Evidence map›Paper›PMID 29506910›Full record

ArticleMolecular metabolism2018

GPR142 prompts glucagon-like Peptide-1 release from islets to improve β cell function.

Hua V Lin, Jingru Wang, Jie Wang, Weiji Li, Xuesong Wang, James T Alston, Melissa K Thomas, Daniel A Briere, Samreen K Syed, Alexander M Efanov

Open access · goldAbstract read
In one paragraph

Article in Molecular metabolism, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
5.4field-weighted citation impact, top 4% 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

18 citing papers in PubMed, 34 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Review
  5. Article
  6. Review
  7. Article
  8. Article
  9. Review
  10. Article
  11. Review
  12. Review
  13. Review
  14. Review
  15. Glucagon-like peptide 1 (GLP-1).Molecular metabolism · 2019 · on this map
    Review
  16. Article
  17. Article
  18. 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

10 authors at 2 institutions in 2 countries.

Hua V LinLilly Research Laboratories, Lilly Corporate Center, Indianapolis, IN, USA. Electronic address: lin_hua@lilly.com.
Jingru WangLilly China Research and Development Center, Shanghai, China.
Jie WangLilly China Research and Development Center, Shanghai, China.
Weiji LiLilly China Research and Development Center, Shanghai, China.
Xuesong WangLilly China Research and Development Center, Shanghai, China.
James T AlstonLilly Research Laboratories, Lilly Corporate Center, Indianapolis, IN, USA.
Melissa K ThomasLilly Research Laboratories, Lilly Corporate Center, Indianapolis, IN, USA.
Daniel A BriereLilly Research Laboratories, Lilly Corporate Center, Indianapolis, IN, USA.
Samreen K SyedLilly Research Laboratories, Lilly Corporate Center, Indianapolis, IN, USA.
Alexander M EfanovLilly Research Laboratories, Lilly Corporate Center, Indianapolis, IN, USA.
Eli Lilly (United States) · USLilly (China) · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

objectiveGPR142 agonists are being pursued as novel diabetes therapies by virtue of their insulin secretagogue effects. But it is undetermined whether GPR142's functions in pancreatic islets are limited to regulating insulin secretion. The current study expands research on its action. METHODS AND

resultsWe demonstrated by in situ hybridization and immunostaining that GPR142 is expressed not only in β cells but also in a subset of α cells. Stimulation of GPR142 by a selective agonist increased glucagon secretion in both human and mouse islets. More importantly, the GPR142 agonist also potentiated glucagon-like peptide-1 (GLP-1) production and its release from islets through a mechanism that involves upregulation of prohormone convertase 1/3 expression. Strikingly, stimulation of insulin secretion and increase in insulin content via GPR142 engagement requires intact GLP-1 receptor signaling. Furthermore, GPR142 agonist increased β cell proliferation and protected both mouse and human islets against stress-induced apoptosis.

conclusionsCollectively, we provide here evidence that local GLP-1 release from α cells defines GPR142's beneficial effects on improving β cell function and mass, and we propose that GPR142 agonism may have translatable and durable efficacy for the treatment of type 2 diabetes.

Indexed as

AnimalsApoptosisCell ProliferationCells, CulturedGlucagon-Like Peptide 1Glucagon-Like Peptide-1 ReceptorGlucagon-Secreting CellsHumansInsulin-Secreting CellsInsulin SecretionMaleMiceMice, Inbred C57BLProprotein Convertase 1Receptors, G-Protein-CoupledGlucagon-Like Peptide 1Glucagon-Like Peptide-1 ReceptorGPR142 protein, mouseProprotein Convertase 1Receptors, G-Protein-CoupledGPR142Intra-islet GLP-1PC1/3α cell

Identifiers

PMID29506910
PMCPMC6001353
OpenAlexW2792229274

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.