Evidence map›Paper›PMID 24946098›Full record

ArticleMolecular and cellular endocrinology2014

FOXO1-dependent up-regulation of MAP kinase phosphatase 3 (MKP-3) mediates glucocorticoid-induced hepatic lipid accumulation in mice.

Bin Feng, Qin He, Haiyan Xu

Abstract read
In one paragraph

Article in Molecular and cellular endocrinology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
2.0field-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

16 citing papers in PubMed, 34 citations in OpenAlex.

  1. Review
  2. Article
  3. MAP kinase phosphatases in metabolic diseases.Trends in endocrinology and metabolism: TEM · 2026
    Review
  4. Review
  5. Review
  6. Article
  7. Article
  8. Article
  9. Article
  10. Review
  11. Article
  12. Glucose metabolism in Cushing's syndrome.Current opinion in endocrinology, diabetes, and obesity · 2020
    Review
  13. Glucocorticoid-Induced Fatty Liver Disease.Diabetes, metabolic syndrome and obesity : targets and therapy · 2020
    Review
  14. Article
  15. Article
  16. 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

3 authors at 2 institutions in 1 country.

Bin FengHallett Center for Diabetes and Endocrinology, Rhode Island Hospital, Warren Alpert Medical School of Brown University, Providence, RI 02903, USA. Electronic address: bfeng@lifespan.org.
Qin HeHallett Center for Diabetes and Endocrinology, Rhode Island Hospital, Warren Alpert Medical School of Brown University, Providence, RI 02903, USA. Electronic address: qinh123d@gmail.com.
Haiyan XuHallett Center for Diabetes and Endocrinology, Rhode Island Hospital, Warren Alpert Medical School of Brown University, Providence, RI 02903, USA. Electronic address: hxu@lifespan.org.
Rhode Island Hospital · USBrown University · 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 3R01 DK080746-02S1NIDDK NIH HHS 5R01 DK080746NIDDK NIH HHS R01 DK080746
6 · The paper itself

Abstract

Long-term treatment with glucocorticoids (GCs) or dysregulation of endogenous GC levels induces a series of metabolic diseases, such as insulin resistance, obesity and type 2 diabetes. We previously showed that MAP kinase phosphatase-3 (MKP-3) plays an important role in glucose metabolism. The aim of this study is to investigate the role of MKP-3 in GC-induced metabolic disorders. Dexamethasone (Dex), a synthetic GC, increases MKP-3 protein expression both in cultured hepatoma cells and in the liver of lean mice. This effect is likely mediated by forkhead box protein O1 (FOXO1) because disruption of endogenous FOXO1 function by either interfering RNA mediated FOXO1 knockdown or overexpression of a dominant negative FOXO1 mutant blocks Dex-induced upregulation of MKP-3 protein. In addition, overexpression of FOXO1 is sufficient to induce MKP-3 protein expression. MKP-3 deficient mice are protected from several side effects of chronic Dex exposure, such as body weight gain, adipose tissue enlargement, hepatic lipid accumulation, and insulin resistance. The beneficial phenotypes in mice lacking MKP-3 are largely attributed to the absence of MKP-3 in the liver since only hepatic insulin signaling has been preserved among the three insulin target tissues (liver, muscle and adipose tissue).

Indexed as

Up-RegulationAnimalsCarcinoma, HepatocellularCell Line, TumorCells, CulturedDexamethasoneDual Specificity Phosphatase 6Fatty LiverForkhead Box Protein O1Forkhead Transcription FactorsGlucocorticoidsLiverLiver NeoplasmsMiceMice, KnockoutSignal TransductionDexamethasoneDual Specificity Phosphatase 6Forkhead Box Protein O1Forkhead Transcription FactorsFOXO1 protein, humanGlucocorticoidsDexamethasoneHepatosteatosisInsulin resistanceLipogenesisObesity

Identifiers

PMID24946098
PMCPMC4130747
OpenAlexW1971211736

What OpenQuestion holds

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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.