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

Li, Xiang; Kitamura, Takayuki; Kawamura, Gaku; Mori, Yoichi; Sato, Kanako; Araki, Yuko; Sato, Ryugo; Yamada, Yosuke

doi:10.5582/bst.2014.01060

Cited by 13 publications

(17 citation statements)

References 23 publications

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“…[ 3 ] On the other hand, propofol has been reported to promote insulin resistance but concomitantly increases insulin secretion and preserves glucose utilization in animal models. [ 4 5 ]…”

Section: Introductionmentioning

confidence: 99%

Randomized trial to compare plasma glucose trends in patients undergoing surgery for supratentorial gliomas under maintenance of sevoflurane, desflurane, and propofol

et al. 2020

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Background: Anesthetic agents influence the glycemic response by affecting the neuroendocrine surgical response or directly modifying pancreatic insulin release. Due to chances of neuronal damage, intraoperative hyperglycemia and hypoglycemia both are detrimental for patients undergoing neurosurgeries. Inhalational (sevoflurane and desflurane) and intravenous (propofol) agents have been found to raise intraoperative glucose levels in nonneurological surgeries. Aim: We aimed to compare the intraoperative glucose levels in supratentorial glioma surgeries under the maintenance of three anesthetic agents such as sevoflurane, desflurane, and propofol. Materials and Methods: This randomized trial was conducted with 90 nondiabetic adults with supratentorial glioma. Thirty patients were allocated randomly to the three groups receiving sevoflurane, desflurane, and propofol. Baseline and hourly plasma glucose levels were recorded. Postoperatively, the time required to achieve an Aldrete score of 9 and complications were assessed. Results: Baseline plasma glucose levels were 111.23 ± 11.67, 109.47 ± 19.75, and 111.7 ± 13.88 mg/dL ( P = 0.84) in sevoflurance, desflurane, and propofol group, respectively. All of them showed an elevation of plasma glucose in relation to the time of surgery with variable trends. In the 4 th and 5 th h, the elevations in the inhalational groups (sevoflurane and desflurane) were significantly higher than the propofol group ( P = 0.003 and 0.002, respectively). The time for achieving Aldrete's score of 9 was higher in the propofol group ( P < 0.0001). No differences were observed in the duration of hospital stay or complications. Conclusions: Maintenance of anesthesia in nondiabetic patients showed clinically modest rise of plasma glucose which is higher in patients under sevoflurane and desflurane than under propofol. However, the immediate recovery was faster with inhalational agents compared to propofol-based anesthesia.

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“…[ 3 ] On the other hand, propofol has been reported to promote insulin resistance but concomitantly increases insulin secretion and preserves glucose utilization in animal models. [ 4 5 ]…”

Section: Introductionmentioning

confidence: 99%

Randomized trial to compare plasma glucose trends in patients undergoing surgery for supratentorial gliomas under maintenance of sevoflurane, desflurane, and propofol

et al. 2020

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“…However, experimental findings regarding propofol’s effects on glucose metabolism are contradictory. Anesthesia involving propofol in unstressed rats slightly induces insulin resistance due to the tumor necrosis factor α (TNF-α) elevation and acute lipid load [ 8 , 9 , 10 , 11 , 12 ], whereas in stressed rats and rhesus monkeys, propofol increases insulin secretion and improves glucose metabolism, and reduces TNF-α-induced hepatic insulin resistance [ 13 , 14 , 15 ]. Therefore, propofol has a regulatory effect on glucose metabolism, and its consequences are dependent upon a patient’s stress levels, environment, and disease status.…”

Section: Introductionmentioning

confidence: 99%

Propofol Improved Glucose Tolerance Associated with Increased FGF-21 and GLP-1 Production in Male Sprague-Dawley Rats

Hung

Wang

et al. 2020

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Anesthetics, particularly volatile anesthetics, have been shown to impair glucose metabolism and cause hyperglycemia, closely linking them with mortality and morbidity as related to surgery. Beyond being an anesthetic used for general anesthesia and sedation, intravenous hypnotic propofol displays an effect on glucose metabolism. To extend the scope of propofol studies, its effects on glucose metabolism were evaluated in male Sprague-Dawley rats of various ages. Unlike chloral hydrate and isoflurane, propofol had little effect on basal glucose levels in rats at 2 months of age, although it did reduce chloral hydrate- and isoflurane-induced hyperglycemia. Propofol reduced postload glucose levels after either intraperitoneal or oral administration of glucose in both 7- and 12-month-old rats, but not those at 2 months of age. These improved effects regarding propofol on glucose metabolism were accompanied by an increase in insulin, fibroblast growth factor-21 (FGF-21), and glucagon-like peptide-1 (GLP-1) secretion. Additionally, an increase in hepatic FGF-21 expression, GLP-1 signaling, and FGF-21 signaling, along with a decrease in endoplasmic reticulum (ER) stress, were noted in propofol-treated rats at 7 months of age. Current findings imply that propofol may turn into insulin-sensitizing molecules during situations of existing insulin resistance, which involve FGF-21, GLP-1, and ER stress.

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“…Manuscript to be reviewed plays a critical role in glycemic control (Ashcroft 2005). It is reported that propofol anesthesia enhances insulin secretion and concomitantly exaggerates insulin resistance, compared with sevoflurane anesthesia (Li et al 2014). Another report indicates that glucose levels in rats anesthetized with sevoflurane were significantly higher than those in rats anesthetized with propofol, and insulin levels in rats anesthetized with sevoflurane were significantly lower than those in rats anesthetized with propofol (Kitamura et al 2012).…”

Section: Introductionmentioning

confidence: 99%

Peer Review #1 of "Propofol inhibits stromatoxin-1-sensitive voltage-dependent K+ channels in pancreatic β-cells and enhances insulin secretion (v0.2)"

2019

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Proper glycemic control is an important goal of critical care medicine, including perioperative patient care that can influence patients' prognosis. Insulin secretion from pancreatic β-cells is generally assumed to play a critical role in glycemic control in response to an elevated blood glucose concentration. Many animal and human studies have demonstrated that perioperative drugs, including volatile anesthetics, have an impact on glucose-stimulated insulin secretion (GSIS). However, the effects of the intravenous anesthetic propofol on glucose metabolism and insulin sensitivity are largely unknown at present. Methods: The effect of propofol on insulin secretion under low glucose or high glucose was examined in mouse MIN6 cells, rat INS-1 cells, and mouse pancreatic β-cells/islets. Cellular oxygen or energy metabolism was measured by Extracellular Flux Analyzer. Expression of glucose transporter 2 (GLUT2), potassium channels, and insulin mRNA was assessed by qRT-PCR. Protein expression of voltagedependent potassium channels (Kv2) was also assessed by immunoblot. Propofol's effects on potassium channels including stromatoxin-1-sensitive Kv channels and cellular oxygen and energy metabolisms were also examined. Results: We showed that propofol, at clinically relevant doses, facilitates insulin secretion under low glucose conditions and GSIS in MIN6, INS-1 cells, and pancreatic β-cells/islets. Propofol did not affect intracellular ATP or ADP concentrations and cellular oxygen or energy metabolism. The mRNA expression of GLUT2 and channels including the voltage-dependent calcium channels Cav1.2, Kir6.2, and SUR1 subunit of K ATP , and Kv2 were not affected by glucose or propofol. Finally, we demonstrated that propofol specifically blocks Kv currents in β-cells, resulting in insulin secretion in the presence of glucose. Conclusions: Our data support the hypothesis that glucose induces membrane depolarization at the distal site, leading to K ATP channel closure, and that the closure of Kv channels by propofol depolarization in β-cells enhances Ca 2+ entry, leading to insulin secretion. Because its activity is dependent on GSIS, propofol and its derivatives are potential compounds that enhance and initiate β-cell electrical activity.

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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

Cited by 13 publications

References 23 publications

Randomized trial to compare plasma glucose trends in patients undergoing surgery for supratentorial gliomas under maintenance of sevoflurane, desflurane, and propofol

Randomized trial to compare plasma glucose trends in patients undergoing surgery for supratentorial gliomas under maintenance of sevoflurane, desflurane, and propofol

Propofol Improved Glucose Tolerance Associated with Increased FGF-21 and GLP-1 Production in Male Sprague-Dawley Rats

Peer Review #1 of "Propofol inhibits stromatoxin-1-sensitive voltage-dependent K+ channels in pancreatic β-cells and enhances insulin secretion (v0.2)"

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