Evidence map›Paper›PMID 10575028›Full record

ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience1999

Identification and characterization of glucoresponsive neurons in the enteric nervous system.

M Liu, S Seino, A L Kirchgessner

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 1999. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 46 papers.

0numbers the graph read from it
0cells of the map it votes in
46citing papers in PubMed
8.6field-weighted citation impact, top 2% 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

46 citing papers in PubMed, 149 citations in OpenAlex.

  1. Trial
  2. Article
  3. The Enteric Neuronal Circuitry: A Key Ignored Player in Nutrient Sensing Along the Gut-Brain Axis.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2025
    Review
  4. Article
  5. Review
  6. Neuroimmunometabolism: A New Pathological Nexus Underlying Neurodegenerative Disorders.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2022
    Review
  7. Disorders of the enteric nervous system - a holistic view.Nature reviews. Gastroenterology & hepatology · 2021
    Review
  8. Identification of Patulin fromMolecules (Basel, Switzerland) · 2019
    Article
  9. Review
  10. Article
  11. Glucosensing in the gastrointestinal tract: Impact on glucose metabolism.American journal of physiology. Gastrointestinal and liver physiology · 2016
    Review
  12. Review
  13. Review
  14. Gut chemosensing mechanisms.The Journal of clinical investigation · 2015
    Review
  15. Review
  16. Review
  17. Review
  18. ATP-sensitive K(+) channels in rat colonic epithelium.Pflugers Archiv : European journal of physiology · 2013
    Article
  19. Article
  20. Xenin-25 increases cytosolic free calcium levels and acetylcholine release from a subset of myenteric neurons.American journal of physiology. Gastrointestinal and liver physiology · 2012
    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

3 authors at 3 institutions in 2 countries.

M LiuDepartment of Physiology, State University of New York Health Science Center at Brooklyn, Brooklyn, New York 11203, USA.
S Seino
A L Kirchgessner
Chiba University · JPColumbia University · USState University of New York · US

Funding

ENTERIC INNERVATION AND ITS PANCREATIC PROJECTIONSR01NS027645 · NINDS · SUNY DOWNSTATE MEDICAL CENTER · PI KIRCHGESSNER, ANNETTE LORRAINE · 1989 to 2003
$966k
NINDS NIH HHS NS27645
6 · The paper itself

Abstract

We tested the hypothesis that a subset of enteric neurons is glucoresponsive and expresses ATP-sensitive K(+) (K(ATP)) channels. The immunoreactivities of the inwardly rectifying K(+) channel 6.2 (Kir6.2) and the sulfonylurea receptor (SUR), now renamed SUR1, subunits of pancreatic beta-cell K(ATP) channels, were detected on cholinergic neurons in the guinea pig ileum, many of which were identified as sensory by their costorage of substance P and/or calbindin. Glucoresponsive neurons were distinguished in the myenteric plexus because of the hyperpolarization and decrease in membrane input resistance that were observed in response to removal of extracellular glucose. The effects of no-glucose were reversed on the reintroduction of glucose or by the K(ATP) channel inhibitor tolbutamide. No reversal of the hyperpolarization was observed when D- mannoheptulose, a hexokinase inhibitor, was present on the reintroduction of glucose. Application of the K(ATP) channel opener diazoxide or the ob gene product leptin mimicked the effect of glucose removal in a reversible manner; moreover, hyperpolarizations evoked by either agent were inhibited by tolbutamide. Glucoresponsive neurons displayed leptin receptor immunoreactivity, which was widespread in both enteric plexuses. Superfusion of diazoxide inhibited fast synaptic activity in myenteric neurons, via activation of presynaptic K(ATP) channels. Diazoxide also produced a decrease in colonic motility. These experiments demonstrate for the first time the presence of glucoresponsive neurons in the gut. We propose that the glucose-induced excitation of these neurons be mediated by inhibition of K(ATP) channels. The results support the idea that enteric K(ATP) channels play a role in glucose-evoked reflexes.

Indexed as

Adenosine TriphosphateAnimalsColonDiazoxideElectrophysiologyEnteric Nervous SystemGastrointestinal MotilityGlucoseGuinea PigsLeptinMaleMyenteric PlexusNeuronsPotassium ChannelsSynaptic TransmissionTolbutamideAdenosine TriphosphateDiazoxideGlucoseLeptinPotassium ChannelsTolbutamide

Identifiers

PMID10575028
PMCPMC6782413
OpenAlexW1827038840

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.