Evidence map›Paper›PMID 26643367›Full record

ArticleScientific reports2015

Erythropoietin alleviates hepatic insulin resistance via PPARγ-dependent AKT activation.

Zhijuan Ge, Pengzi Zhang, Ting Hong, Sunyinyan Tang, Ran Meng, Yan Bi, Dalong Zhu

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed
2.1field-weighted citation impact, top 12% 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

24 citing papers in PubMed, 40 citations in OpenAlex.

  1. Article
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  9. N-Frontiers in pharmacology · 2024
    Article
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  13. Article
  14. Article
  15. Characterization and Treatment of Inflammation and Insulin Resistance in Obese Adipose Tissue.Diabetes, metabolic syndrome and obesity : targets and therapy · 2020
    Review
  16. Article
  17. Article
  18. Review
  19. PPARPPAR research · 2018
    Article
  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

7 authors at 2 institutions in 1 country.

Zhijuan GeDepartment of Endocrinology, DrumTower hospital affiliated to Nanjing University Medical School, No321 Zhongshan Road, Nanjing, 210008, China.
Pengzi ZhangDepartment of Endocrinology, DrumTower hospital affiliated to Nanjing University Medical School, No321 Zhongshan Road, Nanjing, 210008, China.
Ting HongDepartment of Endocrinology, Drum Tower Clinical Medical College of Nanjing Medical University, Nanjing, 210008, China.
Sunyinyan TangDepartment of Endocrinology, DrumTower hospital affiliated to Nanjing University Medical School, No321 Zhongshan Road, Nanjing, 210008, China.
Ran MengDepartment of Endocrinology, DrumTower hospital affiliated to Nanjing University Medical School, No321 Zhongshan Road, Nanjing, 210008, China.
Yan BiDepartment of Endocrinology, DrumTower hospital affiliated to Nanjing University Medical School, No321 Zhongshan Road, Nanjing, 210008, China.
Dalong ZhuDepartment of Endocrinology, DrumTower hospital affiliated to Nanjing University Medical School, No321 Zhongshan Road, Nanjing, 210008, China.
Nanjing Drum Tower Hospital · CNNanjing Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Erythropoietin (EPO) has beneficial effects on glucose metabolism and insulin resistance. However, the mechanism underlying these effects has not yet been elucidated. This study aimed to investigate how EPO affects hepatic glucose metabolism. Here, we report that EPO administration promoted phosphatidylinositol 3-kinase (PI3K)/AKT pathway activation in palmitic acid (PA)-treated HepG2 cells and in the liver of high-fat diet (HFD)-fed mice, whereas adenovirus-mediated silencing of the erythropoietin receptor (EPOR) blocked EPO-induced AKT signalling in HepG2 cells. Importantly, a peroxisome proliferator-activated receptor γ (PPARγ) antagonist and PPARγ small interfering RNA (siRNA) abrogated the EPO-induced increase in p-AKT in HepG2 cells. Lentiviral vector-mediated hepatic PPARγ silencing in HFD-fed C57BL/6 mice impaired EPO-mediated increases in glucose tolerance, insulin sensitivity and hepatic AKT activation. Furthermore, EPO activated the AMP-activated protein kinase (AMPK)/sirtuin 1 (SIRT1) signalling pathway, and AMPKα and SIRT1 knockdown each attenuated the EPO-induced PPARγ expression and deacetylation and PPARγ-dependent AKT activation in HepG2 cells. In summary, these findings suggest that PPARγ is involved in EPO/EPOR-induced AKT activation, and targeting the PPARγ/AKT pathway via EPO may have therapeutic implications for hepatic insulin resistance and type 2 diabetes.

Indexed as

Insulin ResistanceAMP-Activated Protein KinasesAnimalsCalcium-Calmodulin-Dependent Protein Kinase KinaseEnzyme ActivationErythropoietinGlucoseGlucose Tolerance TestHepatocytesHep G2 CellsHumansMaleMicePPAR gammaProto-Oncogene Proteins c-aktReceptors, ErythropoietinAMP-Activated Protein KinasesCalcium-Calmodulin-Dependent Protein Kinase KinaseErythropoietinGlucosePPAR gammaProto-Oncogene Proteins c-aktReceptors, ErythropoietinSirtuin 1

Identifiers

PMID26643367
PMCPMC4672330
OpenAlexW2414121742

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.