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Glucose‐stimulated insulin secretion: A newer perspective
Existing concepts and models for glucose‐stimulated insulin secretion (GSIS) are overviewed and a newer perspective has been formulated toward the physiological understanding of GSIS. A conventional model has been created on the basis of in vitro data on application of a square wave high glucose in...
Autores principales: | , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Wiley-Blackwell
2013
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4020243/ https://www.ncbi.nlm.nih.gov/pubmed/24843702 http://dx.doi.org/10.1111/jdi.12094 |
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author | Komatsu, Mitsuhisa Takei, Masahiro Ishii, Hiroaki Sato, Yoshihiko |
author_facet | Komatsu, Mitsuhisa Takei, Masahiro Ishii, Hiroaki Sato, Yoshihiko |
author_sort | Komatsu, Mitsuhisa |
collection | PubMed |
description | Existing concepts and models for glucose‐stimulated insulin secretion (GSIS) are overviewed and a newer perspective has been formulated toward the physiological understanding of GSIS. A conventional model has been created on the basis of in vitro data on application of a square wave high glucose in the absence of any other stimulatory inputs. Glucose elicits rapid insulin release through an adenosine triphosphate‐sensitive K(+) channel (K(ATP) channel)‐dependent mechanism, which is gradually augmented in a K(ATP) channel‐independent manner. Biphasic GSIS thus occurs. In the body, the β‐cells are constantly exposed to stimulatory signals, such as glucagon‐like peptide 1 (GLP‐1), parasympathetic inputs, free fatty acid (FFA), amino acids and slightly suprathreshold levels of glucose, even at fasting. GLP‐1 increases cellular cyclic adenosine monophosphate, parasympathetic stimulation activates protein kinase C, and FFA, amino acids and glucose generate metabolic amplification factors. Plasma glucose concentration gradually rises postprandially under such tonic stimulation. We hypothesize that these stimulatory inputs together make the β‐cells responsive to glucose independently from its action on K(ATP) channels. Robust GSIS in patients with a loss of function mutation of the sulfonylurea receptor, a subunit of K(ATP) channels, is compatible with this hypothesis. Furthermore, pre‐exposure of the islets to an activator of protein kinase A and/or C makes β‐cells responsive to glucose in a K(ATP) channel‐ and Ca(2+)‐independent manner. We hypothesize that GSIS occurs in islet β‐cells without glucose regulation of K(ATP) channels in vivo, for which priming with cyclic adenosine monophosphate, protein kinase C and non‐glucose nutrients are required. To understand the physiology of GSIS, comprehensive integration of accumulated knowledge is required. |
format | Online Article Text |
id | pubmed-4020243 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2013 |
publisher | Wiley-Blackwell |
record_format | MEDLINE/PubMed |
spelling | pubmed-40202432014-05-19 Glucose‐stimulated insulin secretion: A newer perspective Komatsu, Mitsuhisa Takei, Masahiro Ishii, Hiroaki Sato, Yoshihiko J Diabetes Investig Mini Review Existing concepts and models for glucose‐stimulated insulin secretion (GSIS) are overviewed and a newer perspective has been formulated toward the physiological understanding of GSIS. A conventional model has been created on the basis of in vitro data on application of a square wave high glucose in the absence of any other stimulatory inputs. Glucose elicits rapid insulin release through an adenosine triphosphate‐sensitive K(+) channel (K(ATP) channel)‐dependent mechanism, which is gradually augmented in a K(ATP) channel‐independent manner. Biphasic GSIS thus occurs. In the body, the β‐cells are constantly exposed to stimulatory signals, such as glucagon‐like peptide 1 (GLP‐1), parasympathetic inputs, free fatty acid (FFA), amino acids and slightly suprathreshold levels of glucose, even at fasting. GLP‐1 increases cellular cyclic adenosine monophosphate, parasympathetic stimulation activates protein kinase C, and FFA, amino acids and glucose generate metabolic amplification factors. Plasma glucose concentration gradually rises postprandially under such tonic stimulation. We hypothesize that these stimulatory inputs together make the β‐cells responsive to glucose independently from its action on K(ATP) channels. Robust GSIS in patients with a loss of function mutation of the sulfonylurea receptor, a subunit of K(ATP) channels, is compatible with this hypothesis. Furthermore, pre‐exposure of the islets to an activator of protein kinase A and/or C makes β‐cells responsive to glucose in a K(ATP) channel‐ and Ca(2+)‐independent manner. We hypothesize that GSIS occurs in islet β‐cells without glucose regulation of K(ATP) channels in vivo, for which priming with cyclic adenosine monophosphate, protein kinase C and non‐glucose nutrients are required. To understand the physiology of GSIS, comprehensive integration of accumulated knowledge is required. Wiley-Blackwell 2013-05-15 2013-11-27 /pmc/articles/PMC4020243/ /pubmed/24843702 http://dx.doi.org/10.1111/jdi.12094 Text en Copyright © 2013 Asian Association for the Study of Diabetes and Wiley Publishing Asia Pty Ltd |
spellingShingle | Mini Review Komatsu, Mitsuhisa Takei, Masahiro Ishii, Hiroaki Sato, Yoshihiko Glucose‐stimulated insulin secretion: A newer perspective |
title | Glucose‐stimulated insulin secretion: A newer perspective |
title_full | Glucose‐stimulated insulin secretion: A newer perspective |
title_fullStr | Glucose‐stimulated insulin secretion: A newer perspective |
title_full_unstemmed | Glucose‐stimulated insulin secretion: A newer perspective |
title_short | Glucose‐stimulated insulin secretion: A newer perspective |
title_sort | glucose‐stimulated insulin secretion: a newer perspective |
topic | Mini Review |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4020243/ https://www.ncbi.nlm.nih.gov/pubmed/24843702 http://dx.doi.org/10.1111/jdi.12094 |
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