Evidence map›Paper›PMID 30156060›Full record

ArticlePhysiological reports2018

Chronic administration of the angiotensin type 2 receptor agonist C21 improves insulin sensitivity in C57BL/6 mice.

Diego Tomás Quiroga, Marina C Muñoz, Carolina Gil, Marlies Pffeifer, Jorge E Toblli, Ulrike M Steckelings, Jorge F Giani, Fernando P Dominici

Open access · goldAbstract read
In one paragraph

Article in Physiological reports, 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
2.4field-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

15 citing papers in PubMed, 22 citations in OpenAlex.

  1. Review
  2. Article
  3. The Angiotensin ATPharmacological reviews · 2022
    Review
  4. Article
  5. Review
  6. Activation of ATBritish journal of pharmacology · 2020
    Article
  7. Article
  8. Article
  9. Article
  10. Review
  11. Review
  12. Article
  13. Article
  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

8 authors at 5 institutions in 3 countries.

Diego Tomás QuirogaDepartamento de Química Biológica-Instituto de Química y Fisicoquímica Biológicas (CONICET), Facultad de Farmacia y Bioquímica, Universidad de Buenos Aires, Buenos Aires, Argentina.
Marina C MuñozDepartamento de Química Biológica-Instituto de Química y Fisicoquímica Biológicas (CONICET), Facultad de Farmacia y Bioquímica, Universidad de Buenos Aires, Buenos Aires, Argentina.
Carolina GilDepartamento de Química Biológica-Instituto de Química y Fisicoquímica Biológicas (CONICET), Facultad de Farmacia y Bioquímica, Universidad de Buenos Aires, Buenos Aires, Argentina.
Marlies PffeiferDepartamento de Química Biológica-Instituto de Química y Fisicoquímica Biológicas (CONICET), Facultad de Farmacia y Bioquímica, Universidad de Buenos Aires, Buenos Aires, Argentina.
Jorge E ToblliLaboratory of Experimental Medicine, Hospital Alemán de Buenos Aires, Buenos Aires, Argentina.
Ulrike M SteckelingsIMM - Deptartment of Cardiovascular & Renal Research, University of Southern Denmark, Odense, Denmark.
Jorge F GianiDepartment of Biomedical Sciences, Cedars-Sinai Medical Center, Los Angeles, California.
Fernando P DominiciDepartamento de Química Biológica-Instituto de Química y Fisicoquímica Biológicas (CONICET), Facultad de Farmacia y Bioquímica, Universidad de Buenos Aires, Buenos Aires, Argentina.
Instituto de Química y Fisicoquímica Biológicas · ARConsejo Nacional de Investigaciones Científicas y Técnicas · ARCedars-Sinai Medical Center · USHospital Alemán · ARUniversity of Southern Denmark · DK

Funding

Transgenic & Knock-out MouseP30DK063491 · NIDDK · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI Andrea L Hevener · 2003 to 2026
$40.4M
NIDDK NIH HHS P30 DK063491
6 · The paper itself

Abstract

The renin-angiotensin system modulates insulin action. Angiotensin type 1 receptor exerts a deleterious effect, whereas the angiotensin type 2 receptor (AT2R) appears to have beneficial effects providing protection against insulin resistance and type 2 diabetes. To further explore the role of the AT2R on insulin action and glucose homeostasis, in this study we administered C57Bl/6 mice with the synthetic agonist of the AT2R C21 for 12 weeks (1 mg/kg per day; ip). Vehicle-treated animals were used as control. Metabolic parameters, glucose, and insulin tolerance, in vivo insulin signaling in main insulin-target tissues as well as adipose tissue levels of adiponectin, and TNF-α were assessed. C21-treated animals displayed decreased glycemia together with unaltered insulinemia, increased insulin sensitivity, and increased glucose tolerance compared to nontreated controls. This was accompanied by a significant decrease in adipocytes size in epididymal adipose tissue and significant increases in both adiponectin and UCP-1 expression in this tissue. C21-treated mice showed an increase in both basal Akt and ERK1/2 phosphorylation levels in the liver, and increased insulin-stimulated Akt activation in adipose tissue. This positive modulation of insulin action induced by C21 appeared not to involve the insulin receptor. In C21-treated mice, adipose tissue and skeletal muscle became unresponsive to insulin in terms of ERK1/2 phosphorylation levels. Present data show that chronic pharmacological activation of AT2R with C21 increases insulin sensitivity in mice and indicate that the AT2R has a physiological role in the conservation of insulin action.

Indexed as

AdipocytesAdiponectinAdipose TissueAnimalsBlood GlucoseCell SizeDiabetes Mellitus, ExperimentalDiabetes Mellitus, Type 2Drug Administration ScheduleDrug Evaluation, PreclinicalGlucose Tolerance TestInsulin ResistanceMaleMAP Kinase Signaling SystemMice, Inbred C57BLReceptor, Angiotensin, Type 2AdiponectinBlood GlucoseN-butyloxycarbonyl-3-(4-imidazol-1-ylmethylphenyl)-5-isobutylthiophene-2-sulfonamideReceptor, Angiotensin, Type 2SulfonamidesThiophenesTumor Necrosis Factor-alphaAdiponectinangiotensin type 2 receptorcompound 21insulin sensitivityrenin-angiotensin system

Identifiers

PMID30156060
PMCPMC6113135
OpenAlexW2888846790

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.