Evidence map›Paper›PMID 29925501›Full record

ArticleDiabetes2018

Glucagon Receptor Signaling Regulates Energy Metabolism via Hepatic Farnesoid X Receptor and Fibroblast Growth Factor 21.

Teayoun Kim, Shelly Nason, Cassie Holleman, Mark Pepin, Landon Wilson, Taylor F Berryhill, Adam R Wende, Chad Steele, Martin E Young, Stephen Barnes and 6 more

Open access · bronzeAbstract readComparative Study
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 60 papers.

0numbers the graph read from it
0cells of the map it votes in
60citing papers in PubMed
3.4field-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

60 citing papers in PubMed, 92 citations in OpenAlex.

  1. Trial
  2. Dose-response effects on HbADiabetologia · 2024
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  6. Improving incretin-mediated body weight loss via energy expenditure.Trends in endocrinology and metabolism: TEM · 2026
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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

16 authors at 5 institutions in 3 countries.

Teayoun KimComprehensive 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.
Cassie HollemanComprehensive Diabetes Center and Division of Endocrinology, Diabetes and Metabolism, Department of Medicine, University of Alabama at Birmingham, Birmingham, AL.
Mark PepinDivision of Molecular and Cellular Pathology, Department of Pathology, University of Alabama at Birmingham, AL.
Landon WilsonDepartment of Pharmacology, University of Alabama at Birmingham, Birmingham, AL.
Taylor F BerryhillDepartment of Pharmacology, University of Alabama at Birmingham, Birmingham, AL.
Adam R WendeDivision of Molecular and Cellular Pathology, Department of Pathology, University of Alabama at Birmingham, AL.
Chad SteeleDivision of Pulmonary, Allergy and Critical Care Medicine, Department of Medicine, University of Alabama at Birmingham, Birmingham, AL.
Martin E YoungDivision of Cardiovascular Disease, Department of Medicine, University of Alabama at Birmingham, Birmingham, AL.
Stephen BarnesDepartment of Pharmacology, University of Alabama at Birmingham, Birmingham, AL.
Daniel J DruckerDepartment of Medicine, Lunenfeld-Tanenbaum Research Institute, Sinai Health System, University of Toronto, Toronto, Ontario, Canada.ORCID 0000-0001-6688-8127
Brian FinanNovo Nordisk Research Center Indianapolis, Indianapolis, IN.
Richard DiMarchiNovo Nordisk Research Center Indianapolis, Indianapolis, IN.
Diego Perez-TilveDivision of Endocrinology, Diabetes and Metabolism, Metabolic Diseases Institute, University of Cincinnati, Cincinnati, OH.
Matthias TschöpInstitute for Diabetes and Obesity, Helmholtz Zentrum München, München, Germany.
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.ORCID 0000-0002-0342-5480
University of Alabama at Birmingham · USNovo Nordisk (United States) · USHelmholtz Zentrum München · DEUniversity of Cincinnati · USUniversity of Toronto · CA

Funding

Why is the prevalence of obesity so high in U.S. Southern States? Regional predictors of BMI and obesity treatment response.P30DK056336 · NIDDK · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI BARBARA A GOWER · 2000 to 2026
$31.9M
University of Alabama at Birmingham's Diabetes Research CenterP30DK079626 · NIDDK · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI Kirk Michael Habegger · 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
Neuroendocrine Regulation of Adipocyte MetabolismR01DK077975 · NIDDK · UNIVERSITY OF CINCINNATI · PI PEREZ-TILVE, DIEGO · 2009 to 2013
$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
GADD45B and Metabolic Memory in Diabetic Heart FailureF30HL137240 · NHLBI · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI PEPIN, MARK EMILE · 2018 to 2019
$83k
NHLBI NIH HHS F30 HL137240NHLBI NIH HHS T32 HL105349NIDDK NIH HHS K01 DK098319NIDDK NIH HHS P30 DK056336NIDDK NIH HHS P30 DK079626NIDDK NIH HHS R01 DK077975NIDDK NIH HHS R01 DK112934
6 · The paper itself

Abstract

Glucagon, an essential regulator of glucose and lipid metabolism, also promotes weight loss, in part through potentiation of fibroblast growth factor 21 (FGF21) secretion. However, FGF21 is only a partial mediator of metabolic actions ensuing from glucagon receptor (GCGR) activation, prompting us to search for additional pathways. Intriguingly, chronic GCGR agonism increases plasma bile acid levels. We hypothesized that GCGR agonism regulates energy metabolism, at least in part, through farnesoid X receptor (FXR). To test this hypothesis, we studied whole-body and liver-specific FXR-knockout (

Indexed as

AdiposityAnimalsAnti-Obesity AgentsCalorimetry, IndirectCells, CulturedDiet, High-FatEnergy MetabolismFibroblast Growth FactorsGene Expression RegulationLiverMaleMice, Inbred C57BLMice, KnockoutMitochondria, LiverObesityOrgan SpecificityAnti-Obesity Agentsfibroblast growth factor 21Fibroblast Growth FactorsIUB288PeptidesReceptor, Farnesoid X-ActivatedReceptors, Cytoplasmic and NuclearReceptors, Glucagon

Identifiers

PMID29925501
PMCPMC6110317
OpenAlexW2809364083

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.