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Am J Physiol Endocrinol Metab 281: E93-E99, 2001;
0193-1849/01 $5.00
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Vol. 281, Issue 1, E93-E99, July 2001

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

Stephen J. Vore1, E. Dale Aycock1, Johannes D. Veldhuis2, and Peter C. Butler3

1 Department of Comparative Medicine, East Carolina School of Medicine, Greenville, North Carolina 27858; 2 Department of Medicine and National Science Foundation Center for Biological Timing, Charlottesville, Virginia 22908; and 3 Division of Endocrinology and Diabetes, Keck School of Medicine, University of Southern California, Los Angeles, California 90033

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 beta -cells' secretory activity in vivo.

sodium thiamylal; nitrous oxide; isoflurane; pulsatile insulin


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