Evidence map›Paper›PMID 34799628›Full record

ArticleScientific reports2021

A glucagon analogue decreases body weight in mice via signalling in the liver.

Charlotte E Hinds, Bryn M Owen, David C D Hope, Philip Pickford, Ben Jones, Tricia M Tan, James S Minnion, Stephen R Bloom

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing 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

12 citing papers in PubMed, 14 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Class B1 GPCRs: insights into multireceptor pharmacology for the treatment of metabolic disease.American journal of physiology. Endocrinology and metabolism · 2024
    Review
  5. Article
  6. Article
  7. Glucagon and Its Receptors in the Mammalian Heart.International journal of molecular sciences · 2023
    Review
  8. Review
  9. Article
  10. Review
  11. Review
  12. 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 1 institution in 1 country.

Charlotte E Hinds *Section of Investigative Medicine, Department of Metabolism, Digestion, and Reproduction, Imperial College London, London, W12 0NN, UK.
Bryn M Owen *Section of Investigative Medicine, Department of Metabolism, Digestion, and Reproduction, Imperial College London, London, W12 0NN, UK.
David C D HopeSection of Investigative Medicine, Department of Metabolism, Digestion, and Reproduction, Imperial College London, London, W12 0NN, UK.
Philip PickfordSection of Investigative Medicine, Department of Metabolism, Digestion, and Reproduction, Imperial College London, London, W12 0NN, UK.
Ben JonesSection of Investigative Medicine, Department of Metabolism, Digestion, and Reproduction, Imperial College London, London, W12 0NN, UK.
Tricia M TanSection of Investigative Medicine, Department of Metabolism, Digestion, and Reproduction, Imperial College London, London, W12 0NN, UK.
James S MinnionSection of Investigative Medicine, Department of Metabolism, Digestion, and Reproduction, Imperial College London, London, W12 0NN, UK.
Stephen R BloomSection of Investigative Medicine, Department of Metabolism, Digestion, and Reproduction, Imperial College London, London, W12 0NN, UK. s.bloom@imperial.ac.uk.
Imperial College London · GB

Funding

Medical Research Council MR/J010731/1Medical Research Council MR/K023667/1Medical Research Council MR/R010676/1Medical Research Council MR/S02171X/1
6 · The paper itself

Abstract

Glucagon receptor agonists show promise as components of next generation metabolic syndrome pharmacotherapies. However, the biology of glucagon action is complex, controversial, and likely context dependent. As such, a better understanding of chronic glucagon receptor (GCGR) agonism is essential to identify and mitigate potential clinical side-effects. Herein we present a novel, long-acting glucagon analogue (GCG104) with high receptor-specificity and potent in vivo action. It has allowed us to make two important observations about the biology of sustained GCGR agonism. First, it causes weight loss in mice by direct receptor signalling at the level of the liver. Second, subtle changes in GCG104-sensitivity, possibly due to interindividual variation, may be sufficient to alter its effects on metabolic parameters. Together, these findings confirm the liver as a principal target for glucagon-mediated weight loss and provide new insights into the biology of glucagon analogues.

Indexed as

AnimalsAnti-Obesity AgentsBiological Variation, PopulationDose-Response Relationship, DrugFemaleGlucagonHEK293 CellsHepatocytesHumansLiverMaleMiceMice, Inbred C57BLMice, KnockoutRatsRats, WistarAnti-Obesity AgentsGlucagonReceptors, Glucagon

Identifiers

PMID34799628
PMCPMC8604983
OpenAlexW3214720893

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.