Evidence map›Paper›PMID 18644868›Full record

ArticleMolecular and cellular biology2008

Prep1 deficiency induces protection from diabetes and increased insulin sensitivity through a p160-mediated mechanism.

Francesco Oriente, Luis Cesar Fernandez Diaz, Claudia Miele, Salvatore Iovino, Silvia Mori, Victor Manuel Diaz, Giancarlo Troncone, Angela Cassese, Pietro Formisano, Francesco Blasi and 1 more

Open access · greenAbstract read
In one paragraph

Article in Molecular and cellular biology, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.

0numbers the graph read from it
0cells of the map it votes in
28citing papers in PubMed
2.5field-weighted citation impact, top 11% 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

28 citing papers in PubMed, 46 citations in OpenAlex.

  1. Article
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  3. Article
  4. Review
  5. The Role of Prep1 in the Regulation of Mesenchymal Stromal Cells.International journal of molecular sciences · 2019
    Article
  6. Article
  7. Review
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  11. Article
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  14. Myotubes derived from human-induced pluripotent stem cells mirror in vivo insulin resistance.Proceedings of the National Academy of Sciences of the United States of America · 2016
    Article
  15. Article
  16. Article
  17. Article
  18. Article
  19. Biochemistry of the tale transcription factors PREP, MEIS, and PBX in vertebrates.Developmental dynamics : an official publication of the American Association of Anatomists · 2014
    Review
  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

11 authors at 4 institutions in 1 country.

Francesco OrienteDipartimento di Biologia e Patologia Cellulare e Molecolare, Università di Napoli Federico II, Via Sergio Pansini, 5, Naples 80131, Italy.
Luis Cesar Fernandez Diaz
Claudia Miele
Salvatore Iovino
Silvia Mori
Victor Manuel Diaz
Giancarlo Troncone
Angela Cassese
Pietro Formisano
Francesco Blasi
Francesco Beguinot
Institute for Experimental Endocrinology and Oncology · ITIFOM · ITVita-Salute San Raffaele University · ITUniversity of Naples Federico II · IT

Funding

Telethon GGP06028
6 · The paper itself

Abstract

We have examined glucose homeostasis in mice hypomorphic for the homeotic transcription factor gene Prep1. Prep1-hypomorphic (Prep1(i/i)) mice exhibit an absolute reduction in circulating insulin levels but normal glucose tolerance. In addition, these mice exhibit protection from streptozotocin-induced diabetes and enhanced insulin sensitivity with improved glucose uptake and insulin-dependent glucose disposal by skeletal muscle. This muscle phenotype does not depend on reduced expression of the known Prep1 transcription partner, Pbx1. Instead, in Prep1(i/i) muscle, we find normal Pbx1 but reduced levels of the recently identified novel Prep1 interactor p160. Consistent with this reduction, we find a muscle-selective increase in mRNA and protein levels of PGC-1alpha, accompanied by enhanced expression of the GLUT4 transporter, responsible for insulin-stimulated glucose uptake in muscle. Indeed, using L6 skeletal muscle cells, we induced the opposite effects by overexpressing Prep1 or p160, but not Pbx1. In vivo skeletal muscle delivery of p160 cDNA in Prep1(i/i) mice also reverses the molecular phenotype. Finally, we show that Prep1 controls the stability of the p160 protein. We conclude that Prep1 controls insulin sensitivity through the p160-GLUT4 pathway.

Indexed as

Diabetes Mellitus, ExperimentalAnimalsBlood GlucoseCarrier ProteinsDNA-Binding ProteinsFemaleGlucagonGlucose Tolerance TestGlucose Transporter Type 4Homeodomain ProteinsHomeostasisHumansInsulinIslets of LangerhansMaleMiceBlood GlucoseCarrier ProteinsDNA-Binding ProteinsGlucagonGlucose Transporter Type 4Homeodomain ProteinsInsulinMybbp1a protein, mouseNuclear ProteinsPbx1 protein, mousePeroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alphaPknox1 protein, mousePpargc1a protein, mousePre-B-Cell Leukemia Transcription Factor 1RNA-Binding ProteinsSlc2a4 protein, mouseTrans-ActivatorsTranscription Factors

Identifiers

PMID18644868
PMCPMC2546928
OpenAlexW2097079519

What OpenQuestion holds

Textmetadata
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.