Evidence map›Paper›PMID 27829151›Full record

ArticleCell reports2016

A Genetic Screen Identifies Hypothalamic Fgf15 as a Regulator of Glucagon Secretion.

Alexandre Picard, Josselin Soyer, Xavier Berney, David Tarussio, Simon Quenneville, Maxime Jan, Eric Grouzmann, Frédéric Burdet, Mark Ibberson, Bernard Thorens

Open access · goldAbstract read
In one paragraph

Article in Cell reports, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed, 2 pooled it
2.5field-weighted citation impact, top 11% 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

25 citing papers in PubMed, 2 syntheses or guidelines pooled it, 36 citations in OpenAlex.

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  11. Molecular Basis of Bile Acid-FXR-FGF15/19 Signaling Axis.International journal of molecular sciences · 2022
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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 3 institutions in 1 country.

Alexandre PicardCenter for Integrative Genomics, University of Lausanne, 1015 Lausanne, Switzerland.
Josselin SoyerCenter for Integrative Genomics, University of Lausanne, 1015 Lausanne, Switzerland.
Xavier BerneyCenter for Integrative Genomics, University of Lausanne, 1015 Lausanne, Switzerland.
David TarussioCenter for Integrative Genomics, University of Lausanne, 1015 Lausanne, Switzerland.
Simon QuennevilleCenter for Integrative Genomics, University of Lausanne, 1015 Lausanne, Switzerland.
Maxime JanVital-IT, Swiss Institute of Bioinformatics, 1015 Lausanne, Switzerland.
Eric GrouzmannService de Biomédicine, Laboratoire des Catécholamines et Peptides, Centre Hospitalier Universitaire Vaudois CHUV, 1011 Lausanne, Switzerland.
Frédéric BurdetVital-IT, Swiss Institute of Bioinformatics, 1015 Lausanne, Switzerland.
Mark IbbersonVital-IT, Swiss Institute of Bioinformatics, 1015 Lausanne, Switzerland.
Bernard ThorensCenter for Integrative Genomics, University of Lausanne, 1015 Lausanne, Switzerland. Electronic address: bernard.thorens@unil.ch.
University of Lausanne · CHSIB Swiss Institute of Bioinformatics · CHUniversity Hospital of Lausanne · CH

Funding

European Research Council 268946
6 · The paper itself

Abstract

The counterregulatory response to hypoglycemia, which restores normal blood glucose levels to ensure sufficient provision of glucose to the brain, is critical for survival. To discover underlying brain regulatory systems, we performed a genetic screen in recombinant inbred mice for quantitative trait loci (QTL) controlling glucagon secretion in response to neuroglucopenia. We identified a QTL on the distal part of chromosome 7 and combined this genetic information with transcriptomic analysis of hypothalami. This revealed Fgf15 as the strongest candidate to control the glucagon response. Fgf15 was expressed by neurons of the dorsomedial hypothalamus and the perifornical area. Intracerebroventricular injection of FGF19, the human ortholog of Fgf15, reduced activation by neuroglucopenia of dorsal vagal complex neurons, of the parasympathetic nerve, and lowered glucagon secretion. In contrast, silencing Fgf15 in the dorsomedial hypothalamus increased neuroglucopenia-induced glucagon secretion. These data identify hypothalamic Fgf15 as a regulator of glucagon secretion.

Indexed as

Genetic TestingAgingAnimalsChromosomes, MammalianDeoxyglucoseFibroblast Growth FactorsGene SilencingGenomeGlucagonHypothalamusMice, Inbred C57BLParasympathetic Nervous SystemQuantitative Trait LociDeoxyglucosefibroblast growth factor 15, mouseFibroblast Growth FactorsGlucagonautonomic nervous systemdorsal vagal complexFGF15FGF19genetic screenglucagon secretionglucose sensinghypothalamusneuroglucopeniaQTL mapping

Identifiers

PMID27829151
PMCPMC5120348
OpenAlexW2556766149

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.