Evidence map›Paper›PMID 27026049›Full record

ArticleScientific reports2016

Ghrelin Regulates Glucose and Glutamate Transporters in Hypothalamic Astrocytes.

Esther Fuente-Martín, Cristina García-Cáceres, Pilar Argente-Arizón, Francisca Díaz, Miriam Granado, Alejandra Freire-Regatillo, David Castro-González, María L Ceballos, Laura M Frago, Suzanne L Dickson and 2 more

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 48 papers.

0numbers the graph read from it
0cells of the map it votes in
48citing papers in PubMed
5.6field-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

48 citing papers in PubMed, 91 citations in OpenAlex.

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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

12 authors at 5 institutions in 2 countries.

Esther Fuente-MartínHospital Infantil Universitario Niño Jesús, Department of Endocrinology, Instituto de Investigación La Princesa, University Autónoma of Madrid and Centro de Investigación Biomédica en Red (CIBER) de la Fisiopatología de la Obesidad y Nutrición (CIBEROBN), Instituto de Salud Carlos III, Madrid, Spain.
Cristina García-CáceresHospital Infantil Universitario Niño Jesús, Department of Endocrinology, Instituto de Investigación La Princesa, University Autónoma of Madrid and Centro de Investigación Biomédica en Red (CIBER) de la Fisiopatología de la Obesidad y Nutrición (CIBEROBN), Instituto de Salud Carlos III, Madrid, Spain.
Pilar Argente-ArizónHospital Infantil Universitario Niño Jesús, Department of Endocrinology, Instituto de Investigación La Princesa, University Autónoma of Madrid and Centro de Investigación Biomédica en Red (CIBER) de la Fisiopatología de la Obesidad y Nutrición (CIBEROBN), Instituto de Salud Carlos III, Madrid, Spain.
Francisca DíazHospital Infantil Universitario Niño Jesús, Department of Endocrinology, Instituto de Investigación La Princesa, University Autónoma of Madrid and Centro de Investigación Biomédica en Red (CIBER) de la Fisiopatología de la Obesidad y Nutrición (CIBEROBN), Instituto de Salud Carlos III, Madrid, Spain.
Miriam GranadoHospital Infantil Universitario Niño Jesús, Department of Endocrinology, Instituto de Investigación La Princesa, University Autónoma of Madrid and Centro de Investigación Biomédica en Red (CIBER) de la Fisiopatología de la Obesidad y Nutrición (CIBEROBN), Instituto de Salud Carlos III, Madrid, Spain.
Alejandra Freire-RegatilloHospital Infantil Universitario Niño Jesús, Department of Endocrinology, Instituto de Investigación La Princesa, University Autónoma of Madrid and Centro de Investigación Biomédica en Red (CIBER) de la Fisiopatología de la Obesidad y Nutrición (CIBEROBN), Instituto de Salud Carlos III, Madrid, Spain.
David Castro-GonzálezHospital Infantil Universitario Niño Jesús, Department of Endocrinology, Instituto de Investigación La Princesa, University Autónoma of Madrid and Centro de Investigación Biomédica en Red (CIBER) de la Fisiopatología de la Obesidad y Nutrición (CIBEROBN), Instituto de Salud Carlos III, Madrid, Spain.
María L CeballosInstituto Cajal, Dept. of Cellular, Molecular and Developmental Neurobiology, and CIBERNED, CSIC, Madrid, Spain.
Laura M FragoHospital Infantil Universitario Niño Jesús, Department of Endocrinology, Instituto de Investigación La Princesa, University Autónoma of Madrid and Centro de Investigación Biomédica en Red (CIBER) de la Fisiopatología de la Obesidad y Nutrición (CIBEROBN), Instituto de Salud Carlos III, Madrid, Spain.
Suzanne L DicksonDept. Physiology/Endocrine, The Sahlgrenska Academy at the University of Gothenburg, Gothenburg, Sweden.
Jesús ArgenteHospital Infantil Universitario Niño Jesús, Department of Endocrinology, Instituto de Investigación La Princesa, University Autónoma of Madrid and Centro de Investigación Biomédica en Red (CIBER) de la Fisiopatología de la Obesidad y Nutrición (CIBEROBN), Instituto de Salud Carlos III, Madrid, Spain.
Julie A ChowenHospital Infantil Universitario Niño Jesús, Department of Endocrinology, Instituto de Investigación La Princesa, University Autónoma of Madrid and Centro de Investigación Biomédica en Red (CIBER) de la Fisiopatología de la Obesidad y Nutrición (CIBEROBN), Instituto de Salud Carlos III, Madrid, Spain.
Hospital Infantil Universitario Niño Jesús · ESCentro de Investigación Biomédica en Red · ESInstituto de Salud Carlos III · ESInstituto Cajal · ESUniversity of Gothenburg · SE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Hypothalamic astrocytes can respond to metabolic signals, such as leptin and insulin, to modulate adjacent neuronal circuits and systemic metabolism. Ghrelin regulates appetite, adiposity and glucose metabolism, but little is known regarding the response of astrocytes to this orexigenic hormone. We have used both in vivo and in vitro approaches to demonstrate that acylated ghrelin (acyl-ghrelin) rapidly stimulates glutamate transporter expression and glutamate uptake by astrocytes. Moreover, acyl-ghrelin rapidly reduces glucose transporter (GLUT) 2 levels and glucose uptake by these glial cells. Glutamine synthetase and lactate dehydrogenase decrease, while glycogen phosphorylase and lactate transporters increase in response to acyl-ghrelin, suggesting a change in glutamate and glucose metabolism, as well as glycogen storage by astrocytes. These effects are partially mediated through ghrelin receptor 1A (GHSR-1A) as astrocytes do not respond equally to desacyl-ghrelin, an isoform that does not activate GHSR-1A. Moreover, primary astrocyte cultures from GHSR-1A knock-out mice do not change glutamate transporter or GLUT2 levels in response to acyl-ghrelin. Our results indicate that acyl-ghrelin may mediate part of its metabolic actions through modulation of hypothalamic astrocytes and that this effect could involve astrocyte mediated changes in local glucose and glutamate metabolism that alter the signals/nutrients reaching neighboring neurons.

Indexed as

AnimalsAstrocytesCells, CulturedGhrelinGlucoseGlucose Transporter Type 2Glutamic AcidHypothalamusMaleMice, KnockoutRats, WistarReceptors, GhrelinGhrelinGhsr protein, MouseGlucoseGlucose Transporter Type 2Glutamic AcidReceptors, GhrelinSlc2a2 protein, mouse

Identifiers

PMID27026049
PMCPMC4812252
OpenAlexW2316235633

What OpenQuestion holds

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LicenceCC BY
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Registered trials

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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.