• Takayuki Kitamura, Gaku Kawamura, Yoshiteru Mori, Rui Sato, and Yoshitsugu Yamada.
• Department of Anesthesiology, Faculty of Medicine, University of Tokyo, 7-3-1 Hongo, Bunkyo-ku, Tokyo 113-8655, Japan. tyy-kitamura@m7.dion.ne.j.
• Anesth. Analg.. 2013 Sep 1;117(3):627-33.

BackgroundWe previously reported the marked differences in the effects of sevoflurane anesthesia and propofol anesthesia on glucose use in fed rats; however, we could not elucidate mechanisms underlying the differences.MethodsWe used fasted rats in this study. After surgical preparation under sevoflurane anesthesia, rats were divided into 3 groups: awake rats, rats under sevoflurane anesthesia, and rats under propofol anesthesia. All rats underwent the IV glucose tolerance test (IVGTT); 0.5 g/kg glucose was administered IV to rats. Just before IVGTT, some rats were pretreated with glibenclamide or diazoxide. We measured glucose, insulin, tumor necrosis factor-α (TNF-α), and high molecular weight adiponectin levels during IVGTT and calculated the quantitative insulin sensitivity check index (QUICKI) using glucose and insulin levels before glucose administration in each rat.ResultsBefore glucose administration, rats under sevoflurane anesthesia showed similar glucose and insulin levels with significantly higher QUICKI compared with awake rats, while rats under propofol anesthesia showed similar glucose levels and significantly higher insulin levels with significantly lower QUICKI compared with awake rats. After glucose administration, rats under sevoflurane anesthesia showed significantly higher glucose levels and similar insulin levels compared with awake rats, while rats under propofol anesthesia showed similar glucose levels and significantly higher insulin levels compared with awake rats. Before glucose administration, TNF-α levels in rats under sevoflurane anesthesia and rats under propofol anesthesia were similar to those in awake rats. After glucose administration, TNF-α was undetectable in all awake rats and all rats under sevoflurane anesthesia, whereas TNF-α was detectable in all rats under propofol anesthesia; TNF-α levels in rats under propofol anesthesia were significantly higher than those in awake rats. High molecular weight adiponectin levels in rats under sevoflurane anesthesia and rats under propofol anesthesia were similar to those in awake rats throughout the experimental period. In rats under sevoflurane anesthesia, glibenclamide significantly decreased glucose levels and significantly increased insulin levels; however, diazoxide produced no significant effects on glucose and insulin levels. In rats under propofol anesthesia, glibenclamide significantly decreased glucose levels and significantly increased insulin levels, while diazoxide significantly decreased glucose levels without changing insulin levels.ConclusionsSevoflurane anesthesia attenuates glucose-induced insulin secretion without affecting basic insulin secretion, while propofol anesthesia enhances insulin secretion. Propofol anesthesia exaggerates insulin-resistive conditions, whereas sevoflurane anesthesia dose not impair insulin sensitivity; there may be a possible association of TNF-α with insulin-resistive conditions under propofol anesthesia.

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