Evidence map›Paper›PMID 28925407›Full record

ArticleInternational journal of obesity (2005)2018

Foxc2 coordinates inflammation and browning of white adipose by leptin-STAT3-PRDM16 signal in mice.

L Gan, Z Liu, F Feng, T Wu, D Luo, C Hu, C Sun

Abstract read
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In one paragraph

Article in International journal of obesity (2005), 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.

0numbers the graph read from it
0cells of the map it votes in
29citing papers in PubMed
–field-weighted citation impact
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

29 citing papers in PubMed.

  1. Trial
  2. Article
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  4. Article
  5. Review
  6. Article
  7. Review
  8. Article
  9. Review
  10. Article
  11. Article
  12. Impaired Leptin Signalling in Obesity: Is Leptin a New Thermolipokine?International journal of molecular sciences · 2021
    Review
  13. Review
  14. Article
  15. Review
  16. There and Back Again: Leptin Actions in White Adipose Tissue.International journal of molecular sciences · 2020
    Review
  17. Article
  18. Article
  19. Impact of adipokines and myokines on fat browning.Journal of physiology and biochemistry · 2020
    Review
  20. Incendiary Leptin.Nutrients · 2020
    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

7 authors.

L GanCollege of Animal Science and Technology, Northwest A&F University, Yangling, Shaanxi, China.
Z LiuCollege of Animal Science and Technology, Northwest A&F University, Yangling, Shaanxi, China.
F FengCollege of Animal Science and Technology, Northwest A&F University, Yangling, Shaanxi, China.
T WuCollege of Animal Science and Technology, Northwest A&F University, Yangling, Shaanxi, China.
D LuoCollege of Animal Science and Technology, Northwest A&F University, Yangling, Shaanxi, China.
C HuDepartment of Human Nutrition, Food and Animal Sciences, College of Tropical Agriculture and Human Resources, University of Hawaii at Manoa, Honolulu, HI, USA.
C SunCollege of Animal Science and Technology, Northwest A&F University, Yangling, Shaanxi, China.ORCID 0000-0001-7222-4028

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

aimsThe objective of this study is to characterize the relationship between forkhead box C2 protein (Foxc2) and leptin under adipose inflammatory response.

methodsLipopolysaccharide (LPS)-induced inflammatory model was conducted. Data from wild-type and ob/ob mice were used to compare the alternative role of leptin on Foxc2-mediated inflammation and browning. Transcriptional regulation and protein-protein interaction were analyzed by bioinformatics and proved by chromatin immunoprecipitation and co-immunoprecipitation experiment.

resultsFoxc2 and leptin correlated with inflammation and browning of white adipose tissue (WAT) in LPS-treated mice. Moreover, Foxc2-mediated inhibition of inflammation involved downstream activation of leptin signal and promoted WAT browning. We then determined CREB, the potential transcriptional factor of leptin, was required for Foxc2-mediated inflammation in the regulation of WAT browning. Foxc2 alleviated adipocyte inflammation by reducing leptin-mediated Janus-activated kinase 2/signal transducer and activator of transcription 3 (STAT3) pathway. Importantly, STAT3 physically interacted with PRDM16 and formed a complex to promote WAT browning. Exogenous Foxc2 overexpression also ameliorated inflammation and promoted adipose browning in high fat diet (HFD)-induced obese mice.

conclusionsOur results indicated that Foxc2 inhibited inflammation and promoted browning of WAT through positive regulation of leptin signal and the STAT3-PRDM16 complex. These findings identify a new potential means to prevent and treat obese caused metabolic syndrome of mammals.

Indexed as

Adipose Tissue, BrownAdipose Tissue, WhiteAdiposityAnimalsDisease Models, AnimalDNA-Binding ProteinsForkhead Transcription FactorsInflammationLeptinMaleMiceMice, Inbred C57BLObesitySignal TransductionSTAT3 Transcription FactorTranscription FactorsDNA-Binding ProteinsForkhead Transcription FactorsLeptinmesenchyme fork head 1 proteinPrdm16 protein, mouseSTAT3 Transcription FactorTranscription Factors

Identifiers

PMID28925407

What OpenQuestion holds

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Registered trials

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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.