Evidence map›Paper›PMID 28660492›Full record

ArticleDiabetologia2017

Deficiency in plasmacytoid dendritic cells and type I interferon signalling prevents diet-induced obesity and insulin resistance in mice.

Tine D Hannibal, Anja Schmidt-Christensen, Julia Nilsson, Nina Fransén-Pettersson, Lisbeth Hansen, Dan Holmberg

Open access · hybridAbstract read
In one paragraph

Article in Diabetologia, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers.

0numbers the graph read from it
0cells of the map it votes in
35citing papers in PubMed
2.1field-weighted citation impact, top 13% 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

35 citing papers in PubMed, 53 citations in OpenAlex.

  1. Trial
  2. Article
  3. Review
  4. Review
  5. Review
  6. Article
  7. Review
  8. Immunometabolism at the Heart of Cardiovascular Disease.JACC. Basic to translational science · 2023
    Review
  9. Review
  10. Review
  11. Review
  12. Article
  13. Article
  14. Review
  15. Article
  16. Article
  17. Article
  18. Type 2 diabetes and viral infection; cause and effect of disease.Diabetes research and clinical practice · 2021
    Review
  19. Review
  20. Review
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 2 countries.

Tine D HannibalDepartment of Experimental Medical Sciences, Lund University, Biomedical Center, CRC, 205 02, Malmö, Sweden.
Anja Schmidt-ChristensenDepartment of Experimental Medical Sciences, Lund University, Biomedical Center, CRC, 205 02, Malmö, Sweden.
Julia NilssonDepartment of Experimental Medical Sciences, Lund University, Biomedical Center, CRC, 205 02, Malmö, Sweden.
Nina Fransén-PetterssonDepartment of Experimental Medical Sciences, Lund University, Biomedical Center, CRC, 205 02, Malmö, Sweden.
Lisbeth HansenDepartment of Experimental Medical Sciences, Lund University, Biomedical Center, CRC, 205 02, Malmö, Sweden.
Dan HolmbergDepartment of Experimental Medical Sciences, Lund University, Biomedical Center, CRC, 205 02, Malmö, Sweden. dan.holmberg@med.lu.se.
Lund University · SEUniversity of Copenhagen · DK

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

aims/hypothesisObesity is associated with glucose intolerance and insulin resistance and is closely linked to the increasing prevalence of type 2 diabetes. In mouse models of diet-induced obesity (DIO) and type 2 diabetes, an increased fat intake results in adipose tissue expansion and the secretion of proinflammatory cytokines. The innate immune system not only plays a crucial role in obesity-associated chronic low-grade inflammation but it is also proposed to play a role in modulating energy metabolism. However, little is known about how the modulation of metabolism by the immune system may promote increased adiposity in the early stages of increased dietary intake. Here we aimed to define the role of type I IFNs in DIO and insulin resistance.

methodsMice lacking the receptor for IFN-α (IFNAR

resultsWe found that the development of obesity was inhibited by an inability to respond to type I IFNs. Furthermore, the development of obesity and insulin resistance in this model was associated with pDC recruitment to the fatty tissues and liver of obese mice (a 4.3-fold and 2.7-fold increase, respectively). Finally, we demonstrated that the depletion of pDCs protects mice from DIO and from developing obesity-associated metabolic complications. CONCLUSIONS/

interpretationOur results provide genetic evidence that pDCs, via type I IFNs, regulate energy metabolism and promote the development of obesity.

Indexed as

Adipose TissueAnimalsBlood GlucoseDendritic CellsDiet, High-FatInsulin ResistanceInterferon Type IMaleMiceObesityReceptor, Interferon alpha-betaSignal TransductionBlood GlucoseInterferon Type IReceptor, Interferon alpha-betaAdipose tissueObesitypDCsType I interferons

Identifiers

PMID28660492
PMCPMC6448810
OpenAlexW2728603801

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.