve function that, in turn, mediates key neuroimmune effects upon systemic metabolism. The insights gained may open therapeutic opportunities for the treatment of obesity.

Indexed as

Adipose Tissue, BrownAnimalsCatecholaminesCells, CulturedEnergy MetabolismGene DeletionInsulin Receptor Substrate ProteinsMaleMiceMice, Inbred C57BLMonocyte-Macrophage Precursor CellsObesitySignal TransductionSympathetic Nervous SystemCatecholaminesInsulin Receptor Substrate ProteinsIrs2 protein, mouseBATInflammationIrs2MacrophageObesitySympathetic neurons

Identifiers

PMID30553769
PMCPMC6358539
OpenAlexW2902026079

What OpenQuestion 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 OpenQuestion graph.