Evidence map›Paper›PMID 21719535›Full record

ArticleMolecular endocrinology (Baltimore, Md.)2011

Ghrelin directly stimulates glucagon secretion from pancreatic alpha-cells.

Jen-Chieh Chuang, Ichiro Sakata, Daisuke Kohno, Mario Perello, Sherri Osborne-Lawrence, Joyce J Repa, Jeffrey M Zigman

Open access · bronzeAbstract read
In one paragraph

Article in Molecular endocrinology (Baltimore, Md.), 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 81 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
81citing papers in PubMed, 1 pooled it
3.6field-weighted citation impact, top 6% 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

81 citing papers in PubMed, 1 synthesis or guideline pooled it, 132 citations in OpenAlex.

  1. Systematic Review: Does Exercise Training Influence Ghrelin Levels?International journal of molecular sciences · 2025
    Pooled it
  2. Review
  3. Review
  4. Article
  5. Article
  6. Review
  7. Article
  8. Review
  9. An Emerging Role for Gut-Brain Signaling Involving Ghrelin in Chronic Stress.Advances in experimental medicine and biology · 2025
    Review
  10. Article
  11. Review
  12. Review
  13. Article
  14. Ghrelin receptor signaling in health and disease: a biased view.Trends in endocrinology and metabolism: TEM · 2023
    Review
  15. Article
  16. Article
  17. Review
  18. Article
  19. "Sibling" battle or harmony: crosstalk between nesfatin-1 and ghrelin.Cellular and molecular life sciences : CMLS · 2022
    Review
  20. Article

21 more citing papers are in PubMed but not listed here.

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 1 institution in 1 country.

Jen-Chieh ChuangDepartment of Internal Medicine, Division of Hypothalamic Research, University of Texas Southwestern Medical Center, Dallas, Texas 75390-9077, USA.
Ichiro Sakata
Daisuke Kohno
Mario Perello
Sherri Osborne-Lawrence
Joyce J Repa
Jeffrey M Zigman
The University of Texas Southwestern Medical Center · US

Funding

Identification of Central Targets of GhrelinK08DK068069 · NIDDK · UT SOUTHWESTERN MEDICAL CENTER · PI ZIGMAN, JEFFREY M · 2006 to 2010
$627k
NIDDK NIH HHS 1K08DK068069NIDDK NIH HHS 5R01DK07132006NIDDK NIH HHS 5RL1DK08118504NIDDK NIH HHS K08 DK068069
6 · The paper itself

Abstract

Previous work has demonstrated that the peptide hormone ghrelin raises blood glucose. Such has been attributed to ghrelin's ability to enhance GH secretion, restrict insulin release, and/or reduce insulin sensitivity. Ghrelin's reported effects on glucagon have been inconsistent. Here, both animal- and cell-based systems were used to determine the role of glucagon in mediating ghrelin's effects on blood glucose. The tissue and cell distribution of ghrelin receptors (GHSR) was evaluated by quantitative PCR and histochemistry. Plasma glucagon levels were determined following acute acyl-ghrelin injections and in pharmacological and/or transgenic mouse models of ghrelin overexpression and GHSR deletion. Isolated mouse islets and the α-cell lines αTC1 and InR1G9 were used to evaluate ghrelin's effects on glucagon secretion and the role of calcium and ERK in this activity. GHSR mRNA was abundantly expressed in mouse islets and colocalized with glucagon in α-cells. Elevation of acyl-ghrelin acutely (after sc administration, such that physiologically relevant plasma ghrelin levels were achieved) and chronically (by slow-releasing osmotic pumps and as observed in transgenic mice harboring ghrelinomas) led to higher plasma glucagon and increased blood glucose. Conversely, genetic GHSR deletion was associated with lower plasma glucagon and reduced fasting blood glucose. Acyl-ghrelin increased glucagon secretion in a dose-dependent manner from mouse islets and α-cell lines, in a manner requiring elevation of intracellular calcium and phosphorylation of ERK. Our study shows that ghrelin's regulation of blood glucose involves direct stimulation of glucagon secretion from α-cells and introduces the ghrelin-glucagon axis as an important mechanism controlling glycemia under fasting conditions.

Indexed as

AnimalsBlood GlucoseCalciumCell LineDown-RegulationEnzyme ActivationExtracellular Signal-Regulated MAP KinasesGhrelinGlucagonGlucagon-Secreting CellsInjections, SubcutaneousMaleMiceMice, Inbred C57BLMice, TransgenicRatsBlood GlucoseCalciumExtracellular Signal-Regulated MAP KinasesGhrelinGlucagonReceptors, Ghrelin

Identifiers

PMID21719535
PMCPMC3165914
OpenAlexW2014093079

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.