Differential effects of propofol and isoflurane on glucose utilization and insulin secretion

Functional roles of ATP-sensitive potassium channel as related to anesthesia

“…In contrast, propofol, an intravenously administered anesthetic, did not affect glucose-induced insulin secretion from isolated rat pancreatic islet cells; similar results were also observed in an in vivo IVGTT study [12]. The frequently used combination of propofol and opioids also does not impair glucose homeostasis in rats [10].…”

“…The frequently used combination of propofol and opioids also does not impair glucose homeostasis in rats [10]. Clinically relevant concentrations of propofol had no effect on pancreatic K ATP -channel activity in different patch-clamp configurations [12]. Therefore, the different effects of isoflurane and propofol on insulin release may be caused by the difference in K ATP -channel sensitivity in pancreatic b cells.…”

“…Furthermore, using an in vivo rabbit model, we demonstrated that inhalation of 1.0 minimum alveolar concentration (MAC) isoflurane inhibits glibenclamide-induced insulin secretion during the late phase of an intravenously administered glucose tolerance test (IVGTT) [11]. Furthermore, patch-clamp experiments showed that isoflurane significantly decreases ATP sensitivity of pancreatic K ATP channels in the presence of 10 mM glucose, resulting in the opening of these channels in pancreatic b cells [12]. These results indicate that the isoflurane-induced inhibition of insulin secretion from pancreatic b cells is mediated by isoflurane-induced activation of K ATP channels in these cells.…”

Biophysical and Pharmacological Properties of Glucagon-Like Peptide-1 in Rats Under Isoflurane Anesthesia

“…9 Briefly, collagenase (Type IV, Sigma-Aldrich) was injected into the pancreas through the pancreatic duct; the pancreas was then dissected and incubated at 37°C. After washing the pancreatic digest, individual islets were separated from the adjacent acinar tissue by applying a discontinuous density gradient.…”

“…Recently, we showed that isoflurane impairs insulin release mediated by suppression of glucose-induced depolarization via modulation of pancreatic adenosine triphosphate (ATP)-sensitive K ϩ (K ATP ) channels. 8,9 Conversely, GLP-1 depolarizes pancreatic ␤-cells through a cyclic adenosine monophosphate-dependent mechanism, resulting in enhanced insulin secretion. 10 Overall, these data indicate that isoflurane and GLP-1 have opposite effects on the electrical activity of pancreatic ␤-cells in response to glucose stimulation.…”