Evidence map›Paper›PMID 23520131›Full record

ArticleDiabetes2013

Identification of sucrose non-fermenting-related kinase (SNRK) as a suppressor of adipocyte inflammation.

Yujie Li, Yaohui Nie, Ynes Helou, Guoxian Ding, Bin Feng, Gang Xu, Arthur Salomon, Haiyan Xu

Open access · hybridAbstract read
In one paragraph

Article in Diabetes, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
0.8field-weighted citation impact, top 25% 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

20 citing papers in PubMed, 23 citations in OpenAlex.

  1. Article
  2. Article
  3. SNRK modulates mTOR-autophagy pathway for liver lipid homeostasis in MAFLD.Molecular therapy : the journal of the American Society of Gene Therapy · 2025
    Article
  4. SNRK tames mTOR against metabolic dysfunction-associated steatotic liver disease.Molecular therapy : the journal of the American Society of Gene Therapy · 2025
    Article
  5. Review
  6. Article
  7. Article
  8. Article
  9. Human bone marrow mesenchymal stem cell-derived extracellular vesicles reduce inflammation and pyroptosis in acute kidney injury via miR-223-3p/HDAC2/SNRK.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2023
    Article
  10. Article
  11. Cardiomyocyte-SpecificJournal of the American Heart Association · 2019
    Article
  12. Article
  13. Article
  14. Article
  15. SNRK (Sucrose Nonfermenting 1-Related Kinase) Promotes Angiogenesis In Vivo.Arteriosclerosis, thrombosis, and vascular biology · 2018
    Article
  16. Article
  17. Article
  18. Article
  19. Article
  20. 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

8 authors at 3 institutions in 2 countries.

Yujie LiHallett Center for Diabetes and Endocrinology, Rhode Island Hospital, Warren Alpert Medical School of Brown University, Providence, Rhode Island, USA.
Yaohui Nie
Ynes Helou
Guoxian Ding
Bin Feng
Gang Xu
Arthur Salomon
Haiyan Xu
Brown University · USJiangsu Province Hospital · CNRhode Island Hospital · US

Funding

MAP Kinase Phosphatase 3 (MKP-3) and Obesity-related GluconeogenesisR01DK080746 · NIDDK · RHODE ISLAND HOSPITAL · PI XU, HAIYAN · 2009 to 2013
$1.7M
NIDDK NIH HHS R01 DK 080746NIDDK NIH HHS R01 DK080746
6 · The paper itself

Abstract

In this study, the role of sucrose non-fermenting-related kinase (SNRK) in white adipocyte biology was investigated. SNRK is abundantly expressed in adipose tissue, and the expression level is decreased in obese mice. SNRK expression is repressed by inflammatory signals but increased by insulin sensitizer in cultured adipocytes. In vivo, adipose tissue SNRK expression can be decreased by lipid injection but enhanced by macrophage ablation. Knocking down SNRK in cultured adipocytes activates both JNK and IKKβ pathways as well as promotes lipolysis. Insulin-stimulated Akt phosphorylation and glucose uptake are impaired in SNRK knockdown adipocytes. Phosphoproteomic analysis with SNRK knockdown adipocytes revealed significantly decreased phosphorylation of 49 proteins by 25% or more, which are involved in various aspects of adipocyte function with a clear indication of attenuated mTORC1 signaling. Phosphorylation of 43 proteins is significantly increased by onefold or higher, among which several proteins are known to be involved in inflammatory pathways. The inflammatory responses in SNRK knockdown adipocytes can be partially attributable to defective mTORC1 signaling, since rapamycin treatment activates IKKβ and induces lipolysis in adipocytes. In summary, SNRK may act as a suppressor of adipocyte inflammation and its presence is necessary for maintaining normal adipocyte function.

Indexed as

3T3-L1 CellsAdipocytesAdipose Tissue, WhiteAnimalsI-kappa B KinaseInflammationInsulinJNK Mitogen-Activated Protein KinasesLipolysisMaleMechanistic Target of Rapamycin Complex 1MiceMultiprotein ComplexesPhosphorylationProtein Serine-Threonine KinasesProto-Oncogene Proteins c-aktI-kappa B KinaseIkbkb protein, mouseInsulinJNK Mitogen-Activated Protein KinasesMechanistic Target of Rapamycin Complex 1Multiprotein ComplexesProtein Serine-Threonine KinasesProto-Oncogene Proteins c-aktSnrk protein, mouseTOR Serine-Threonine Kinases

Identifiers

PMID23520131
PMCPMC3712026
OpenAlexW2106909277

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.