Evidence map›Paper›PMID 21885869›Full record

ArticleDiabetes2011

CCK stimulation of GLP-1 neurons involves α1-adrenoceptor-mediated increase in glutamatergic synaptic inputs.

Kazunari Hisadome, Frank Reimann, Fiona M Gribble, Stefan Trapp

Open access · bronzeAbstract read
In one paragraph

Article in Diabetes, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 64 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
64citing papers in PubMed, 1 pooled it
3.2field-weighted citation impact, top 7% 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

64 citing papers in PubMed, 1 synthesis or guideline pooled it, 99 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Review
  4. Review
  5. Article
  6. Review
  7. Review
  8. Article
  9. CCK-sensitive C fibers activate NTS leptin receptor-expressing neurons via NMDA receptors.American journal of physiology. Regulatory, integrative and comparative physiology · 2024
    Article
  10. Article
  11. Review
  12. Glucagon-Like Peptide-1 Receptors in the Gustatory Cortex Influence Food Intake.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2023
    Article
  13. Signaling pathways in obesity: mechanisms and therapeutic interventions.Signal transduction and targeted therapy · 2022
    Review
  14. Review
  15. Review
  16. Review
  17. The Enteroendocrine System in Obesity.Handbook of experimental pharmacology · 2022
    Article
  18. Review
  19. Article
  20. Article

4 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

4 authors at 2 institutions in 2 countries.

Kazunari HisadomeDepartment of Surgery and Cancer, Imperial College London, London, UK.
Frank Reimann
Fiona M Gribble
Stefan Trapp
Imperial College London · GBUniversity of Cambridge · GB

Funding

Medical Research Council G0600717Medical Research Council G0600928Medical Research Council G0600928(79140)Wellcome Trust 084210Wellcome Trust 088357
6 · The paper itself

Abstract

objectiveGlucagon-like peptide 1 (GLP-1) is involved in the central regulation of food intake. It is produced within the brain by preproglucagon (PPG) neurons, which are located primarily within the brain stem. These neurons project widely throughout the brain, including to the appetite centers in the hypothalamus, and are believed to convey signals related to satiety. Previous work demonstrated that they are directly activated by leptin and electrical activity of the afferent vagus. Another satiety hormone, cholecystokinin (CCK), has also been linked to activation of brain stem neurons, suggesting that it might act partially via centrally projecting neurons from the nucleus tractus solitarius (NTS). The aim of this study was to investigate the neuronal circuitry linking CCK to the population of NTS-PPG neurons. RESEARCH DESIGN AND

methodsTransgenic mice expressing yellow fluorescent protein (Venus) under the control of the PPG promoter were used to identify PPG neurons in vitro and to record their electrical and pharmacological profile.

resultsPPG neurons in the NTS were excited by CCK and epinephrine, but not by the melanocortin receptor agonist melanotan II. Both CCK and epinephrine acted to increase glutamatergic transmission to the PPG neurons, and this involved activation of α(1)-adrenergic receptors. Inhibition of adrenergic signaling abolished the excitatory action of CCK.

conclusionsCCK activates NTS-PPG cells by a circuit involving adrenergic and glutamatergic neurons. NTS-PPG neurons integrate a variety of peripheral signals that indicate both long-term energy balance and short-term nutritional and digestional status to produce an output signal to feeding and autonomic circuits.

Indexed as

Excitatory Postsynaptic PotentialsAnimalsCells, CulturedCholecystokininEpinephrineFemaleGenes, ReporterGlucagon-Like Peptide 1In Vitro TechniquesMaleMiceMice, Inbred C57BLMice, TransgenicNeuronsNeurotransmitter AgentsProglucagonCholecystokininEpinephrineGlucagon-Like Peptide 1Neurotransmitter AgentsProglucagonProtein IsoformsReceptors, Adrenergic, alpha-1Receptors, CholecystokininReceptors, GlutamateRNA, Messenger

Identifiers

PMID21885869
PMCPMC3198097
OpenAlexW2170256989

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.