Evidence map›Paper›PMID 30150304›Full record

ArticleDiabetes2018

Hepatic Glucagon Receptor Signaling Enhances Insulin-Stimulated Glucose Disposal in Rodents.

Teayoun Kim, Cassie L Holleman, Shelly Nason, Deanna M Arble, Nickki Ottaway, Joseph Chabenne, Christine Loyd, Jeong-A Kim, Darleen Sandoval, Daniel J Drucker and 3 more

Open access · bronzeAbstract read
In one paragraph

Article in Diabetes, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 papers.

0numbers the graph read from it
0cells of the map it votes in
41citing papers in PubMed
4.4field-weighted citation impact, top 4% 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

41 citing papers in PubMed, 65 citations in OpenAlex.

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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

13 authors at 6 institutions in 2 countries.

Teayoun KimComprehensive Diabetes Center and Division of Endocrinology, Diabetes, and Metabolism, Department of Medicine, University of Alabama at Birmingham, Birmingham, AL.
Cassie L HollemanComprehensive Diabetes Center and Division of Endocrinology, Diabetes, and Metabolism, Department of Medicine, University of Alabama at Birmingham, Birmingham, AL.
Shelly NasonComprehensive Diabetes Center and Division of Endocrinology, Diabetes, and Metabolism, Department of Medicine, University of Alabama at Birmingham, Birmingham, AL.
Deanna M ArbleDepartment of Biological Sciences, Marquette University, Milwaukee, WI.
Nickki OttawayMetabolic Diseases Institute and Division of Endocrinology, Diabetes, and Metabolism, Department of Medicine, University of Cincinnati, Cincinnati, OH.
Joseph ChabenneNovo Nordisk Research Center, Indianapolis, IN.
Christine LoydComprehensive Diabetes Center and Division of Endocrinology, Diabetes, and Metabolism, Department of Medicine, University of Alabama at Birmingham, Birmingham, AL.
Jeong-A KimComprehensive Diabetes Center and Division of Endocrinology, Diabetes, and Metabolism, Department of Medicine, University of Alabama at Birmingham, Birmingham, AL.
Darleen SandovalDepartment of Surgery, University of Michigan, Ann Arbor, MI.
Daniel J DruckerLunenfeld-Tanenbaum Research Institute, Mt. Sinai Hospital, Department of Medicine, University of Toronto, Toronto, Ontario, Canada.ORCID 0000-0001-6688-8127
Richard DiMarchiNovo Nordisk Research Center, Indianapolis, IN.
Diego Perez-TilveMetabolic Diseases Institute and Division of Endocrinology, Diabetes, and Metabolism, Department of Medicine, University of Cincinnati, Cincinnati, OH kirkhabegger@uabmc.edu pereztdo@ucmail.uc.edu.
Kirk M HabeggerComprehensive Diabetes Center and Division of Endocrinology, Diabetes, and Metabolism, Department of Medicine, University of Alabama at Birmingham, Birmingham, AL kirkhabegger@uabmc.edu pereztdo@ucmail.uc.edu.ORCID 0000-0002-0342-5480
University of Alabama at Birmingham · USNovo Nordisk (United States) · USUniversity of Cincinnati · USMarquette University · USUniversity of Michigan · USUniversity of Toronto · CA

Funding

Regional Pilot And Feasibility Study Grants ProgramP30DK020572 · NIDDK · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI Mehboob A Hussain · 2013 to 2026
$24.3M
University of Alabama at Birmingham's Diabetes Research CenterP30DK079626 · NIDDK · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI BARBARA A GOWER · 2013 to 2026
$19.5M
UAB Pre-Doctoral Training Program in Obesity-Related ResearchT32HL105349 · NHLBI · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI BARBARA A GOWER · 2010 to 2026
$5.7M
Saturated Fatty Acid-induced Autophagy in Vascular EndotheliumR01HL128695 · NHLBI · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI KIM, JEONGA · 2016 to 2019
$1.8M
Neuroendocrine Regulation of Adipocyte MetabolismR01DK077975 · NIDDK · UNIVERSITY OF CINCINNATI · PI PEREZ-TILVE, DIEGO · 2009 to 2013
$1.7M
Role of Glucokinase in GLP-1 Regulation of Energy and Glucose HomeostasisR01DK082480 · NIDDK · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI SANDOVAL, DARLEEN A. · 2010 to 2014
$1.7M
Glucagon Mediated Potentiation of Insulin Sensitivity in Glucose MetabolismR01DK112934 · NIDDK · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI HABEGGER, KIRK MICHAEL · 2017 to 2021
$1.7M
Duodenal nutrient exclusion enhances glucose metabolism via CNS regulationK01DK098319 · NIDDK · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI HABEGGER, KIRK MICHAEL · 2014 to 2016
$456k
NHLBI NIH HHS R01 HL128695NHLBI NIH HHS T32 HL105349NIDDK NIH HHS K01 DK098319NIDDK NIH HHS P30 DK020572NIDDK NIH HHS P30 DK079626NIDDK NIH HHS R01 DK077975NIDDK NIH HHS R01 DK082480NIDDK NIH HHS R01 DK112934
6 · The paper itself

Abstract

Glucagon receptor (GCGR) agonists cause hyperglycemia but also weight loss. However, GCG-like peptide 1 receptor (GLP1R)/GCGR mixed agonists do not exhibit the diabetogenic effects often attributed to GCGR activity. Thus, we sought to investigate the effect of glucagon agonism on insulin action and glucose homeostasis. Acute GCGR agonism induced immediate hyperglycemia, followed by improved glucose tolerance and enhanced glucose-stimulated insulin secretion. Moreover, acute GCGR agonism improved insulin tolerance in a dose-dependent manner in both lean and obese mice. Improved insulin tolerance was independent of GLP1R, FGF21, and hepatic glycogenolysis. Moreover, we observed increased glucose infusion rate, disposal, uptake, and suppressed endogenous glucose production during euglycemic clamps. Mice treated with insulin and GCGR agonist had enhanced phosphorylation of hepatic AKT at Ser

Indexed as

AnimalsGlucagon-Like Peptide-1 ReceptorGlucoseGlucose Tolerance TestInsulinInsulin ResistanceLiverMiceMice, KnockoutObesityPeptidesPhosphorylationProto-Oncogene Proteins c-aktReceptors, GlucagonGlp1r protein, mouseGlucagon-Like Peptide-1 ReceptorGlucoseInsulinIUB288PeptidesProto-Oncogene Proteins c-aktReceptors, Glucagon

Identifiers

PMID30150304
PMCPMC6198333
OpenAlexW2889408384

What Socratic 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 Socratic graph.