Volatile anesthetics suppress glucose-stimulated insulin secretion in MIN6 cells by inhibiting glucose-induced activation of hypoxia-inducible factor 1

Proper glycemic control is one of the most important goals in perioperative patient management. Insulin secretion from pancreatic β-cells in response to an increased blood glucose concentration plays the most critical role in glycemic control. Several animal and human studies have indicated that vol...

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Glavni autori: Kengo Suzuki, Yoshifumi Sato, Shinichi Kai, Kenichiro Nishi, Takehiko Adachi, Yoshiyuki Matsuo, Kiichi Hirota
Format: Članak
Jezik:English
Izdano: PeerJ Inc. 2015-12-01
Serija:PeerJ
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Online pristup:https://peerj.com/articles/1498.pdf
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author Kengo Suzuki
Yoshifumi Sato
Shinichi Kai
Kenichiro Nishi
Takehiko Adachi
Yoshiyuki Matsuo
Kiichi Hirota
author_facet Kengo Suzuki
Yoshifumi Sato
Shinichi Kai
Kenichiro Nishi
Takehiko Adachi
Yoshiyuki Matsuo
Kiichi Hirota
author_sort Kengo Suzuki
collection DOAJ
description Proper glycemic control is one of the most important goals in perioperative patient management. Insulin secretion from pancreatic β-cells in response to an increased blood glucose concentration plays the most critical role in glycemic control. Several animal and human studies have indicated that volatile anesthetics impair glucose-stimulated insulin secretion (GSIS). A convincing GSIS model has been established, in which the activity of ATP-dependent potassium channels (KATP) under the control of intracellular ATP plays a critical role. We previously reported that pimonidazole adduct formation and stabilization of hypoxia-inducible factor-1α (HIF-1α) were detected in response to glucose stimulation and that MIN6 cells overexpressing HIF-1α were resistant to glucose-induced hypoxia. Genetic ablation of HIF-1α or HIF-1β significantly inhibited GSIS in mice. Moreover, we previously reported that volatile anesthetics suppressed hypoxia-induced HIF activation in vitro and in vivo.To examine the direct effect of volatile anesthetics on GSIS, we used the MIN6 cell line, derived from mouse pancreatic β-cells. We performed a series of experiments to examine the effects of volatile anesthetics (sevoflurane and isoflurane) on GSIS and demonstrated that these compounds inhibited the glucose-induced ATP increase, which is dependent on intracellular hypoxia-induced HIF-1 activity, and suppressed GSIS at a clinically relevant dose in these cells.
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spelling doaj.art-56c38feba69e4d2492b13676469712392023-12-03T10:03:27ZengPeerJ Inc.PeerJ2167-83592015-12-013e149810.7717/peerj.1498Volatile anesthetics suppress glucose-stimulated insulin secretion in MIN6 cells by inhibiting glucose-induced activation of hypoxia-inducible factor 1Kengo Suzuki0Yoshifumi Sato1Shinichi Kai2Kenichiro Nishi3Takehiko Adachi4Yoshiyuki Matsuo5Kiichi Hirota6Department of Anesthesiology, Kansai Medical University, Hirakata, Osaka, JapanDepartment of Medical Biochemistry, Faculty of Life Sciences, Kumamoto University, Kumamoto, JapanDepartment of Anesthesiology, Kansai Medical University, Hirakata, Osaka, JapanDepartment of Anesthesiology, Kansai Medical University, Hirakata, Osaka, JapanDepartment of Anesthesia, Tazuke Kofukai Medical Research Institute Kitano Hospital, Osaka, JapanDepartment of Anesthesiology, Kansai Medical University, Hirakata, Osaka, JapanDepartment of Anesthesiology, Kansai Medical University, Hirakata, Osaka, JapanProper glycemic control is one of the most important goals in perioperative patient management. Insulin secretion from pancreatic β-cells in response to an increased blood glucose concentration plays the most critical role in glycemic control. Several animal and human studies have indicated that volatile anesthetics impair glucose-stimulated insulin secretion (GSIS). A convincing GSIS model has been established, in which the activity of ATP-dependent potassium channels (KATP) under the control of intracellular ATP plays a critical role. We previously reported that pimonidazole adduct formation and stabilization of hypoxia-inducible factor-1α (HIF-1α) were detected in response to glucose stimulation and that MIN6 cells overexpressing HIF-1α were resistant to glucose-induced hypoxia. Genetic ablation of HIF-1α or HIF-1β significantly inhibited GSIS in mice. Moreover, we previously reported that volatile anesthetics suppressed hypoxia-induced HIF activation in vitro and in vivo.To examine the direct effect of volatile anesthetics on GSIS, we used the MIN6 cell line, derived from mouse pancreatic β-cells. We performed a series of experiments to examine the effects of volatile anesthetics (sevoflurane and isoflurane) on GSIS and demonstrated that these compounds inhibited the glucose-induced ATP increase, which is dependent on intracellular hypoxia-induced HIF-1 activity, and suppressed GSIS at a clinically relevant dose in these cells.https://peerj.com/articles/1498.pdfInsulin secretionVolatile anestheticPanreactic β-cellHIF-1MIN6 cellATP
spellingShingle Kengo Suzuki
Yoshifumi Sato
Shinichi Kai
Kenichiro Nishi
Takehiko Adachi
Yoshiyuki Matsuo
Kiichi Hirota
Volatile anesthetics suppress glucose-stimulated insulin secretion in MIN6 cells by inhibiting glucose-induced activation of hypoxia-inducible factor 1
PeerJ
Insulin secretion
Volatile anesthetic
Panreactic β-cell
HIF-1
MIN6 cell
ATP
title Volatile anesthetics suppress glucose-stimulated insulin secretion in MIN6 cells by inhibiting glucose-induced activation of hypoxia-inducible factor 1
title_full Volatile anesthetics suppress glucose-stimulated insulin secretion in MIN6 cells by inhibiting glucose-induced activation of hypoxia-inducible factor 1
title_fullStr Volatile anesthetics suppress glucose-stimulated insulin secretion in MIN6 cells by inhibiting glucose-induced activation of hypoxia-inducible factor 1
title_full_unstemmed Volatile anesthetics suppress glucose-stimulated insulin secretion in MIN6 cells by inhibiting glucose-induced activation of hypoxia-inducible factor 1
title_short Volatile anesthetics suppress glucose-stimulated insulin secretion in MIN6 cells by inhibiting glucose-induced activation of hypoxia-inducible factor 1
title_sort volatile anesthetics suppress glucose stimulated insulin secretion in min6 cells by inhibiting glucose induced activation of hypoxia inducible factor 1
topic Insulin secretion
Volatile anesthetic
Panreactic β-cell
HIF-1
MIN6 cell
ATP
url https://peerj.com/articles/1498.pdf
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