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פותח על ידי קלירמאש פתרונות בע"מ -
CRF type 2 receptors mediate the metabolic effects of ghrelin in C2C12 cells
Year:
2014
Source of publication :
obesity (source)
Authors :
גרשון, ערן
;
.
Volume :
22
Co-Authors:
Gershon, E., Clayton Foundation Laboratories for Peptide Biology, Salk Institute for Biological Studies, North Torrey Pines Road, San Diego 10010 ,CA, United States, Department of Ruminant Science, Volcani Center, Bet Dagan, Israel
Vale, W.W., Clayton Foundation Laboratories for Peptide Biology, Salk Institute for Biological Studies, North Torrey Pines Road, San Diego 10010 ,CA, United States
Facilitators :
From page:
380
To page:
389
(
Total pages:
10
)
Abstract:
Objective Ghrelin is known to regulate appetite control and cellular metabolism. The corticotropin-releasing factor (CRF) family is also known to regulate energy balance. In this study, the links between ghrelin and the CRF family in C2C12 cells, a mouse myoblast cell line was investigated. Design and Methods C2C12 cells were treated with ghrelin in the presence or absence of CRF receptor antagonists and then subjected to different metabolic analyses. Results Ghrelin enhanced glucose uptake by C2C12 cells, induced GLUT4 translocation to the cell surface and decreased RBP4 expression. A CRF-R2 selective antagonist, anti-sauvagine-30, blocked ghrelin-induced glucose uptake, Ghrelin upregulated CRF-R2 but not CRF-R1 levels. Moreover, ghrelin-treated C2C12 cells displayed a cAMP and pERK activation in response to Ucn3, a CRF-R2 specific ligand, but not in response to CRF or stressin, CRF-R1 specific ligands. Ghrelin also induced UCP2 and UCP3 expression, which were blocked by anti- sauvagine-30. Ghrelin did not induce fatty acids uptake by C2C12 cells or ACC expression. Even though C2C12 cells clearly exhibited responses to ghrelin, the known ghrelin receptor, GHSR1a, was not detectable in C2C12 cells. Conclusion The results suggest that, ghrelin plays a role in regulating muscle glucose and, raise the possibility that suppression of the CRF-R2 pathway might provide benefits in high ghrelin states. © 2013 The Obesity Society.
Note:
Related Files :
Animals
cell membrane
Ghrelin
mice
Pyrroles
Retinol-Binding Proteins, Plasma
Urocortins
עוד תגיות
תוכן קשור
More details
DOI :
10.1002/oby.20535
Article number:
Affiliations:
Database:
סקופוס
Publication Type:
מאמר
;
.
Language:
אנגלית
Editors' remarks:
ID:
18399
Last updated date:
02/03/2022 17:27
Creation date:
16/04/2018 23:21
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Scientific Publication
CRF type 2 receptors mediate the metabolic effects of ghrelin in C2C12 cells
22
Gershon, E., Clayton Foundation Laboratories for Peptide Biology, Salk Institute for Biological Studies, North Torrey Pines Road, San Diego 10010 ,CA, United States, Department of Ruminant Science, Volcani Center, Bet Dagan, Israel
Vale, W.W., Clayton Foundation Laboratories for Peptide Biology, Salk Institute for Biological Studies, North Torrey Pines Road, San Diego 10010 ,CA, United States
CRF type 2 receptors mediate the metabolic effects of ghrelin in C2C12 cells
Objective Ghrelin is known to regulate appetite control and cellular metabolism. The corticotropin-releasing factor (CRF) family is also known to regulate energy balance. In this study, the links between ghrelin and the CRF family in C2C12 cells, a mouse myoblast cell line was investigated. Design and Methods C2C12 cells were treated with ghrelin in the presence or absence of CRF receptor antagonists and then subjected to different metabolic analyses. Results Ghrelin enhanced glucose uptake by C2C12 cells, induced GLUT4 translocation to the cell surface and decreased RBP4 expression. A CRF-R2 selective antagonist, anti-sauvagine-30, blocked ghrelin-induced glucose uptake, Ghrelin upregulated CRF-R2 but not CRF-R1 levels. Moreover, ghrelin-treated C2C12 cells displayed a cAMP and pERK activation in response to Ucn3, a CRF-R2 specific ligand, but not in response to CRF or stressin, CRF-R1 specific ligands. Ghrelin also induced UCP2 and UCP3 expression, which were blocked by anti- sauvagine-30. Ghrelin did not induce fatty acids uptake by C2C12 cells or ACC expression. Even though C2C12 cells clearly exhibited responses to ghrelin, the known ghrelin receptor, GHSR1a, was not detectable in C2C12 cells. Conclusion The results suggest that, ghrelin plays a role in regulating muscle glucose and, raise the possibility that suppression of the CRF-R2 pathway might provide benefits in high ghrelin states. © 2013 The Obesity Society.
Scientific Publication
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