Evidence map›Paper›PMID 21788571›Full record

ArticleDiabetes2011

Ghrelin attenuates cAMP-PKA signaling to evoke insulinostatic cascade in islet β-cells.

Katsuya Dezaki, Boldbaatar Damdindorj, Hideyuki Sone, Oleg Dyachok, Anders Tengholm, Erik Gylfe, Tomoyuki Kurashina, Masashi Yoshida, Masafumi Kakei, Toshihiko Yada

Open access · bronzeAbstract read
In one paragraph

Article in Diabetes, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.

0numbers the graph read from it
0cells of the map it votes in
26citing papers in PubMed
3.0field-weighted citation impact, top 8% 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

26 citing papers in PubMed, 62 citations in OpenAlex.

  1. Review
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  8. The Difference δ-Cells Make in Glucose Control.Physiology (Bethesda, Md.) · 2018
    Review
  9. [Association of leptin, adiponectin, and ghrelin in breast milk with the growth of infants with exclusive breastfeeding].Zhongguo dang dai er ke za zhi = Chinese journal of contemporary pediatrics · 2018
    Article
  10. Article
  11. Review
  12. Involvement of thermosensitive TRP channels in energy metabolism.The journal of physiological sciences : JPS · 2017
    Review
  13. Article
  14. Article
  15. Review
  16. Article
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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

10 authors at 2 institutions in 2 countries.

Katsuya DezakiDivision of Integrative Physiology, Department of Physiology, Jichi Medical University School of Medicine, Tochigi, Japan. dezaki@jichi.ac.jp
Boldbaatar Damdindorj
Hideyuki Sone
Oleg Dyachok
Anders Tengholm
Erik Gylfe
Tomoyuki Kurashina
Masashi Yoshida
Masafumi Kakei
Toshihiko Yada
Jichi Medical University · JPUppsala University · SE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

objectiveGhrelin reportedly restricts insulin release in islet β-cells via the Gα(i2) subtype of G-proteins and thereby regulates glucose homeostasis. This study explored whether ghrelin regulates cAMP signaling and whether this regulation induces insulinostatic cascade in islet β-cells. RESEARCH DESIGN AND

methodsInsulin release was measured in rat perfused pancreas and isolated islets and cAMP production in isolated islets. Cytosolic cAMP concentrations ([cAMP](i)) were monitored in mouse MIN6 cells using evanescent-wave fluorescence imaging. In rat single β-cells, cytosolic protein kinase-A activity ([PKA](i)) and Ca(2+) concentration ([Ca(2+)](i)) were measured by DR-II and fura-2 microfluorometry, respectively, and whole cell currents by patch-clamp technique.

resultsGhrelin suppressed glucose (8.3 mmol/L)-induced insulin release in rat perfused pancreas and isolated islets, and these effects of ghrelin were blunted in the presence of cAMP analogs or adenylate cyclase inhibitor. Glucose-induced cAMP production in isolated islets was attenuated by ghrelin and enhanced by ghrelin receptor antagonist and anti-ghrelin antiserum, which counteract endogenous islet-derived ghrelin. Ghrelin inhibited the glucose-induced [cAMP](i) elevation and [PKA](i) activation in MIN6 and rat β-cells, respectively. Furthermore, ghrelin potentiated voltage-dependent K(+) (Kv) channel currents without altering Ca(2+) channel currents and attenuated glucose-induced [Ca(2+)](i) increases in rat β-cells in a PKA-dependent manner.

conclusionsGhrelin directly interacts with islet β-cells to attenuate glucose-induced cAMP production and PKA activation, which lead to activation of Kv channels and suppression of glucose-induced [Ca(2+)](i) increase and insulin release.

Indexed as

AnimalsCyclic AMPCyclic AMP-Dependent Protein KinasesGhrelinGlucoseInsulinInsulin-Secreting CellsInsulin SecretionMaleMiceRatsRats, WistarSignal TransductionCyclic AMPCyclic AMP-Dependent Protein KinasesGhrelinGlucoseInsulin

Identifiers

PMID21788571
PMCPMC3161328
OpenAlexW2120892371

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.