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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...
Autores principales: | , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
John Wiley and Sons Inc.
2021
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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. |
format | Online Article Text |
id | pubmed-7814488 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2021 |
publisher | John Wiley and Sons Inc. |
record_format | MEDLINE/PubMed |
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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