Evidence map›Paper›PMID 29330456›Full record

ArticleNature communications2018

20-HETE promotes glucose-stimulated insulin secretion in an autocrine manner through FFAR1.

Sorin Tunaru, Remy Bonnavion, Isabell Brandenburger, Jens Preussner, Dominique Thomas, Klaus Scholich, Stefan Offermanns

Open access · goldAbstract read
In one paragraph

Article in Nature communications, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 56 papers.

0numbers the graph read from it
0cells of the map it votes in
56citing papers in PubMed
6.1field-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

56 citing papers in PubMed, 92 citations in OpenAlex.

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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

7 authors at 2 institutions in 1 country.

Sorin TunaruMax Planck Institute for Heart and Lung Research, Department of Pharmacology, Ludwigstr. 43, 61231, Bad Nauheim, Germany.
Remy BonnavionMax Planck Institute for Heart and Lung Research, Department of Pharmacology, Ludwigstr. 43, 61231, Bad Nauheim, Germany.
Isabell BrandenburgerMax Planck Institute for Heart and Lung Research, Department of Pharmacology, Ludwigstr. 43, 61231, Bad Nauheim, Germany.
Jens PreussnerECCPS Bioinformatics Facility, Max Planck Institute for Heart and Lung Research, Ludwigstr 43, 61231, Bad Nauheim, Germany.
Dominique ThomasInstitut für Klinische Pharmakologie, Pharmazentrum Frankfurt, ZAFES, Klinikum der Goethe-Universität Frankfurt, 60590 Frankfurt, Germany.
Klaus ScholichInstitut für Klinische Pharmakologie, Pharmazentrum Frankfurt, ZAFES, Klinikum der Goethe-Universität Frankfurt, 60590 Frankfurt, Germany.
Stefan OffermannsMax Planck Institute for Heart and Lung Research, Department of Pharmacology, Ludwigstr. 43, 61231, Bad Nauheim, Germany. stefan.offermanns@mpi-bn.mpg.de.
Max Planck Institute for Heart and Lung Research · DEGoethe University Frankfurt · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The long-chain fatty acid receptor FFAR1 is highly expressed in pancreatic β-cells. Synthetic FFAR1 agonists can be used as antidiabetic drugs to promote glucose-stimulated insulin secretion (GSIS). However, the physiological role of FFAR1 in β-cells remains poorly understood. Here we show that 20-HETE activates FFAR1 and promotes GSIS via FFAR1 with higher potency and efficacy than dietary fatty acids such as palmitic, linoleic, and α-linolenic acid. Murine and human β-cells produce 20-HETE, and the ω-hydroxylase-mediated formation and release of 20-HETE is strongly stimulated by glucose. Pharmacological inhibition of 20-HETE formation and blockade of FFAR1 in islets inhibits GSIS. In islets from type-2 diabetic humans and mice, glucose-stimulated 20-HETE formation and 20-HETE-dependent stimulation of GSIS are strongly reduced. We show that 20-HETE is an FFAR1 agonist, which functions as an autocrine positive feed-forward regulator of GSIS, and that a reduced glucose-induced 20-HETE formation contributes to inefficient GSIS in type-2 diabetes.

Indexed as

AdultAnimalsAutocrine CommunicationCell LineCell Line, TumorCells, CulturedChlorocebus aethiopsCOS CellsDiabetes Mellitus, Type 2FemaleGlucoseHumansHydroxyeicosatetraenoic AcidsInsulinInsulin-Secreting CellsInsulin Secretion20-hydroxy-5,8,11,14-eicosatetraenoic acidFFAR1 protein, humanGlucoseHydroxyeicosatetraenoic AcidsInsulinReceptors, G-Protein-Coupled

Identifiers

PMID29330456
PMCPMC5766607
OpenAlexW2782927392

What Socratic holds

Textmetadata
LicenceCC BY
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 Socratic graph.