Evidence map›Paper›PMID 23066908›Full record

ArticleCardiovascular diabetology2012

Obestatin induced recovery of myocardial dysfunction in type 1 diabetic rats: underlying mechanisms.

Manuela Aragno, Raffaella Mastrocola, Corrado Ghé, Elisa Arnoletti, Eleonora Bassino, Giuseppe Alloatti, Giampiero Muccioli

Open access · goldAbstract read
In one paragraph

Article in Cardiovascular diabetology, 2012. 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
9.1field-weighted citation impact, top 2% 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

29 citing papers in PubMed, 58 citations in OpenAlex.

  1. Article
  2. Obestatin: canonical and unexpected functions.Reviews in endocrine & metabolic disorders · 2026
    Review
  3. Article
  4. Review
  5. Article
  6. Review
  7. Review
  8. Article
  9. Article
  10. Article
  11. Review
  12. Article
  13. Article
  14. Erythropoietin and diabetes mellitus.World journal of diabetes · 2015
    Review
  15. Review
  16. Article
  17. Review
  18. Review
  19. New Insights for Oxidative Stress and Diabetes Mellitus.Oxidative medicine and cellular longevity · 2015
    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

7 authors at 2 institutions in 1 country.

Manuela AragnoDepartment of Experimental Medicine and Oncology, University of Turin, Corso Raffaello 30, Turin, 10125, Italy. manuela.aragno@unito.it
Raffaella Mastrocola
Corrado Ghé
Elisa Arnoletti
Eleonora Bassino
Giuseppe Alloatti
Giampiero Muccioli
University of Turin · ITAccademia Albertina delle Belle Arti · IT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundThe aim of this study was to investigate whether obestatin (OB), a peptide mediator encoded by the ghrelin gene exerting a protective effect in ischemic reperfused heart, is able to reduce cardiac dysfunctions in adult diabetic rats.

methodsDiabetes was induced by STZ injection (50 mg/kg) in Wistar rats (DM). OB was administered (25 μg/kg) twice a day for 6 weeks. Non-diabetic (ND) rats and DM rats were distributed into four groups: untreated ND, OB-treated ND, untreated DM, OB-treated DM. Cardiac contractility and ß-adrenergic response were studied on isolated papillary muscles. Phosphorylation of AMPK, Akt, ERK1/2 and GSK3ß as well ß-1 adrenoreceptors levels were detected by western blot, while α-MHC was measured by RT-PCR.

resultsOB preserved papillary muscle contractility (85 vs 27% of ND), ß-adrenergic response (103 vs 65% of ND), as well ß1-adrenoreceptors and α-MHC levels in diabetic myocardial tissue. Moreover, OB up-regulated the survival kinases Akt and ERK1/2, and enhanced AMPK and GSK3ß phosphorylation. OB corrected oxidative unbalance, reduced pro-inflammatory cytokine TNF-α plasma levels, NFkB translocation and pro-fibrogenic factors expression in diabetic myocardium.

conclusionsOB displays a significant beneficial effect against the alterations of contractility and ß-adrenergic response in the heart of STZ-treated diabetic rats, which was mainly associated with the ability of OB to up-regulate the transcription of ß1-adrenergic receptors and α-MHC; this protective effect was accompanied by the ability to restore oxidative balance and to promote phosphorylation/modulation of AMPK and pro-survival kinases such as Akt, ERK1/2 and GSK3ß.

Indexed as

AMP-Activated Protein KinasesAnimalsBlotting, WesternCardiotonic AgentsCell LineDiabetes Mellitus, ExperimentalDiabetes Mellitus, Type 1Glycogen Synthase Kinase 3Glycogen Synthase Kinase 3 betaHeart DiseasesHypoglycemic AgentsInflammation MediatorsMaleMetforminMitogen-Activated Protein Kinase 1Mitogen-Activated Protein Kinase 3AMP-Activated Protein KinasesCardiotonic AgentsGlycogen Synthase Kinase 3Glycogen Synthase Kinase 3 betaHypoglycemic AgentsInflammation MediatorsMapk1 protein, ratMetforminMitogen-Activated Protein Kinase 1Mitogen-Activated Protein Kinase 3Myosin Heavy ChainsNF-kappa Bobestatin, ratPeptide HormonesProto-Oncogene Proteins c-aktReceptors, Adrenergic, beta-1Tumor Necrosis Factor-alphaVentricular Myosins

Identifiers

PMID23066908
PMCPMC3537569
OpenAlexW2143565379

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.