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- Publisher Website: 10.1080/19382014.2019.1601490
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Article: Palmitate is not an effective fuel for pancreatic islets and amplifies insulin secretion independent of calcium release from endoplasmic reticulum
Title | Palmitate is not an effective fuel for pancreatic islets and amplifies insulin secretion independent of calcium release from endoplasmic reticulum |
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Authors | |
Keywords | calcium cytochrome c endoplasmic reticulum islets L-type calcium channels |
Issue Date | 2019 |
Publisher | Taylor & Francis Inc.. The Journal's web site is located at http://www.tandfonline.com/kisl |
Citation | Islets, 2019, v. 11 n. 3, p. 51-64 How to Cite? |
Abstract | The aim of the study was to determine the acute contribution of fuel oxidation in mediating the increase in insulin secretion rate (ISR) in response to fatty acids. Measures of mitochondrial metabolism, as reflected by oxygen consumption rate (OCR) and cytochrome c reduction, calcium signaling, and ISR by rat islets were used to evaluate processes stimulated by acute exposure to palmitic acid (PA). The contribution of mitochondrial oxidation of PA was determined in the presence and absence of a blocker of mitochondrial transport of fatty acids (etomoxir) at different glucose concentrations. Subsequent to increasing glucose from 3 to 20 mM, PA caused small increases in OCR and cytosolic calcium (about 20% of the effect of glucose). In contrast, the effect of PA on ISR was almost 3 times that by glucose, suggesting that the metabolism of PA is not the dominant mechanism mediating PA’s effect on ISR. This was further supported by lack of inhibition of PA-stimulated OCR and ISR when blocking entry of PA into mitochondria (with etomoxir), and PA’s lack of stimulation of reduced cytochrome c in the presence of high glucose. Consistent with the lack of metabolic stimulation by PA, an inhibitor of calcium release from the endoplasmic reticulum, but not a blocker of L-type calcium channels, abolished the PA-induced elevation of cytosolic calcium. Notably, ISR was unaffected by thapsigargin showing the dissociation of endoplasmic reticulum calcium release and second phase insulin secretion. In conclusion, stimulation of ISR by PA was mediated by mechanisms largely independent of the oxidation of the fuel. © 2019, © 2019 The Author(s). Published with license by Taylor & Francis Group, LLC. |
Persistent Identifier | http://hdl.handle.net/10722/274538 |
ISSN | 2023 Impact Factor: 1.9 2023 SCImago Journal Rankings: 0.612 |
ISI Accession Number ID |
DC Field | Value | Language |
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dc.contributor.author | Kuok, IT | - |
dc.contributor.author | Rountree, AM | - |
dc.contributor.author | Jung, SR | - |
dc.contributor.author | Sweet, IR | - |
dc.date.accessioned | 2019-08-18T15:03:42Z | - |
dc.date.available | 2019-08-18T15:03:42Z | - |
dc.date.issued | 2019 | - |
dc.identifier.citation | Islets, 2019, v. 11 n. 3, p. 51-64 | - |
dc.identifier.issn | 1938-2014 | - |
dc.identifier.uri | http://hdl.handle.net/10722/274538 | - |
dc.description.abstract | The aim of the study was to determine the acute contribution of fuel oxidation in mediating the increase in insulin secretion rate (ISR) in response to fatty acids. Measures of mitochondrial metabolism, as reflected by oxygen consumption rate (OCR) and cytochrome c reduction, calcium signaling, and ISR by rat islets were used to evaluate processes stimulated by acute exposure to palmitic acid (PA). The contribution of mitochondrial oxidation of PA was determined in the presence and absence of a blocker of mitochondrial transport of fatty acids (etomoxir) at different glucose concentrations. Subsequent to increasing glucose from 3 to 20 mM, PA caused small increases in OCR and cytosolic calcium (about 20% of the effect of glucose). In contrast, the effect of PA on ISR was almost 3 times that by glucose, suggesting that the metabolism of PA is not the dominant mechanism mediating PA’s effect on ISR. This was further supported by lack of inhibition of PA-stimulated OCR and ISR when blocking entry of PA into mitochondria (with etomoxir), and PA’s lack of stimulation of reduced cytochrome c in the presence of high glucose. Consistent with the lack of metabolic stimulation by PA, an inhibitor of calcium release from the endoplasmic reticulum, but not a blocker of L-type calcium channels, abolished the PA-induced elevation of cytosolic calcium. Notably, ISR was unaffected by thapsigargin showing the dissociation of endoplasmic reticulum calcium release and second phase insulin secretion. In conclusion, stimulation of ISR by PA was mediated by mechanisms largely independent of the oxidation of the fuel. © 2019, © 2019 The Author(s). Published with license by Taylor & Francis Group, LLC. | - |
dc.language | eng | - |
dc.publisher | Taylor & Francis Inc.. The Journal's web site is located at http://www.tandfonline.com/kisl | - |
dc.relation.ispartof | Islets | - |
dc.rights | AOM/Preprint Before Accepted: his article has been accepted for publication in [JOURNAL TITLE], published by Taylor & Francis. AOM/Preprint After Accepted: This is an [original manuscript / preprint] of an article published by Taylor & Francis in [JOURNAL TITLE] on [date of publication], available online: http://www.tandfonline.com/[Article DOI]. Accepted Manuscript (AM) i.e. Postprint This is an Accepted Manuscript of an article published by Taylor & Francis in [JOURNAL TITLE] on [date of publication], available online: http://www.tandfonline.com/[Article DOI]. | - |
dc.rights | This work is licensed under a Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International License. | - |
dc.subject | calcium | - |
dc.subject | cytochrome c | - |
dc.subject | endoplasmic reticulum | - |
dc.subject | islets | - |
dc.subject | L-type calcium channels | - |
dc.title | Palmitate is not an effective fuel for pancreatic islets and amplifies insulin secretion independent of calcium release from endoplasmic reticulum | - |
dc.type | Article | - |
dc.identifier.email | Kuok, IT: dkuok@hku.hk | - |
dc.description.nature | published_or_final_version | - |
dc.identifier.doi | 10.1080/19382014.2019.1601490 | - |
dc.identifier.pmid | 31084524 | - |
dc.identifier.scopus | eid_2-s2.0-85065791385 | - |
dc.identifier.hkuros | 302099 | - |
dc.identifier.volume | 11 | - |
dc.identifier.issue | 3 | - |
dc.identifier.spage | 51 | - |
dc.identifier.epage | 64 | - |
dc.identifier.isi | WOS:000473791800001 | - |
dc.publisher.place | United States | - |
dc.identifier.issnl | 1938-2022 | - |