Evidence map›Paper›PMID 16418280›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America2006

IA-2beta, but not IA-2, is induced by ghrelin and inhibits glucose-stimulated insulin secretion.

Asako Doi, Takeshi Shono, Masahiro Nishi, Hiroto Furuta, Hideyuki Sasaki, Kishio Nanjo

Abstract read
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed
2.5field-weighted citation impact, top 10% 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

22 citing papers in PubMed, 70 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Review
  5. Article
  6. Ghrelin regulation of glucose metabolism.Journal of neuroendocrinology · 2019
    Review
  7. Review
  8. Article
  9. Review
  10. Immunohistochemical analysis of IA-2 family of protein tyrosine phosphatases in rat gastrointestinal endocrine cells.The journal of histochemistry and cytochemistry : official journal of the Histochemistry Society · 2013
    Article
  11. Review
  12. Review
  13. Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. Exogenous ghrelin enhances endocrine and exocrine regeneration in pancreatectomized rats.Journal of gastrointestinal surgery : official journal of the Society for Surgery of the Alimentary Tract · 2009
    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

6 authors at 2 institutions in 2 countries.

Asako DoiThe First Department of Medicine, Wakayama Medical University, 811-1 Kimiidera, Wakayama 641-8509, Japan.
Takeshi Shono
Masahiro Nishi
Hiroto Furuta
Hideyuki Sasaki
Kishio Nanjo
University of Chicago · USWakayama Medical University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Ghrelin is a newly discovered peptide and an endogenous ligand for growth hormone (GH) secretagogue (GHS) receptor. It has been shown to possess various central and peripheral effects, including GH secretion, food intake, and gastric and cardiac effects. Ghrelin and the GHS receptor are expressed also in pancreatic islets. We have identified several ghrelin-induced genes by PCR-select subtraction methods, among which is a beta-cell autoantigen for type 1 diabetes, IA-2beta. Administration of ghrelin increased IA-2beta mRNA in mouse brain, pancreas, and insulinoma cell lines (MIN6 and betaTC3). However, the expression of IA-2, another structurally related beta-cell autoantigen, was not induced by ghrelin. Administration of ghrelin or overexpression of IA-2beta, but not overexpression of IA-2, inhibited glucose-stimulated insulin secretion in MIN6 insulinoma cells and, moreover, inhibition of IA-2beta expression by the RNA interference technique ameliorated ghrelin's inhibitory effects on glucose-stimulated insulin secretion. These findings strongly suggest that inhibitory effects of ghrelin on glucose-stimulated insulin secretion are at least partly due to increased expression of IA-2beta induced by ghrelin. Our data demonstrate the link among ghrelin, IA-2beta, and glucose-stimulated insulin secretion.

Indexed as

AnimalsAutoantibodiesBlotting, NorthernBlotting, WesternCell LineCell Line, TumorDose-Response Relationship, DrugEnzyme-Linked Immunosorbent AssayGene Expression RegulationGhrelinGlucoseGrowth HormoneInsulinInsulinomaInsulin-Secreting CellsInsulin SecretionAutoantibodiesGhrelinGlucoseGrowth HormoneICA512 autoantibodyInsulinLigandsMembrane ProteinsPeptide HormonesProtein Tyrosine Phosphatase, Non-Receptor Type 1Protein Tyrosine PhosphatasesPTPRN2 protein, humanReceptor-Like Protein Tyrosine Phosphatases, Class 8RNA, MessengerRNA, Small Interfering

Identifiers

PMID16418280
PMCPMC1347964
OpenAlexW2076987540

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.