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

Stephen J. Vore, E. Dale Aycock, Johannes D. Veldhuis, Peter C. Butler

Research output: Contribution to journalArticlepeer-review

14 Scopus citations


Induction of anesthesia is accompanied by modest hyperglycemia and a decreased plasma insulin concentration. Most insulin is secreted in discrete pulses occurring at ∼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 ∼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 β-cells' secretory activity in vivo.

Original languageEnglish (US)
Pages (from-to)E93-E99
JournalAmerican Journal of Physiology - Endocrinology and Metabolism
Issue number1 44-1
StatePublished - 2001


  • Isoflurane
  • Nitrous oxide
  • Pulsatile insulin
  • Sodium thiamylal

ASJC Scopus subject areas

  • Endocrinology, Diabetes and Metabolism
  • Physiology
  • Physiology (medical)


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