title: Comparison of mechanisms underlying changes in glucose utilization in fasted rats anesthetized with propofol or sevoflurane: Hyperinsulinemia is exaggerated by propofol with concomitant insulin resistance induced by an acute lipid load.
abstract: The effects of anesthesia with sevoflurane and with propofol on glucose utilization in rats were investigated. Sevoflurane significantly impairs glucose utilization whereas propofol does not. Both insulin secretion and sensitivity affect glucose utilization. Propofol is hydrophobic, and anesthesia with this agent is always accompanied by an acute lipid load, which can exaggerate insulin resistance. The role of the acute lipid load in the effects of anesthesia with sevoflurane and propofol on glucose utilization in fasted rats was investigated. Rats were allocated to groups anesthetized with sevoflurane and infused with physiological saline (group S) or 10% w/v lipid (group SL), or those anesthetized with propofol (group P). Intravenous glucose tolerance tests and insulin tolerance tests were then performed to measure glucose utilization, and blood glucose, plasma insulin, and plasma TNF-α levels were measured. In the intravenous glucose tolerance test, groups SL and P showed significantly higher plasma insulin levels than group S, and group P showed significantly higher plasma insulin levels than group SL. In the insulin tolerance test, groups SL and P showed insulin resistance compared to group S, but no significant difference was observed between groups SL and P. In summary, propofol anesthesia enhances insulin secretion and concomitantly exaggerates insulin resistance, compared with sevoflurane anesthesia. Propofol appears to be the main cause of hyperinsulinemia, and the acute lipid load exaggerates insulin resistance.
authors.affiliation: Department of Anesthesiology, Graduate School of Medicine, The University of Tokyo.
authors.forename: Xiang
authors.initials: X
authors.lastname: Li
authors.forename: Takayuki
authors.initials: T
authors.lastname: Kitamura
authors.forename: Gaku
authors.initials: G
authors.lastname: Kawamura
authors.forename: Yoshiteru
authors.initials: Y
authors.lastname: Mori
authors.forename: Kanako
authors.initials: K
authors.lastname: Sato
authors.forename: Yuko
authors.initials: Y
authors.lastname: Araki
authors.forename: Rui
authors.initials: R
authors.lastname: Sato
authors.forename: Yoshitsugu
authors.initials: Y
authors.lastname: Yamada
mesh_terms: D000818:Animals; D005215:Fasting / Q000097:blood / Q000378:metabolism*; D005947:Glucose / Q000378:metabolism*; D006946:Hyperinsulinism / Q000139:chemically induced*; D007333:Insulin Resistance / Q000502:physiology; D008297:Male; D008738:Methyl Ethers / Q000627:therapeutic use*; D015742:Propofol / Q000627:therapeutic use*; D051381:Rats; D017208:Rats, Wistar; D000077149:Sevoflurane
chemical_list: D008738:Methyl Ethers; D000077149:Sevoflurane; D005947:Glucose; D015742:Propofol