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Ghrelin, via corticotropin‐releasing factor receptors, reduces glucose uptake and increases lipid content in mouse myoblasts cells

Ghrelin and the corticotropin‐releasing factor (CRF) family are known regulators of cellular metabolism and energy balance. We previously demonstrated that myoblast glucose metabolism is regulated by ghrelin and that this effect is mediated by CRF receptor type 2 (CRF‐R2). Here we explored the effec...

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Autores principales: Elbaz, Michal, Gershon, Eran
Formato: Online Artículo Texto
Lenguaje:English
Publicado: John Wiley and Sons Inc. 2021
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7814488/
https://www.ncbi.nlm.nih.gov/pubmed/33463908
http://dx.doi.org/10.14814/phy2.14654
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author Elbaz, Michal
Gershon, Eran
author_facet Elbaz, Michal
Gershon, Eran
author_sort Elbaz, Michal
collection PubMed
description Ghrelin and the corticotropin‐releasing factor (CRF) family are known regulators of cellular metabolism and energy balance. We previously demonstrated that myoblast glucose metabolism is regulated by ghrelin and that this effect is mediated by CRF receptor type 2 (CRF‐R2). Here we explored the effect of des‐acyl ghrelin, the major circulating isoform of ghrelin, on cellular metabolism in mouse myoblast C2C12 cells, and examined whether CRF family receptors mediate its metabolic effects in muscle cells. C2C12 cells were exposed to des‐acyl ghrelin with or without the CRF‐R1‐ and CRF‐R2‐specific antagonists antalarmin or antisauvagine‐30, respectively. Des‐acyl ghrelin reduced glucose uptake and expression of the glucose transporter GLUT4, but induced retinol‐binding protein 4 (RBP4) expression. Antalarmin and antisauvagine‐30 inhibited the induction of glucose uptake by des‐acyl ghrelin and its effect on GLUT4 and RBP4 expression. Moreover, treating C2C12 cells with des‐acyl ghrelin resulted in cAMP activation in response to the CRF‐R1‐specific ligand stressin, and the CRF‐R2‐specific ligand Ucn3. Furthermore, des‐acyl ghrelin reduced the expression of uncoupling proteins UCP2 and UCP3. Adding antalarmin or antisauvagine‐30 to the medium reversed this effect. Finally, des‐acyl ghrelin elevated lipid content and acetyl‐CoA carboxylase expression in C2C12 cells. Our results suggest that during food deprivation, des‐acyl ghrelin signals the muscle cells that glucose levels are low and that they should switch to fatty acids for their metabolic fuel.
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spelling pubmed-78144882021-01-26 Ghrelin, via corticotropin‐releasing factor receptors, reduces glucose uptake and increases lipid content in mouse myoblasts cells Elbaz, Michal Gershon, Eran Physiol Rep Original Research Ghrelin and the corticotropin‐releasing factor (CRF) family are known regulators of cellular metabolism and energy balance. We previously demonstrated that myoblast glucose metabolism is regulated by ghrelin and that this effect is mediated by CRF receptor type 2 (CRF‐R2). Here we explored the effect of des‐acyl ghrelin, the major circulating isoform of ghrelin, on cellular metabolism in mouse myoblast C2C12 cells, and examined whether CRF family receptors mediate its metabolic effects in muscle cells. C2C12 cells were exposed to des‐acyl ghrelin with or without the CRF‐R1‐ and CRF‐R2‐specific antagonists antalarmin or antisauvagine‐30, respectively. Des‐acyl ghrelin reduced glucose uptake and expression of the glucose transporter GLUT4, but induced retinol‐binding protein 4 (RBP4) expression. Antalarmin and antisauvagine‐30 inhibited the induction of glucose uptake by des‐acyl ghrelin and its effect on GLUT4 and RBP4 expression. Moreover, treating C2C12 cells with des‐acyl ghrelin resulted in cAMP activation in response to the CRF‐R1‐specific ligand stressin, and the CRF‐R2‐specific ligand Ucn3. Furthermore, des‐acyl ghrelin reduced the expression of uncoupling proteins UCP2 and UCP3. Adding antalarmin or antisauvagine‐30 to the medium reversed this effect. Finally, des‐acyl ghrelin elevated lipid content and acetyl‐CoA carboxylase expression in C2C12 cells. Our results suggest that during food deprivation, des‐acyl ghrelin signals the muscle cells that glucose levels are low and that they should switch to fatty acids for their metabolic fuel. John Wiley and Sons Inc. 2021-01-19 /pmc/articles/PMC7814488/ /pubmed/33463908 http://dx.doi.org/10.14814/phy2.14654 Text en © 2021 The Authors. Physiological Reports published by Wiley Periodicals LLC on behalf of The Physiological Society and the American Physiological Society This is an open access article under the terms of the http://creativecommons.org/licenses/by/4.0/ License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited.
spellingShingle Original Research
Elbaz, Michal
Gershon, Eran
Ghrelin, via corticotropin‐releasing factor receptors, reduces glucose uptake and increases lipid content in mouse myoblasts cells
title Ghrelin, via corticotropin‐releasing factor receptors, reduces glucose uptake and increases lipid content in mouse myoblasts cells
title_full Ghrelin, via corticotropin‐releasing factor receptors, reduces glucose uptake and increases lipid content in mouse myoblasts cells
title_fullStr Ghrelin, via corticotropin‐releasing factor receptors, reduces glucose uptake and increases lipid content in mouse myoblasts cells
title_full_unstemmed Ghrelin, via corticotropin‐releasing factor receptors, reduces glucose uptake and increases lipid content in mouse myoblasts cells
title_short Ghrelin, via corticotropin‐releasing factor receptors, reduces glucose uptake and increases lipid content in mouse myoblasts cells
title_sort ghrelin, via corticotropin‐releasing factor receptors, reduces glucose uptake and increases lipid content in mouse myoblasts cells
topic Original Research
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7814488/
https://www.ncbi.nlm.nih.gov/pubmed/33463908
http://dx.doi.org/10.14814/phy2.14654
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