Anesthesia rapidly suppresses insulin pulse mass but enhances the orderliness of insulin secretory process

Abstract

Induction of anesthesia is accompanied by modest hyperglycemia and a decreased plasma insulin concentration. Most insulin is secreted in discrete pulses occurring at approximately 6- to 8-min intervals. We sought to test the hypothesis that anesthesia inhibits insulin release by disrupting pulsatile insulin secretion in a canine model by use of direct portal vein sampling. We report that induction of anesthesia causes an abrupt decrease in the insulin secretion rate (1.1 +/- 0.2 vs. 0.7 +/- 0.1 pmol. kg(-1). min(-1), P < 0.05) by suppressing insulin pulse mass (630 +/- 121 vs. 270 +/- 31 pmol, P < 0.01). Anesthesia also elicited an approximately 30% higher increase in insulin pulse frequency (P < 0.01) and more orderly insulin concentration profiles (P < 0.01). These effects were evoked by either sodium thiamylal or nitrous oxide and isoflurane. In conclusion, anesthesia represses insulin secretion through the mechanism of a twofold blunting of pulse mass despite an increase in orderly pulse frequency. These data thus unveil independent amplitude and frequency controls of beta-cells' secretory activity in vivo.

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

“…study and in a pancreatic islet perifusion study, whereas propofol did not affect glucose-induced insulin secretion. These results are in agreement with previous evidence indicating that volatile anesthetics impair insulin secretion and glucose utilization (Camu, 1976;Diltoer and Camu, 1988;Iwasaka et al, 1996;Kitamura et al, 2009;Saho et al, 1997;Tanaka et al, 2005;Vore et al, 2001). In addition, our results suggest that isoflurane significantly decreases the ATP sensitivity of pancreatic K ATP channels, resulting in inhibition of insulin secretion during isoflurane anesthesia.…”

“…It has been known since the 1970s that volatile anesthetics can impair insulin secretion and glucose utilization (Camu, 1976;Diltoer and Camu, 1988;Iwasaka et al, 1996;Kitamura et al, 2009;Saho et al, 1997;Tanaka et al, 2005;Vore et al, 2001). Pancreatic adenosine triphosphate-sensitive potassium (K ATP ) channels are known to play an important role in insulin secretion (Henquin, 2000).…”

Sources of endogenous glucose production in the Goto–Kakizaki diabetic rat

“…In a study of 6-hour fasted, conscious rats of similar weights to that used in our study (~300 g), EGP rates of 70-80 μmol/kg per min were reported [20]. Given that anesthesia is accompanied by a decrease in insulin secretion [21], the higher EGP values observed in our study compared to that or Neese et al may be attributable to incomplete suppression of EGP as a result of reduced insulin levels. Moreover, the anesthetic cocktail used did not produce hyperglycaemia per se in Wistar rats since these animals exhibited low glucose levels but may have reduced the clearance of high glucose levels in the blood of GK rats.…”

Remote regulation of glucose homeostasis in mice using genetically encoded nanoparticles

“…In rats, isoflurane decreased glucosestimulated insulin release from isolated islets in vitro 15 , and in electrophysiological studies in rabbits, isoflurane reversed the inhibitory effects of glucose on pancreatic K ATP channel activity in pancreatic β cells 16 . In studies using direct portal vein sampling in dogs, isoflurane decreased insulin secretion rate and insulin pulse mass in vivo 17 . In both rats and rabbits, isoflurane substantially blunted glucose-stimulated insulin release in vivo 16,18 .…”