Evidence map›Paper›PMID 21177288›Full record

ArticleAmerican journal of physiology. Endocrinology and metabolism2011

Glucagon-like peptide-2-stimulated protein synthesis through the PI 3-kinase-dependent Akt-mTOR signaling pathway.

Xuemei Shi, Xiaojie Li, Yi Wang, Keying Zhang, Fuguo Zhou, Lawrence Chan, Defa Li, Xinfu Guan

Open access · greenAbstract read
In one paragraph

Article in American journal of physiology. Endocrinology and metabolism, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
1.3field-weighted citation impact, top 19% 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

11 citing papers in PubMed, 26 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Article
  5. Article
  6. Article
  7. The CNS glucagon-like peptide-2 receptor in the control of energy balance and glucose homeostasis.American journal of physiology. Regulatory, integrative and comparative physiology · 2014
    Review
  8. Article
  9. Article
  10. Review
  11. 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

8 authors at 3 institutions in 2 countries.

Xuemei ShiUSDA/ARS Children's Nutrition Research Center, Dept. of Pediatrics, Baylor College of Medicine, 1100 Bates St., Houston, TX 77030, USA.
Xiaojie Li
Yi Wang
Keying Zhang
Fuguo Zhou
Lawrence Chan
Defa Li
Xinfu Guan
United States Department of Agriculture · USChina Agricultural University · CNBaylor College of Medicine · US

Funding

MODELS FOR ATHEROSCLEROSIS RESEARCHR01HL051586 · NHLBI · BAYLOR COLLEGE OF MEDICINE · PI CHAN, LAWRENCE · 1994 to 2014
$5.5M
Physiological role of GLP-2 receptor in the mouse intestinal growth and functionK01DK075489 · NIDDK · BAYLOR COLLEGE OF MEDICINE · PI GUAN, XINFU · 2006 to 2009
$562k
Physiological Role of CNS GLP-2 Receptor in Energy HomeostasisR03DK084125 · NIDDK · BAYLOR COLLEGE OF MEDICINE · PI GUAN, XINFU · 2009 to 2010
$136k
NHLBI NIH HHS R01 HL051586NIDDK NIH HHS DK-075489NIDDK NIH HHS DK-084125NIDDK NIH HHS K01 DK075489NIDDK NIH HHS R03 DK084125
6 · The paper itself

Abstract

Glucagon-like peptide-2 (GLP-2) is a nutrient-responsive neuropeptide that exerts diverse actions in the gastrointestinal tract, including enhancing mucosal cell survival and proliferation. GLP-2 stimulates mucosal growth in vivo with an increased rate of protein synthesis. However, it was unclear whether GLP-2 can directly stimulate protein synthesis. The objective was to test critically whether GLP-2 receptor (GLP-2R) activation directly stimulates protein synthesis through a PI 3-kinase-dependent Akt-mTOR signaling pathway. HEK 293 cells (transfected with human GLP-2R cDNA) were treated with human GLP-2 with/without pretreatment of PI 3-kinase inhibitor (LY-294002) or mTOR inhibitor (rapamycin). Results show that 1) GLP-2 specifically bound to GLP-2R overexpressed in the HEK cells with K(a) = 0.22 nM and B(max) = 321 fmol/μg protein; 2) GLP-2-stimulated protein synthesis was dependent on the amount of GLP-2R cDNA and the dosage of GLP-2 and reached the plateau among 0.2-2 nM GLP-2; 3) GLP-2-stimulated protein synthesis was abolished by the PI 3-kinase inhibitor and mTOR inhibitor; and 4) GLP-2-mediated stimulation of phosphorylation on Akt and mTOR was dependent on the amount of GLP-2R cDNA transfected and the dosage of GLP-2. In addition, GLP-2-mediated action and signaling in regulation of protein synthesis were confirmed in mouse hippocampal neurons (expressing native GLP-2R). GLP-2 directly stimulated protein synthesis of primary cultured neurons in dosage-dependent, PI 3-kinase-dependent, and rapamycin-sensitive manners, which linked with activation of Akt-mTOR signaling pathway as well. We conclude that GLP-2R activation directly stimulates protein synthesis by activating the PI 3-kinase-dependent Akt-mTOR signaling pathway. GLP-2-stimulated protein synthesis may be physiologically relevant to maintaining neuronal long-term potentiation and providing secondary mediators (namely neuropeptides or growth factors).

Indexed as

AnimalsAnimals, NewbornBlotting, WesternCell ProliferationCells, CulturedDNA, ComplementaryGlucagon-Like Peptide 2HEK293 CellsHippocampusHumansImmunohistochemistryMiceNeuronsOncogene Protein v-aktPhosphatidylinositol 3-KinasesRibosomesDNA, ComplementaryGlucagon-Like Peptide 2mTOR protein, mouseOncogene Protein v-aktPhosphatidylinositol 3-KinasesTOR Serine-Threonine Kinases

Identifiers

PMID21177288
PMCPMC3279303
OpenAlexW2130080167

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.