Evidence mapPaperPMID 28218622Full record

ArticleThe Journal of clinical investigation2017

Activation of murine pre-proglucagon-producing neurons reduces food intake and body weight.

Ronald P Gaykema, Brandon A Newmyer, Matteo Ottolini, Vidisha Raje, Daniel M Warthen, Philip S Lambeth, Maria Niccum, Ting Yao, Yiru Huang, Ira G Schulman and 4 more

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of clinical investigation, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 81 papers.

0numbers the graph read from it
0cells of the map it votes in
81citing papers in PubMed
6.0field-weighted citation impact, top 3% 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

81 citing papers in PubMed, 128 citations in OpenAlex.

  1. The critical role of gut-brain signalling in eating behaviour and obesity.Nature reviews. Gastroenterology & hepatology · 2026
    Review
  2. Article
  3. Hypothalamus-liver talks: whispers in the language of metabolism.Reviews in endocrine & metabolic disorders · 2026
    Review
  4. Article
  5. GLP-1 physiology and pharmacology along the gut-brain axis.The Journal of clinical investigation · 2026
    Review
  6. Review
  7. Review
  8. Article
  9. Mechanisms of glucagon-like-peptide 1 in the brain beyond metabolic effects.Annals of pediatric endocrinology & metabolism · 2025
    Article
  10. Review
  11. Novel neural pathways targeted by GLP-1R agonists and bariatric surgery.Pflugers Archiv : European journal of physiology · 2025
    Review
  12. Article
  13. Review
  14. Review
  15. Review
  16. Review
  17. Review
  18. Review
  19. Molecular Ontology of the Nucleus of Solitary Tract.The Journal of comparative neurology · 2024
    Article
  20. Article

21 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

14 authors at 4 institutions in 2 countries.

Ronald P Gaykema
Brandon A Newmyer
Matteo Ottolini
Vidisha Raje
Daniel M Warthen
Philip S Lambeth
Maria Niccum
Ting Yao
Yiru Huang
Ira G Schulman
Thurl E Harris
Manoj K Patel
Kevin W Williams
Michael M Scott
University of Virginia · USThe University of Texas Southwestern Medical Center · USXi'an Jiaotong University · CNZhujiang Hospital · CN

Funding

TRAINING IN THE PHARMACOLOGICAL SCIENCEST32GM007055 · UNIVERSITY OF VIRGINIA CHARLOTTESVILLE · 1985 to 2005
$1.9M
NIDA NIH HHS R00 DA024719NIDDK NIH HHS F32 DK102294NIDDK NIH HHS R01 DK100699NIDDK NIH HHS R01 DK101946NIGMS NIH HHS T32 GM007055NINDS NIH HHS R01 NS075157
6 · The paper itself

Abstract

Peptides derived from pre-proglucagon (GCG peptides) act in both the periphery and the CNS to change food intake, glucose homeostasis, and metabolic rate while playing a role in anxiety behaviors and physiological responses to stress. Although the actions of GCG peptides produced in the gut and pancreas are well described, the role of glutamatergic GGC peptide-secreting hindbrain neurons in regulating metabolic homeostasis has not been investigated. Here, we have shown that chemogenetic stimulation of GCG-producing neurons reduces metabolic rate and food intake in fed and fasted states and suppresses glucose production without an effect on glucose uptake. Stimulation of GCG neurons had no effect on corticosterone secretion, body weight, or conditioned taste aversion. In the diet-induced obese state, the effects of GCG neuronal stimulation on gluconeogenesis were lost, while the food intake-lowering effects remained, resulting in reductions in body weight and adiposity. Our work suggests that GCG peptide-expressing neurons can alter feeding, metabolic rate, and glucose production independent of their effects on hypothalamic pituitary-adrenal (HPA) axis activation, aversive conditioning, or insulin secretion. We conclude that GCG neurons likely stimulate separate populations of downstream cells to produce a change in food intake and glucose homeostasis and that these effects depend on the metabolic state of the animal.

Indexed as

AnimalsBody WeightEatingGluconeogenesisHypothalamo-Hypophyseal SystemMiceMice, TransgenicNeuronsPituitary-Adrenal SystemProglucagonRhombencephalonProglucagon

Identifiers

PMID28218622
PMCPMC5330725
OpenAlexW2588626605

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.