Evidence map›Paper›PMID 21846840›Full record

ArticleThe Journal of pharmacology and experimental therapeutics2011

Umami receptor activation increases duodenal bicarbonate secretion via glucagon-like peptide-2 release in rats.

Joon-Ho Wang, Takuya Inoue, Masaaki Higashiyama, Paul H Guth, Eli Engel, Jonathan D Kaunitz, Yasutada Akiba

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of pharmacology and experimental therapeutics, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers.

0numbers the graph read from it
0cells of the map it votes in
39citing papers in PubMed
6.6field-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

39 citing papers in PubMed, 73 citations in OpenAlex.

  1. 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
  2. Review
  3. Article
  4. Review
  5. Review
  6. Article
  7. Lipopolysaccharides transport during fat absorption in rodent small intestine.American journal of physiology. Gastrointestinal and liver physiology · 2020
    Article
  8. Article
  9. Review
  10. Article
  11. Duodenal chemosensing.Current opinion in gastroenterology · 2018
    Review
  12. Review
  13. Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. Article
  19. Review
  20. Gastroduodenal mucosal defense mechanisms.Current opinion in gastroenterology · 2015
    Review
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

7 authors at 1 institution in 1 country.

Joon-Ho WangDepartment of Medicine, School of Medicine, University of California, Los Angeles, California, USA.
Takuya Inoue
Masaaki Higashiyama
Paul H Guth
Eli Engel
Jonathan D Kaunitz
Yasutada Akiba
University of California, Los Angeles · US

Funding

Duodenal Muscosal Defense MechanismsR01DK054221 · NIDDK · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI KAUNITZ, JONATHAN D. · 1999 to 2016
$4.4M
BLRD VA I01 BX001245NIDDK NIH HHS P30-DK0413NIDDK NIH HHS R01 DK054221NIDDK NIH HHS R01-DK54221
6 · The paper itself

Abstract

Luminal nutrient chemosensing during meal ingestion is mediated by intestinal endocrine cells, which regulate secretion and motility via the release of gut hormones. We have reported that luminal coperfusion of L-Glu and IMP, common condiments providing the umami or proteinaceous taste, synergistically increases duodenal bicarbonate secretion (DBS) possibly via taste receptor heterodimers, taste receptor type 1, member 1 (T1R1)/R3. We hypothesized that glucose-dependent insulinotropic peptide (GIP) or glucagon-like peptide (GLP) is released by duodenal perfusion with L-Glu/IMP. We measured DBS with pH and CO(2) electrodes through a perfused rat duodenal loop in vivo. GIP, exendin (Ex)-4 (GLP-1 receptor agonist), or GLP-2 was intravenously infused (0.01-1 nmol/kg/h). l-Glu (10 mM) and IMP (0.1 mM) were luminally perfused with or without bolus intravenous injection (3 or 30 nmol/kg) of the receptor antagonists Pro(3)GIP, Ex-3(9-39), or GLP-2(3-33). GIP or GLP-2 infusion dose-dependently increased DBS, whereas Ex-4 infusion gradually decreased DBS. Luminal perfusion of l-Glu/IMP increased DBS, with no effect of Pro(3)GIP or Ex-3(9-39), whereas GLP-2(3-33) inhibited L-Glu/IMP-induced DBS. Vasoactive intestinal peptide (VIP)(6-28) intravenously or N(G)-nitro-L-arginine methyl ester coperfusion inhibited the effect of L-Glu/IMP. Perfusion of L-Glu/IMP increased portal venous concentrations of GLP-2, followed by a delayed increase of GLP-1, with no effect on GIP release. GLP-1/2 and T1R1/R3 were expressed in duodenal endocrine-like cells. These results suggest that luminal L-Glu/IMP-induced DBS is mediated via GLP-2 release and receptor activation followed by VIP and nitric oxide release. Because GLP-1 is insulinotropic and GLP-2 is intestinotrophic, umami receptor activation may have additional benefits in glucose metabolism and duodenal mucosal protection and regeneration.

Indexed as

AnimalsBicarbonatesDuodenumExenatideGastric Inhibitory PolypeptideGlucagon-Like Peptide 1Glucagon-Like Peptide-1 ReceptorGlucagon-Like Peptide 2Glutamic AcidInosine MonophosphateMaleNG-Nitroarginine Methyl EsterNitric Oxide SynthasePeptide FragmentsPeptidesProstaglandin-Endoperoxide SynthasesBicarbonatesExenatideexendin 3Gastric Inhibitory Polypeptidegastric inhibitory polypeptide (1-39)gastric inhibitory polypeptide receptorGlp1r protein, ratGlucagon-Like Peptide 1Glucagon-Like Peptide-1 ReceptorGlucagon-Like Peptide 2Glutamic AcidInosine MonophosphateNG-Nitroarginine Methyl EsterNitric Oxide SynthasePeptide FragmentsPeptidespro-glucose-dependent insulinotropic polypeptideProstaglandin-Endoperoxide SynthasesReceptors, Gastrointestinal HormoneReceptors, GlucagonReceptors, G-Protein-CoupledReceptors, MuscarinicReceptors, Vasoactive Intestinal Peptidetaste receptors, type 1Vasoactive Intestinal Peptidevasoactive intestinal peptide (6-28)Venoms

Identifiers

PMID21846840
PMCPMC3199979
OpenAlexW1974667501

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.