Propofol inhibits stromatoxin-1-sensitive voltage-dependent K
Anesthetic
Glucose
Insulin
Kv channel
Pancreatic β-cells
Propofol
Stromatoxin-1
Journal
PeerJ
ISSN: 2167-8359
Titre abrégé: PeerJ
Pays: United States
ID NLM: 101603425
Informations de publication
Date de publication:
2019
2019
Historique:
received:
23
05
2019
accepted:
04
11
2019
entrez:
12
12
2019
pubmed:
12
12
2019
medline:
12
12
2019
Statut:
epublish
Résumé
Proper glycemic control is an important goal of critical care medicine, including perioperative patient care that can influence patients' prognosis. Insulin secretion from pancreatic β-cells is generally assumed to play a critical role in glycemic control in response to an elevated blood glucose concentration. Many animal and human studies have demonstrated that perioperative drugs, including volatile anesthetics, have an impact on glucose-stimulated insulin secretion (GSIS). However, the effects of the intravenous anesthetic propofol on glucose metabolism and insulin sensitivity are largely unknown at present. The effect of propofol on insulin secretion under low glucose or high glucose was examined in mouse MIN6 cells, rat INS-1 cells, and mouse pancreatic β-cells/islets. Cellular oxygen or energy metabolism was measured by Extracellular Flux Analyzer. Expression of glucose transporter 2 (GLUT2), potassium channels, and insulin mRNA was assessed by We showed that propofol, at clinically relevant doses, facilitates insulin secretion under low glucose conditions and GSIS in MIN6, INS-1 cells, and pancreatic β-cells/islets. Propofol did not affect intracellular ATP or ADP concentrations and cellular oxygen or energy metabolism. The mRNA expression of GLUT2 and channels including the voltage-dependent calcium channels Cav1.2, Kir6.2, and SUR1 subunit of K Our data support the hypothesis that glucose induces membrane depolarization at the distal site, leading to K
Sections du résumé
BACKGROUND
BACKGROUND
Proper glycemic control is an important goal of critical care medicine, including perioperative patient care that can influence patients' prognosis. Insulin secretion from pancreatic β-cells is generally assumed to play a critical role in glycemic control in response to an elevated blood glucose concentration. Many animal and human studies have demonstrated that perioperative drugs, including volatile anesthetics, have an impact on glucose-stimulated insulin secretion (GSIS). However, the effects of the intravenous anesthetic propofol on glucose metabolism and insulin sensitivity are largely unknown at present.
METHODS
METHODS
The effect of propofol on insulin secretion under low glucose or high glucose was examined in mouse MIN6 cells, rat INS-1 cells, and mouse pancreatic β-cells/islets. Cellular oxygen or energy metabolism was measured by Extracellular Flux Analyzer. Expression of glucose transporter 2 (GLUT2), potassium channels, and insulin mRNA was assessed by
RESULTS
RESULTS
We showed that propofol, at clinically relevant doses, facilitates insulin secretion under low glucose conditions and GSIS in MIN6, INS-1 cells, and pancreatic β-cells/islets. Propofol did not affect intracellular ATP or ADP concentrations and cellular oxygen or energy metabolism. The mRNA expression of GLUT2 and channels including the voltage-dependent calcium channels Cav1.2, Kir6.2, and SUR1 subunit of K
CONCLUSIONS
CONCLUSIONS
Our data support the hypothesis that glucose induces membrane depolarization at the distal site, leading to K
Identifiants
pubmed: 31824770
doi: 10.7717/peerj.8157
pii: 8157
pmc: PMC6894434
doi:
Types de publication
Journal Article
Langues
eng
Pagination
e8157Informations de copyright
©2019 Kusunoki et al.
Déclaration de conflit d'intérêts
The authors declare there are no competing interests.
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