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...
Glavni autori: | , , , , , , |
---|---|
Format: | Članak |
Jezik: | English |
Izdano: |
PeerJ Inc.
2015-12-01
|
Serija: | PeerJ |
Teme: | |
Online pristup: | https://peerj.com/articles/1498.pdf |
_version_ | 1827607547011399680 |
---|---|
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. |
first_indexed | 2024-03-09T06:56:02Z |
format | Article |
id | doaj.art-56c38feba69e4d2492b1367646971239 |
institution | Directory Open Access Journal |
issn | 2167-8359 |
language | English |
last_indexed | 2024-03-09T06:56:02Z |
publishDate | 2015-12-01 |
publisher | PeerJ Inc. |
record_format | Article |
series | PeerJ |
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 |
work_keys_str_mv | AT kengosuzuki volatileanestheticssuppressglucosestimulatedinsulinsecretioninmin6cellsbyinhibitingglucoseinducedactivationofhypoxiainduciblefactor1 AT yoshifumisato volatileanestheticssuppressglucosestimulatedinsulinsecretioninmin6cellsbyinhibitingglucoseinducedactivationofhypoxiainduciblefactor1 AT shinichikai volatileanestheticssuppressglucosestimulatedinsulinsecretioninmin6cellsbyinhibitingglucoseinducedactivationofhypoxiainduciblefactor1 AT kenichironishi volatileanestheticssuppressglucosestimulatedinsulinsecretioninmin6cellsbyinhibitingglucoseinducedactivationofhypoxiainduciblefactor1 AT takehikoadachi volatileanestheticssuppressglucosestimulatedinsulinsecretioninmin6cellsbyinhibitingglucoseinducedactivationofhypoxiainduciblefactor1 AT yoshiyukimatsuo volatileanestheticssuppressglucosestimulatedinsulinsecretioninmin6cellsbyinhibitingglucoseinducedactivationofhypoxiainduciblefactor1 AT kiichihirota volatileanestheticssuppressglucosestimulatedinsulinsecretioninmin6cellsbyinhibitingglucoseinducedactivationofhypoxiainduciblefactor1 |