Evidence map›Paper›PMID 22535770›Full record

ArticleEndocrinology2012

Intestinotrophic glucagon-like peptide-2 (GLP-2) activates intestinal gene expression and growth factor-dependent pathways independent of the vasoactive intestinal peptide gene in mice.

Bernardo Yusta, Dianne Holland, James A Waschek, Daniel J Drucker

Open access · bronzeAbstract read
In one paragraph

Article in Endocrinology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
1.7field-weighted citation impact, top 17% 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

17 citing papers in PubMed, 39 citations in OpenAlex.

  1. Article
  2. Article
  3. The enteric nervous system.Physiological reviews · 2023
    Review
  4. Article
  5. Article
  6. Review
  7. Article
  8. Review
  9. Article
  10. Article
  11. The Role of Neuropeptides in Mouse Models of Colitis.Journal of molecular neuroscience : MN · 2016
    Review
  12. Article
  13. Article
  14. Review
  15. Review
  16. The gut as a sensory organ.Nature reviews. Gastroenterology & hepatology · 2013
    Article
  17. 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

4 authors at 4 institutions in 2 countries.

Bernardo YustaDepartment of Medicine, Samuel Lunenfeld Research Institute, Mt. Sinai Hospital, University of Toronto, Toronto, Ontario, Canada M5G 1X5.
Dianne Holland
James A Waschek
Daniel J Drucker
Lunenfeld-Tanenbaum Research Institute · CAMount Sinai Hospital · CAUniversity of California, Los Angeles · USUniversity of Toronto · CA

Funding

Canadian Institutes of Health Research MOP-14799
6 · The paper itself

Abstract

The enteroendocrine and enteric nervous systems convey signals through an overlapping network of regulatory peptides that act either as circulating hormones or as localized neurotransmitters within the gastrointestinal tract. Because recent studies invoke an important role for vasoactive intestinal peptide (VIP) as a downstream mediator of glucagon-like peptide-2 (GLP-2) action in the gut, we examined the importance of the VIP-GLP-2 interaction through analysis of Vip(-/-) mice. Unexpectedly, we detected abnormal villous architecture, expansion of the crypt compartment, increased crypt cell proliferation, enhanced Igf1 and Kgf gene expression, and reduced expression of Paneth cell products in the Vip(-/-) small bowel. These abnormalities were not reproduced by antagonizing VIP action in wild-type mice, and VIP administration did not reverse the intestinal phenotype of Vip(-/-) mice. Exogenous administration of GLP-2 induced the expression of ErbB ligands and immediate-early genes to similar levels in Vip(+/+) vs. Vip(-/-) mice. Moreover, GLP-2 significantly increased crypt cell proliferation and small bowel growth to comparable levels in Vip(+/+) vs. Vip(-/-) mice. Unexpectedly, exogenous GLP-2 administration had no therapeutic effect in mice with dextran sulfate-induced colitis; the severity of colonic injury and weight loss was modestly reduced in female but not male Vip(-/-) mice. Taken together, these findings extend our understanding of the complex intestinal phenotype arising from loss of the Vip gene. Furthermore, although VIP action may be important for the antiinflammatory actions of GLP-2, the Vip gene is not required for induction of a gene expression program linked to small bowel growth after enhancement of GLP-2 receptor signaling.

Indexed as

Adenomatous Polyposis Coli ProteinAnimalsBlotting, WesternCell ProliferationColonEnteric Nervous SystemFemaleGene Expression RegulationGlucagon-Like Peptide 2Glucagon-Like Peptide-2 ReceptorInsulin-Like Growth Factor IIntercellular Signaling Peptides and ProteinsIntestinal MucosaIntestinesIntestine, SmallJejunumAdenomatous Polyposis Coli ProteinGlucagon-Like Peptide 2Glucagon-Like Peptide-2 ReceptorInsulin-Like Growth Factor IIntercellular Signaling Peptides and ProteinsReceptors, GlucagonVasoactive Intestinal Peptide

Identifiers

PMID22535770
PMCPMC3359603
OpenAlexW2045081472

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.