Evidence map›Paper›PMID 22872212›Full record

ArticleDiabetologia2012

Somatostatin receptor 5 and cannabinoid receptor 1 activation inhibit secretion of glucose-dependent insulinotropic polypeptide from intestinal K cells in rodents.

D Hodge, W J Marsh, H E Parker, E Ogunnowo-Bada, C H Riches, A M Habib, M L Evans, F M Gribble, F Reimann

Open access · hybridAbstract read
In one paragraph

Article in Diabetologia, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 44 papers.

0numbers the graph read from it
0cells of the map it votes in
44citing papers in PubMed
4.6field-weighted citation impact, top 5% 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

44 citing papers in PubMed, 85 citations in OpenAlex.

  1. Review
  2. Altered GScience advances · 2026
    Article
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  12. Cellular mechanisms of incretin hormone secretion.Journal of molecular endocrinology · 2024
    Review
  13. Article
  14. Article
  15. Somatostatin Containing δ-Cell Number Is Reduced in Type-2 Diabetes.International journal of molecular sciences · 2023
    Article
  16. Article
  17. Review
  18. Review
  19. Epac-2 ameliorates spontaneous colitis in Il-10Journal of cellular and molecular medicine · 2022
    Article
  20. Targeting the Enteroendocrine System for Treatment of Obesity.Handbook of experimental pharmacology · 2022
    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

9 authors at 2 institutions in 1 country.

D HodgeCambridge Institute for Medical Research, Wellcome Trust/MRC Building, Addenbrooke's Hospital, Box 139, Hills Road, Cambridge CB2 0XY, UK.
W J Marsh
H E Parker
E Ogunnowo-Bada
C H Riches
A M Habib
M L Evans
F M Gribble
F Reimann
Addenbrooke's Hospital · GBWellcome/MRC Cambridge Stem Cell Institute · GB

Funding

Biotechnology and Biological Sciences Research CouncilMedical Research Council G0600717Wellcome TrustWellcome Trust 084210Wellcome Trust 088357
6 · The paper itself

Abstract

aims/hypothesisGlucose-dependent insulinotropic polypeptide (GIP) is an enteroendocrine hormone that promotes storage of glucose and fat. Its secretion from intestinal K cells is triggered by nutrient ingestion and is modulated by intracellular cAMP. In view of the proadipogenic actions of GIP, this study aimed to identify pathways in K cells that lower cAMP levels and GIP secretion.

methodsMurine K cells purified by flow cytometry were analysed for expression of G(αi)-coupled receptors by transcriptomic microarrays. Somatostatin and cannabinoid receptor expression was confirmed by quantitative RT-PCR. Hormone secretion in vitro was measured in GLUTag and primary murine intestinal cultures. cAMP was monitored in GLUTag cells using the genetically encoded sensor Epac2-camps. In vivo tolerance tests were performed in cannulated rats.

resultsPurified murine K cells expressed high mRNA levels for somatostatin receptors (Sstrs) Sstr2, Sstr3 and Sstr5, and cannabinoid receptor type 1 (Cnr1, CB1). Somatostatin inhibited GIP and glucagon-like peptide-1 (GLP-1) secretion from primary small intestinal cultures, in part through SSTR5, and reduced cAMP generation in GLUTag cells. Although the CB1 agonist methanandamide (mAEA) inhibited GIP secretion, no significant effect was observed on GLP-1 secretion from primary cultures. In cannulated rats, treatment with mAEA prior to an oral glucose tolerance test suppressed plasma GIP but not GLP-1 levels, whereas the CB1 antagonist AM251 elevated basal GIP concentrations. CONCLUSIONS/

interpretationGIP release is inhibited by somatostatin and CB1 agonists. The differential effects of CB1 ligands on GIP and GLP-1 release may provide a new tool to dissociate secretion of these incretin hormones and lower GIP but not GLP-1 levels in vivo.

Indexed as

AnimalsColonCyclic AMPEnteroendocrine CellsGastric Inhibitory PolypeptideGlucagon-Like Peptide 1IncretinsIntestine, SmallMaleMiceMice, Inbred C57BLPrimary Cell CultureRatsRats, Sprague-DawleyReceptor, Cannabinoid, CB1Receptors, SomatostatinCNR1 protein, mouseCnr1 protein, ratCyclic AMPGastric Inhibitory PolypeptideGlucagon-Like Peptide 1IncretinsReceptor, Cannabinoid, CB1Receptors, SomatostatinRNA, Messengersomatostatin receptor 3somatostatin receptor 5

Identifiers

PMID22872212
PMCPMC3464380
OpenAlexW1977898912

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
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.