Evidence map›Paper›PMID 26290108›Full record

ReviewAmerican journal of physiology. Regulatory, integrative and comparative physiology2015

PPG neurons of the lower brain stem and their role in brain GLP-1 receptor activation.

Stefan Trapp, Simon C Cork

Abstract readReview
In one paragraph

Review in American journal of physiology. Regulatory, integrative and comparative physiology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 63 papers.

0numbers the graph read from it
0cells of the map it votes in
63citing papers in PubMed
3.1field-weighted citation impact, top 9% 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

63 citing papers in PubMed, 95 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. The effects of glucagon-like peptide-1 receptor agonists on sympathetic neuron activity.Hypertension research : official journal of the Japanese Society of Hypertension · 2026
    Article
  5. Review
  6. Article
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  9. Review
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  12. The expanding role of semaglutide: beyond glycemic control.Journal of diabetes and metabolic disorders · 2025
    Review
  13. GLP-1 Receptor Agonists and Research to Treat Overeating and Substance Use Disorders.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2025
    Review
  14. Review
  15. Article
  16. Article
  17. Review
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  19. Article
  20. Review

3 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

2 authors at 1 institution in 1 country.

Stefan TrappCentre for Cardiovascular and Metabolic Neuroscience, Department of Neuroscience, Physiology and Pharmacology, University College London, London, United Kingdom s.trapp@ucl.ac.uk.ORCID http://orcid.org/0000-0003-0665-4948
Simon C CorkCentre for Cardiovascular and Metabolic Neuroscience, Department of Neuroscience, Physiology and Pharmacology, University College London, London, United Kingdom.
University College London · GB

Funding

British Heart FoundationDiabetes UK 12/0004529Medical Research Council MR/J013293/1Medical Research Council MR/J013293/2
6 · The paper itself

Abstract

Within the brain, glucagon-like peptide-1 (GLP-1) affects central autonomic neurons, including those controlling the cardiovascular system, thermogenesis, and energy balance. Additionally, GLP-1 influences the mesolimbic reward system to modulate the rewarding properties of palatable food. GLP-1 is produced in the gut and by hindbrain preproglucagon (PPG) neurons, located mainly in the nucleus tractus solitarii (NTS) and medullary intermediate reticular nucleus. Transgenic mice expressing glucagon promoter-driven yellow fluorescent protein revealed that PPG neurons not only project to central autonomic control regions and mesolimbic reward centers, but also strongly innervate spinal autonomic neurons. Therefore, these brain stem PPG neurons could directly modulate sympathetic outflow through their spinal inputs to sympathetic preganglionic neurons. Electrical recordings from PPG neurons in vitro have revealed that they receive synaptic inputs from vagal afferents entering via the solitary tract. Vagal afferents convey satiation to the brain from signals like postprandial gastric distention or activation of peripheral GLP-1 receptors. CCK and leptin, short- and long-term satiety peptides, respectively, increased the electrical activity of PPG neurons, while ghrelin, an orexigenic peptide, had no effect. These findings indicate that satiation is a main driver of PPG neuronal activation. They also show that PPG neurons are in a prime position to respond to both immediate and long-term indicators of energy and feeding status, enabling regulation of both energy balance and general autonomic homeostasis. This review discusses the question of whether PPG neurons, rather than gut-derived GLP-1, are providing the physiological substrate for the effects elicited by central nervous system GLP-1 receptor activation.

Indexed as

AnimalsBrain StemGene Expression RegulationGlucagon-Like Peptide-1 ReceptorNeuronsProglucagonGlucagon-Like Peptide-1 ReceptorProglucagonappetitebrain stemglucagon-like peptide-1hippocampusneuroanatomy

Identifiers

PMID26290108
PMCPMC4666945
OpenAlexW1821594354

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.