Stimulation of fat oxidation in rat muscle by unacylated ghrelin persists for 2–3 hours, but is independent of fatty acid transporter translocation

Abstract While a definitive mechanism‐of‐action remains to be identified, recent findings indicate that ghrelin, particularly the unacylated form (UnAG), stimulates skeletal muscle fatty acid oxidation. The biological importance of UnAG‐mediated increases in fat oxidation remains unclear, as UnAG pe...

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Main Authors: Evan M. Hoecht, Joshua M. Budd, Nicole M. Notaro, Graham P. Holloway, David J. Dyck
Format: Article
Language:English
Published: Wiley 2023-09-01
Series:Physiological Reports
Subjects:
Online Access:https://doi.org/10.14814/phy2.15815
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author Evan M. Hoecht
Joshua M. Budd
Nicole M. Notaro
Graham P. Holloway
David J. Dyck
author_facet Evan M. Hoecht
Joshua M. Budd
Nicole M. Notaro
Graham P. Holloway
David J. Dyck
author_sort Evan M. Hoecht
collection DOAJ
description Abstract While a definitive mechanism‐of‐action remains to be identified, recent findings indicate that ghrelin, particularly the unacylated form (UnAG), stimulates skeletal muscle fatty acid oxidation. The biological importance of UnAG‐mediated increases in fat oxidation remains unclear, as UnAG peaks in the circulation before mealtimes, and decreases rapidly during the postprandial situation before increases in postabsorptive circulating lipids. Therefore, we aimed to determine if the UnAG‐mediated stimulation of fat oxidation would persist long enough to affect the oxidation of meal‐derived fatty acids, and if UnAG stimulated the translocation of fatty acid transporters to the sarcolemma as a mechanism‐of‐action. In isolated soleus muscle strips from male rats, short‐term pre‐treatment with UnAG elicited a persisting stimulus on fatty acid oxidation 2 h after the removal of UnAG. UnAG also caused an immediate phosphorylation of AMPK, but not an increase in plasma membrane FAT/CD36 or FABPpm. There was also no increase in AMPK signaling or increased FAT/CD36 or FABPpm content at the plasma membrane at 2 h which might explain the sustained increase in fatty acid oxidation. These findings confirm UnAG as a stimulator of fatty acid oxidation and provide evidence that UnAG may influence the handling of postprandial lipids. The underlying mechanisms are not known.
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spelling doaj.art-98a4d608b1fa46beb85233141b8f97f02023-12-11T04:25:44ZengWileyPhysiological Reports2051-817X2023-09-011118n/an/a10.14814/phy2.15815Stimulation of fat oxidation in rat muscle by unacylated ghrelin persists for 2–3 hours, but is independent of fatty acid transporter translocationEvan M. Hoecht0Joshua M. Budd1Nicole M. Notaro2Graham P. Holloway3David J. Dyck4Department of Human Health and Nutritional Sciences University of Guelph Guelph Ontario CanadaDepartment of Human Health and Nutritional Sciences University of Guelph Guelph Ontario CanadaDepartment of Human Health and Nutritional Sciences University of Guelph Guelph Ontario CanadaDepartment of Human Health and Nutritional Sciences University of Guelph Guelph Ontario CanadaDepartment of Human Health and Nutritional Sciences University of Guelph Guelph Ontario CanadaAbstract While a definitive mechanism‐of‐action remains to be identified, recent findings indicate that ghrelin, particularly the unacylated form (UnAG), stimulates skeletal muscle fatty acid oxidation. The biological importance of UnAG‐mediated increases in fat oxidation remains unclear, as UnAG peaks in the circulation before mealtimes, and decreases rapidly during the postprandial situation before increases in postabsorptive circulating lipids. Therefore, we aimed to determine if the UnAG‐mediated stimulation of fat oxidation would persist long enough to affect the oxidation of meal‐derived fatty acids, and if UnAG stimulated the translocation of fatty acid transporters to the sarcolemma as a mechanism‐of‐action. In isolated soleus muscle strips from male rats, short‐term pre‐treatment with UnAG elicited a persisting stimulus on fatty acid oxidation 2 h after the removal of UnAG. UnAG also caused an immediate phosphorylation of AMPK, but not an increase in plasma membrane FAT/CD36 or FABPpm. There was also no increase in AMPK signaling or increased FAT/CD36 or FABPpm content at the plasma membrane at 2 h which might explain the sustained increase in fatty acid oxidation. These findings confirm UnAG as a stimulator of fatty acid oxidation and provide evidence that UnAG may influence the handling of postprandial lipids. The underlying mechanisms are not known.https://doi.org/10.14814/phy2.15815FABPpmFAT/CD36fatty acid oxidationskeletal muscleunacylated ghrelin
spellingShingle Evan M. Hoecht
Joshua M. Budd
Nicole M. Notaro
Graham P. Holloway
David J. Dyck
Stimulation of fat oxidation in rat muscle by unacylated ghrelin persists for 2–3 hours, but is independent of fatty acid transporter translocation
Physiological Reports
FABPpm
FAT/CD36
fatty acid oxidation
skeletal muscle
unacylated ghrelin
title Stimulation of fat oxidation in rat muscle by unacylated ghrelin persists for 2–3 hours, but is independent of fatty acid transporter translocation
title_full Stimulation of fat oxidation in rat muscle by unacylated ghrelin persists for 2–3 hours, but is independent of fatty acid transporter translocation
title_fullStr Stimulation of fat oxidation in rat muscle by unacylated ghrelin persists for 2–3 hours, but is independent of fatty acid transporter translocation
title_full_unstemmed Stimulation of fat oxidation in rat muscle by unacylated ghrelin persists for 2–3 hours, but is independent of fatty acid transporter translocation
title_short Stimulation of fat oxidation in rat muscle by unacylated ghrelin persists for 2–3 hours, but is independent of fatty acid transporter translocation
title_sort stimulation of fat oxidation in rat muscle by unacylated ghrelin persists for 2 3 hours but is independent of fatty acid transporter translocation
topic FABPpm
FAT/CD36
fatty acid oxidation
skeletal muscle
unacylated ghrelin
url https://doi.org/10.14814/phy2.15815
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