Growth hormone secretagogue receptor signalling affects high-fat intake independently of plasma levels of ghrelin and LEAP2, in a 4-day binge eating model.


Journal

Journal of neuroendocrinology
ISSN: 1365-2826
Titre abrégé: J Neuroendocrinol
Pays: United States
ID NLM: 8913461

Informations de publication

Date de publication:
10 2019
Historique:
received: 05 06 2019
revised: 16 08 2019
accepted: 27 08 2019
pubmed: 31 8 2019
medline: 15 12 2020
entrez: 31 8 2019
Statut: ppublish

Résumé

The growth hormone secretagogue receptor (GHSR) is a G protein-coupled receptor that is highly expressed in the central nervous system. GHSR acts as a receptor for ghrelin and for liver-expressed antimicrobial peptide 2 (LEAP2), which blocks ghrelin-evoked activity. GHSR also displays ligand-independent activity, including a high constitutive activity that signals in the absence of ghrelin and is reduced by LEAP2. GHSR activity modulates a variety of food intake-related behaviours, including binge eating. Previously, we reported that GHSR-deficient mice daily and time-limited exposed to a high-fat (HF) diet display an attenuated binge-like HF intake compared to wild-type mice. In the present study, we aimed to determine whether ligand-independent GHSR activity affects binge-like HF intake in a 4-day binge-like eating protocol. We found that plasma levels of ghrelin and LEAP2 were not modified in mice exposed to this binge-like eating protocol. Moreover, systemic administration of ghrelin or LEAP2 did not alter HF intake in our experimental conditions. Interestingly, we found that central administration of LEAP2 or K-(D-1-Nal)-FwLL-NH

Identifiants

pubmed: 31469195
doi: 10.1111/jne.12785
doi:

Substances chimiques

Antimicrobial Cationic Peptides 0
GHRP-6, Lys(3)- 0
Ghrelin 0
Leap2 protein, mouse 0
N-(1-(4-(4-methoxybenzyl)-5-phenethyl-4H-1,2,4-triazol-3-yl)-2-(1H-indol-3-yl)ethyl)-2-aminoacetamide 0
Oligopeptides 0
Receptors, Ghrelin 0
Triazoles 0
Glycine TE7660XO1C

Types de publication

Journal Article Research Support, Non-U.S. Gov't

Langues

eng

Sous-ensembles de citation

IM

Pagination

e12785

Informations de copyright

© 2019 British Society for Neuroendocrinology.

Références

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Auteurs

María Paula Cornejo (MP)

Laboratory of Neurophysiology of the Multidisciplinary Institute of Cell Biology, IMBICE, Argentine Research Council (CONICET) and Scientific Research Commission, Province of Buenos Aires (CIC-PBA), National University of La Plata, La Plata, Argentina.

Daniel Castrogiovanni (D)

Laboratory of Neurophysiology of the Multidisciplinary Institute of Cell Biology, IMBICE, Argentine Research Council (CONICET) and Scientific Research Commission, Province of Buenos Aires (CIC-PBA), National University of La Plata, La Plata, Argentina.

Helgi B Schiöth (HB)

Department of Neuroscience, Functional Pharmacology, Uppsala University, Uppsala, Sweden.
Institute for Translational Medicine and Biotechnology, Sechenov First Moscow State Medical University, Moscow, Russia.

Mirta Reynaldo (M)

Laboratory of Neurophysiology of the Multidisciplinary Institute of Cell Biology, IMBICE, Argentine Research Council (CONICET) and Scientific Research Commission, Province of Buenos Aires (CIC-PBA), National University of La Plata, La Plata, Argentina.

Jacky Marie (J)

Faculté de Pharmacie, Institut des Biomolécules Max Mousseron, UMR 5247 CNRS-Université Montpellier-ENSCM, Montpellier, France.

Jean-Alain Fehrentz (JA)

Faculté de Pharmacie, Institut des Biomolécules Max Mousseron, UMR 5247 CNRS-Université Montpellier-ENSCM, Montpellier, France.

Mario Perello (M)

Laboratory of Neurophysiology of the Multidisciplinary Institute of Cell Biology, IMBICE, Argentine Research Council (CONICET) and Scientific Research Commission, Province of Buenos Aires (CIC-PBA), National University of La Plata, La Plata, Argentina.

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