Evidence map›Paper›PMID 29065174›Full record

ArticlePloS one2017

Glucagon like receptor 1/ glucagon dual agonist acutely enhanced hepatic lipid clearance and suppressed de novo lipogenesis in mice.

Vijay R More, Julie Lao, David G McLaren, Anne-Marie Cumiskey, Beth Ann Murphy, Ying Chen, Stephen Previs, Steven Stout, Rajesh Patel, Santhosh Satapati and 7 more

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
2.1field-weighted citation impact, top 12% 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

11 citing papers in PubMed, 21 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Review
  5. Review
  6. Review
  7. Glucagon Receptor Signaling and Glucagon Resistance.International journal of molecular sciences · 2019
    Review
  8. Article
  9. Article
  10. Article
  11. 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

17 authors at 1 institution in 1 country.

Vijay R MoreCardiometabolic Diseases Biology- Discovery, Merck & Co., Inc., Kenilworth, NJ, United States of America.ORCID http://orcid.org/0000-0002-0605-745X
Julie LaoCardiometabolic Diseases Biology- Discovery, Merck & Co., Inc., Kenilworth, NJ, United States of America.
David G McLarenIn Vitro Pharmacology, Merck & Co., Inc., Kenilworth, NJ, United States of America.
Anne-Marie CumiskeyIn-Vivo Pharmacology, Merck & Co., Inc., Kenilworth, NJ, United States of America.
Beth Ann MurphyIn-Vivo Pharmacology, Merck & Co., Inc., Kenilworth, NJ, United States of America.
Ying ChenCardiometabolic Diseases Biology- Discovery, Merck & Co., Inc., Kenilworth, NJ, United States of America.
Stephen PrevisCardiometabolic Diseases Biology- Discovery, Merck & Co., Inc., Kenilworth, NJ, United States of America.
Steven StoutIn Vitro Pharmacology, Merck & Co., Inc., Kenilworth, NJ, United States of America.
Rajesh PatelCardiometabolic Diseases Biology- Discovery, Merck & Co., Inc., Kenilworth, NJ, United States of America.
Santhosh SatapatiCardiometabolic Diseases Biology- Discovery, Merck & Co., Inc., Kenilworth, NJ, United States of America.
Wenyu LiCardiometabolic Diseases Biology- Discovery, Merck & Co., Inc., Kenilworth, NJ, United States of America.
Edward KowalikIn Vitro Pharmacology, Merck & Co., Inc., Kenilworth, NJ, United States of America.
Daphne SzetoIn-Vivo Pharmacology, Merck & Co., Inc., Kenilworth, NJ, United States of America.
Andrea NawrockiIn-Vivo Pharmacology, Merck & Co., Inc., Kenilworth, NJ, United States of America.
Alessandro PocaiCardiometabolic Diseases Biology- Discovery, Merck & Co., Inc., Kenilworth, NJ, United States of America.
Liangsu WangCardiometabolic Diseases Biology- Discovery, Merck & Co., Inc., Kenilworth, NJ, United States of America.
Paul CarringtonCardiometabolic Diseases Biology- Discovery, Merck & Co., Inc., Kenilworth, NJ, United States of America.
Merck & Co., Inc., Rahway, NJ, USA (United States) · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Lipid lowering properties of glucagon have been reported. Blocking glucagon signaling leads to rise in plasma LDL levels. Here, we demonstrate the lipid lowering effects of acute dosing with Glp1r/Gcgr dual agonist (DualAG). All the experiments were performed in 25 week-old male diet-induced (60% kCal fat) obese mice. After 2 hrs of fasting, mice were injected subcutaneously with vehicle, liraglutide (25nmol/kg) and DualAG (25nmol/kg). De novo cholesterol and palmitate synthesis was measured by deuterium incorporation method using D2O. 13C18-oleate infusion was used for measuring fatty acid esterification. Simultaneous activation of Glp1r and Gcgr resulted in decrease in plasma triglyceride and cholesterol levels. DualAG enhanced hepatic LDLr protein levels, along with causing decrease in content of plasma ApoB48 and ApoB100. VLDL secretion, de novo palmitate synthesis and fatty acid esterification decreased with acute DualAG treatment. On the other hand, ketone levels were elevated with DualAG treatment, indicating increased fatty acid oxidation. Lipid relevant changes were absent in liraglutide treated group. In an acute treatment, DualAG demonstrated significant impact on lipid homeostasis, specifically on hepatic uptake, VLDL secretion and de novo synthesis. These effects collectively reveal that lipid lowering abilities of DualAG are primarily through glucagon signaling and are liver centric.

Indexed as

Lipid MetabolismLipogenesisAnimalsCholesterolGlucagonGlucagon-Like Peptide ReceptorsLiverMaleMiceMice, Inbred C57BLTriglyceridesCholesterolGlucagonGlucagon-Like Peptide ReceptorsTriglycerides

Identifiers

PMID29065174
PMCPMC5655430
OpenAlexW2766392360

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.