Evidence mapPaperPMID 30170980Full record

ArticleMolecular metabolism2018

Deletion of the glucagon receptor gene before and after experimental diabetes reveals differential protection from hyperglycemia.

Belen Rivero-Gutierrez, April Haller, Jenna Holland, Emily Yates, Radha Khrisna, Kirk Habegger, Richard Dimarchi, David D'Alessio, Diego Perez-Tilve

Open access · goldAbstract read
In one paragraph

Article in Molecular metabolism, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
1.8field-weighted citation impact, top 14% 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

15 citing papers in PubMed, 20 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Article
  5. Article
  6. Review
  7. Article
  8. Review
  9. Review
  10. Review
  11. Article
  12. Review
  13. Paracrine signaling in islet function and survival.Journal of molecular medicine (Berlin, Germany) · 2020
    Review
  14. Article
  15. 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

9 authors at 4 institutions in 1 country.

Belen Rivero-GutierrezDepartment of Internal Medicine, University of Cincinnati, 2180 E. Galbraith Rd, Cincinnati, OH, USA.
April HallerDepartment of Internal Medicine, University of Cincinnati, 2180 E. Galbraith Rd, Cincinnati, OH, USA.
Jenna HollandDepartment of Internal Medicine, University of Cincinnati, 2180 E. Galbraith Rd, Cincinnati, OH, USA.
Emily YatesDepartment of Internal Medicine, University of Cincinnati, 2180 E. Galbraith Rd, Cincinnati, OH, USA.
Radha KhrisnaDepartment of Medicine, Duke University School of Medicine, NC, USA.
Kirk HabeggerComprehensive Diabetes Center and Department of Medicine - Endocrinology, Diabetes & and Metabolism, University of Alabama at Birmingham, Birmingham, AL, USA.
Richard DimarchiNovo Nordisk Research Center Indianapolis, Indianapolis, IN, USA; Department of Chemistry, Indiana University, Bloomington, IN, USA.
David D'AlessioDepartment of Medicine, Duke University School of Medicine, NC, USA.
Diego Perez-TilveDepartment of Internal Medicine, University of Cincinnati, 2180 E. Galbraith Rd, Cincinnati, OH, USA. Electronic address: pereztdo@ucmail.uc.edu.
University of Cincinnati · USDuke University · USNovo Nordisk (United States) · USUniversity of Alabama at Birmingham · US

Funding

UAB Diabetes Research CenterP30DK079626 · UNIVERSITY OF ALABAMA AT BIRMINGHAM · 2025 to 2025
$1.3M
NIDDK NIH HHS P30 DK079626NIDDK NIH HHS R01 DK112934
6 · The paper itself

Abstract

objectiveMice with congenital loss of the glucagon receptor gene (Gcgr

methodsWe induced experimental T1DM by injecting the beta-cell cytotoxin streptozotocin (STZ) in mice with congenital or temporally-controlled Gcgr loss-of-function using tamoxifen (TMX).

resultsDisruption of Gcgr expression, using either an inducible approach in adult mice or animals with congenital knockout, abolished the response to a long-acting Gcgr agonist. Mice with either developmental Gcgr disruption or inducible deletion several weeks before STZ treatment maintained normoglycemia. However, mice with inducible knockout of the Gcgr one week after the onset of STZ diabetes had only partial correction of hyperglycemia, an effect that was reversed by GLP-1 receptor blockade. Mice with Gcgr deletion for either 2 or 6 weeks had similar patterns of gene expression, although the changes were generally larger with longer GCGR knockout.

conclusionsThese findings demonstrate that the effects of glucagon to mitigate diabetic hyperglycemia are not through acute signaling but require compensations that take weeks to develop.

Indexed as

AnimalsBlood GlucoseDiabetes Mellitus, ExperimentalDisease Models, AnimalGene Expression RegulationGlucagonGlucagon-Like Peptide-1 ReceptorHyperglycemiaInsulinInsulin-Secreting CellsMaleMiceMice, KnockoutReceptors, GlucagonStreptozocinTranscriptomeBlood GlucoseGlucagonGlucagon-Like Peptide-1 ReceptorInsulinReceptors, GlucagonStreptozocinDiabetesGCGRGLP-1RGlucagonInsulinTamoxifen

Identifiers

PMID30170980
PMCPMC6197675
OpenAlexW2888196961

What Socratic 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 Socratic graph.