Evidence map›Paper›PMID 36323234›Full record

ReviewCell metabolism2022

The past, present, and future physiology and pharmacology of glucagon.

Megan E Capozzi, David A D'Alessio, Jonathan E Campbell

Open access · greenAbstract readReview
In one paragraph

Review in Cell metabolism, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 66 papers.

0numbers the graph read from it
0cells of the map it votes in
66citing papers in PubMed
18.7field-weighted citation impact, top 1% 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

66 citing papers in PubMed, 93 citations in OpenAlex.

  1. Trial
  2. Article
  3. Article
  4. Review
  5. Article
  6. Article
  7. Review
  8. Article
  9. Hypothalamus-liver talks: whispers in the language of metabolism.Reviews in endocrine & metabolic disorders · 2026
    Review
  10. Article
  11. Article
  12. Rationale, design and baseline characteristics of the TRANSCEND-CKD trial of retatrutide in patients with chronic kidney disease.Nephrology, dialysis, transplantation : official publication of the European Dialysis and Transplant Association - European Renal Association · 2026
    Article
  13. Article
  14. Review
  15. Article
  16. Article
  17. Article
  18. Review
  19. Article
  20. Article

6 more citing papers are in PubMed but not listed here.

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

3 authors at 1 institution in 1 country.

Megan E CapozziDuke Molecular Physiology Institute, Duke University Medical Center, Durham, NC 27701, USA.
David A D'AlessioDuke Molecular Physiology Institute, Duke University Medical Center, Durham, NC 27701, USA; Department of Medicine, Endocrinology Division, Duke University Medical Center, Durham, NC 27701, USA.
Jonathan E CampbellDuke Molecular Physiology Institute, Duke University Medical Center, Durham, NC 27701, USA; Department of Medicine, Endocrinology Division, Duke University Medical Center, Durham, NC 27701, USA; Department of Pharmacology and Cancer Biology, Duke University Medical Center, Durham, NC 27701, USA. Electronic address: jonathan.campbell@duke.edu.
Duke Medical Center · US

Funding

ENGINEERED GLUCOSE METABOLISM IN INSULIN-SECRETING CELLSR01DK046492 · NIDDK · UNIVERSITY OF TEXAS SW MED CTR/DALLAS · PI NEWGARD, CHRISTOPHER B · 1993 to 2025
$7.8M
Endocrinology and Metabolism Training ProgramT32DK007012 · NIDDK · DUKE UNIVERSITY · PI DAVID A. D'ALESSIO · 1986 to 2026
$6.8M
Novel metabolic actions of GIPR01DK125353 · NIDDK · DUKE UNIVERSITY · PI CAMPBELL, JONATHAN E, D'ALESSIO, DAVID A. · 2020 to 2024
$2.1M
Mechanisms of insulin secretion mediated by alpha cellsR01DK123075 · NIDDK · DUKE UNIVERSITY · PI CAMPBELL, JONATHAN E · 2019 to 2023
$1.9M
Glucagon and insulin act cooperatively in the regulation of prandial hepatic glycogen metabolismK01DK129417 · NIDDK · UNIVERSITY OF WASHINGTON · PI CAPOZZI, MEGAN · 2021 to 2025
$679k
NIDDK NIH HHS K01 DK129417NIDDK NIH HHS R01 DK046492NIDDK NIH HHS R01 DK123075NIDDK NIH HHS R01 DK125353NIDDK NIH HHS T32 DK007012
6 · The paper itself

Abstract

The evolution of glucagon has seen the transition from an impurity in the preparation of insulin to the development of glucagon receptor agonists for use in type 1 diabetes. In type 2 diabetes, glucagon receptor antagonists have been explored to reduce glycemia thought to be induced by hyperglucagonemia. However, the catabolic actions of glucagon are currently being leveraged to target the rise in obesity that paralleled that of diabetes, bringing the pharmacology of glucagon full circle. During this evolution, the physiological importance of glucagon advanced beyond the control of hepatic glucose production, incorporating critical roles for glucagon to regulate both lipid and amino acid metabolism. Thus, it is unsurprising that the study of glucagon has left several paradoxes that make it difficult to distill this hormone down to a simplified action. Here, we describe the history of glucagon from the past to the present and suggest some direction to the future of this field.

Indexed as

Diabetes Mellitus, Type 2Glucagon-Secreting CellsGlucagonHumansInsulinReceptors, GlucagonGlucagonInsulinReceptors, Glucagondiabetesglucagonglucoseinsulinα cells

Identifiers

PMID36323234
PMCPMC9641554
OpenAlexW4308112307

What OpenQuestion holds

Textmetadata
LicenceTDM
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.