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Novel mechanism of impaired metabolism‐secretion coupling in β‐cells: Loss of cytosolic adenosine triphosphate by leakage

Zhang et al. recently proposed a new mechanism of metabolism‐secretion coupling impairment in diabetic β‐cells involving the loss of cytosolic adenosine triphosphate by leakage through plasma membrane. Hyperglycemia increases mistargeting expression of the adenosine triphosphate‐conducting mitochond...

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Detalles Bibliográficos
Autor principal: Fujimoto, Shimpei
Formato: Online Artículo Texto
Lenguaje:English
Publicado: John Wiley and Sons Inc. 2019
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6825920/
https://www.ncbi.nlm.nih.gov/pubmed/31168903
http://dx.doi.org/10.1111/jdi.13094
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author Fujimoto, Shimpei
author_facet Fujimoto, Shimpei
author_sort Fujimoto, Shimpei
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description Zhang et al. recently proposed a new mechanism of metabolism‐secretion coupling impairment in diabetic β‐cells involving the loss of cytosolic adenosine triphosphate by leakage through plasma membrane. Hyperglycemia increases mistargeting expression of the adenosine triphosphate‐conducting mitochondrial outer membrane voltage‐dependent anion channel‐1 on the plasma membrane leading to adenosine triphosphate depletion. The interaction between reactive oxygen species overproduction and voltage‐dependent anion channel‐1 induction is an interesting issue to be resolved.[Image: see text]
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spelling pubmed-68259202019-11-07 Novel mechanism of impaired metabolism‐secretion coupling in β‐cells: Loss of cytosolic adenosine triphosphate by leakage Fujimoto, Shimpei J Diabetes Investig Commentary Zhang et al. recently proposed a new mechanism of metabolism‐secretion coupling impairment in diabetic β‐cells involving the loss of cytosolic adenosine triphosphate by leakage through plasma membrane. Hyperglycemia increases mistargeting expression of the adenosine triphosphate‐conducting mitochondrial outer membrane voltage‐dependent anion channel‐1 on the plasma membrane leading to adenosine triphosphate depletion. The interaction between reactive oxygen species overproduction and voltage‐dependent anion channel‐1 induction is an interesting issue to be resolved.[Image: see text] John Wiley and Sons Inc. 2019-07-02 2019-11 /pmc/articles/PMC6825920/ /pubmed/31168903 http://dx.doi.org/10.1111/jdi.13094 Text en © 2019 The Authors. Journal of Diabetes Investigation published by Asian Association for the Study of Diabetes (AASD) and John Wiley & Sons Australia, Ltd This is an open access article under the terms of the http://creativecommons.org/licenses/by-nc-nd/4.0/ License, which permits use and distribution in any medium, provided the original work is properly cited, the use is non‐commercial and no modifications or adaptations are made.
spellingShingle Commentary
Fujimoto, Shimpei
Novel mechanism of impaired metabolism‐secretion coupling in β‐cells: Loss of cytosolic adenosine triphosphate by leakage
title Novel mechanism of impaired metabolism‐secretion coupling in β‐cells: Loss of cytosolic adenosine triphosphate by leakage
title_full Novel mechanism of impaired metabolism‐secretion coupling in β‐cells: Loss of cytosolic adenosine triphosphate by leakage
title_fullStr Novel mechanism of impaired metabolism‐secretion coupling in β‐cells: Loss of cytosolic adenosine triphosphate by leakage
title_full_unstemmed Novel mechanism of impaired metabolism‐secretion coupling in β‐cells: Loss of cytosolic adenosine triphosphate by leakage
title_short Novel mechanism of impaired metabolism‐secretion coupling in β‐cells: Loss of cytosolic adenosine triphosphate by leakage
title_sort novel mechanism of impaired metabolism‐secretion coupling in β‐cells: loss of cytosolic adenosine triphosphate by leakage
topic Commentary
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6825920/
https://www.ncbi.nlm.nih.gov/pubmed/31168903
http://dx.doi.org/10.1111/jdi.13094
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