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Anesth Analg 2002;95:123-128
© 2002 International Anesthesia Research Society

ANESTHETIC PHARMACOLOGY

Sevoflurane Increases Glucose Transport in Skeletal Muscle Cells

Akira Kudoh, MD*, Hiroshi Katagai, MD{dagger}, and Tomoko Takazawa, MD{dagger}

*Department of Anesthesiology, University of Hirosaki School of Medicine; and {dagger}Department of Anesthesiology, Hirosaki National Hospital, Hirosaki, Aomori, Japan

Address correspondence and reprint requests to Akira Kudoh, MD, Department of Anesthesiology, Hirosaki National Hospital, 1 Tominocho, Hirosaki 036-8545, Aomori, Japan.


   Abstract
Top
 Abstract
Introduction
 Methods
 Results
 Discussion
 References
 
Sevoflurane activates phospholipase C and protein kinase C, leading to an increase in intracellular Ca2+ concentration, which modulates glucose transport. We studied in vitro the effect of sevoflurane on the uptake of 2-deoxyglucose in rat skeletal muscle cells and the mechanism that modulates the glucose transport. Sevoflurane 0.8, 1.2, and 2.0 mM significantly increased glucose uptake from 13.1 ± 1.2 pmol · h-1 · mg protein-1 to 22.6 ± 1.4, 32.1 ± 1.8, and 37.4 ±2.7 pmol · h-1 · mg protein-1, respectively. Tyrphostin A-23 (a highly selective tyrosine kinase inhibitor) 1 and 10 nM significantly decreased the sevoflurane-stimulated glucose uptake from 32.1 ± 1.8 to 25.8 ± 1.1 and 15.2 ± 1.7 pmol · h-1 · mg protein-1, respectively. Genistein (a selective tyrosine kinase inhibitor) 1 and 10 nM also significantly decreased the sevoflurane- stimulated glucose uptake from 32.1 ± 1.8 to 25.7 ± 1.5 and 15.2 ± 1.4 pmol · h-1 · mg protein-1, respectively. The sevoflurane-stimulated glucose uptake was decreased by 100 nM and 1 µM TMB-8 (an intracellular Ca2+ antagonist), from 32.1 ± 1.8 pmol · h-1 · mg protein-1 to 25.6 ± 3.3 and 20.3 ± 1.6 pmol · h-1 · mg protein-1, respectively. Staurosporine (a protein kinase C antagonist) 100 nM significantly decreased sevoflurane-stimulated glucose uptake to 26.1 ± 1.5 pmol · h-1 · mg protein-1. We conclude that sevoflurane increases glucose uptake in skeletal muscle cells and that the sevoflurane-stimulated glucose uptake was associated with tyrosine kinase, protein kinase C, and intracellular Ca2+.

IMPLICATIONS: Sevoflurane anesthesia has an inhibitory effect on insulin secretion. Glucose concentrations in plasma do not significantly change during sevoflurane anesthesia. Plasma glucose concentrations are affected by intracellular glucose metabolism. However, glucose transport into cells during sevoflurane anesthesia remains unclear.


   Introduction
Top
 Abstract
 Introduction
Methods
 Results
 Discussion
 References
 
Sevoflurane diminishes insulin secretion, but glucose concentrations in plasma do not significantly increase during sevoflurane anesthesia (1,2). The major action of insulin is to enhance glucose transport into cells. However, the established glucose transport into cells during sevoflurane anesthesia remains unclear. Of the body tissues, skeletal muscle plays a major role in glucose metabolism, because nearly 90% of the glucose disposal after a meal occurs in the skeletal muscle (3). Thus, we studied the effect of sevoflurane on glucose uptake in skeletal muscle cells.

We previously reported that sevoflurane stimulates inositol 1,4,5-triphosphate (IP3) production in skeletal muscle cells (4). IP3 was released through activation of phospholipase C (PLC), which can cause the release of diacylglycerol as well as IP3. Diacylglycerol triggers the activation of protein kinase C (PKC), and IP3 increases the intracellular Ca2+ concentration. Increased PKC activity (5) and an increase of intracellular Ca2+ (6) can stimulate glucose transport. However, the major stimulation for glucose uptake is insulin. Insulin binds to the insulin receptors of the cell surface and induces the autophosphorylation of its ß subunit, which phosphorylates insulin receptor substrate-1 by tyrosine kinase and leads to the activation of phosphatidylinositol 3-kinase (PI3-kinase). Activation of PI3-kinase leads to the translocation of glucose transporter type 4, which transports glucose across membranes (7). We reported that sevoflurane-stimulated IP3 formation is associated with tyrosine kinase (4). We investigated the effect of sevoflurane on glucose transport in skeletal muscle cells and whether sevoflurane modulates tyrosine kinase, PKC, and concentrations of intracellular Ca2+.


   Methods
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 Abstract
 Introduction
 Methods
Results
 Discussion
 References
 
The study was approved by the medical ethics committee of our institution. L6 rat skeletal muscle cells were grown in Dulbecco’s modified Eagle’s medium supplemented with 10% horse serum on 0.1% gelatin-coated plates. The cells were grown in 5% CO2 in a 100% humidity atmosphere. After 4 days in culture, the cells were used at confluence for this study.

At 24 h before the experiments, the culture medium was changed to a serum-free medium. L6 rat skeletal muscles were incubated for the last 12 h with 5.6 mM glucose. Two hours before the experiment, we added 10 mM 2-deoxyglucose (2-DG) to the glucose culture medium to decrease the basal uptake of [3H]2-DG during the subsequent assay. We assayed 2-DG uptake in medium containing 6 mM KCl, 0.2 mM Na2HPO4, 1.4 mM MgSO2, 1 mM CaCl2, 1 mM NaH2PO4, and 10 mM HEPES-NaOH to obtain a pH of 7.4 and 2% bovine serum albumin. Then, 0.4, 0.8, 1.2, and 2.0 mM of sevoflurane were added directly to the flasks containing L6 rat skeletal muscle cells. The caps of the flasks were immediately closed tightly to minimize vaporization of sevoflurane, and the flasks were incubated at 37°C for 10 min, because exposure of sevoflurane for 10 min was the maximum. Sevoflurane concentrations at 0.4, 0.8, 1.2, and 2.0 mM correspond to 1.3%, 2.6%, 3.9%, and 5.2%, respectively, in the vapor phase (4). The tracer ([3H]2-DG, 2 µCi/mL) was added together with 0.2 µCi/mL of [14C]glucose at the last 5 min of exposure of sevoflurane. The [14C]glucose was used to correct for H2O trapping, nonspecific uptake, or both. The transport was stopped by the addition of 400 µL per well of ice-cold 600 mM phloretin. The dishes were transferred to ice, and the monolayers were washed twice with 3 mL per well of ice-cold 200 mM phloretin. The 2-DG uptake was counted in a liquid scintillation counter 60 min after the addition of 1 mL per well of 0.2 M NaOH. Each experiment was performed in triplicate. The concentrations of sevoflurane soon before adding [3H] and [14C] were measured and confirmed by using gas chromatography (4).

Activation of tyrosine kinase, PKC, and PI3-kinase and increases in intracellular Ca2+ can stimulate glucose transport. Therefore, we evaluated whether tyrosine kinase, intracellular Ca2+, PKC, and PI3-kinase are involved in sevoflurane-induced glucose uptake. We studied this by using their antagonists: genistein (a selective tyrosine kinase inhibitor), tyrphostin A-23 (a highly selective tyrosine kinase inhibitor), tyrphostin A1 (the inactive analog of tyrosine kinase), 8-(N,N-diethylamino)octyl 3,4,5-trimethoxybenzoate(TMB-8, an intracellular Ca2+ antagonist), staurosporine (a PKC antagonist), and wortmannin (a PI3-kinase antagonist). The antagonists were added to the cultures 30 min before exposure to sevoflurane.

TMB-8, staurosporine, wortmannin, cell culture medium, and supplements were purchased from Sigma Chemical Co. (St. Louis, MO). Genistein, tyrphostin A-23, and tyrphostin A1 were purchased from Calbiochem-Novabiochem Co. (La Jolla, CA). 2-Deoxy-D-[3H]glucose was purchased from Amersham (Braunschweig, Germany). The L6 rat skeletal muscle myoblast was obtained from the American Type Culture Collection (Rockville, MD).

Genistein and tyrphostin A1 and A-23 and wortmannin were dissolved in 0.1% dimethyl sulfoxide and kept protected from light. Protein was determined by the method of Bradford (8), with bovine serum albumin used as standard.

The data were expressed as mean ± SEM. Every experiment was repeated eight times with different cell preparations. The significance of differences was determined with analysis of variance. When a significant F value was obtained, comparisons of means were performed with Student’s t-tests for paired and unpaired samples, the Bonferroni test, and the Student-Newman-Keuls multiple comparisons test. Differences in mean values were considered significant at P < 0.05.


   Results
Top
 Abstract
 Introduction
 Methods
 Results
Discussion
 References
 
Sevoflurane 0.8, 1.2, and 2.0 mM significantly increased glucose uptake from a basal level of 13.1 ± 1.2 pmol · h-1 · mg protein-1 to 22.6 ± 1.4, 32.1 ± 1.8, and 37.4 ±2.7 pmol · h-1 · mg protein-1, respectively (Fig. 1).



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  		Figure 1. Effects of sevoflurane on glucose uptake in L6 skeletal muscle cells. L6 cells were incubated for 10 min in the presence of 0.4, 0.8, 1.2, and 2.0 mM sevoflurane. [3H]2-Deoxyglucose uptake was measured for 5 min of incubation. Data are mean ± SEM (n = 8 for each bar). *P < 0.05, **P < 0.01, ***P < 0.001 versus basal conditions.

 
Tyrphostin A-23 10 nM alone or genistein 10 nM alone had no significant effect on basal glucose uptake. Tyrphostin A-23 1 and 10 nM significantly decreased the sevoflurane-stimulated glucose uptake from 32.1 ± 1.8 pmol · h-1 · mg protein-1 to 25.8 ± 1.1 and 15.2 ± 1.7 pmol · h-1 · mg protein-1, respectively. Genistein 1 and 10 nM also significantly decreased the sevoflurane-stimulated glucose uptake from 32.1 ± 1.8 pmol · h-1 · mg protein-1 to 25.7 ± 1.5 and 15.2 ± 1.4 pmol · h-1 · mg protein-1, respectively. Tyrphostin A1, the inactive analog, had no significant effect on basal or sevoflurane-stimulated glucose uptake (Fig. 2).



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  		Figure 2. Effect of genistein and tyrphostin A-23 (tyrosine kinase antagonists) on sevoflurane-stimulated glucose uptake. Cells were incubated with 1 and 10 nM genistein and tyrphostin A-23 for 30 min at 37°C, and 1.2 mM sevoflurane was incubated at 37°C for 10 min (n = 8 for each bar). Data are mean ± SEM. *P < 0.05, ***P < 0.001 versus 0.8 mM sevoflurane-stimulated glucose uptake. ##P < 0.01, ###P < 0.001 between 1 and 10 µM genistein or tyrphostin A-23 in the presence of sevoflurane-stimulated glucose uptake.

 
One micromolar of TMB-8 alone had no significant effect on basal glucose uptake. Sevoflurane-stimulated glucose uptake was decreased by 100 nM and 1 µM TMB-8, from 32.1 ± 1.8 pmol · h-1 · mg protein-1 to 25.6 ± 3.3 and 20.3 ± 1.6 pmol · h-1 · mg protein-1, respectively (Fig. 3).



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  		Figure 3. Effect of TMB-8 (an intracellular calcium antagonist) on sevoflurane-stimulated glucose uptake. The cultures were incubated for 10 min in the presence of 1.2 mM sevoflurane before 100 nM and 1 µM TMB-8 were added for another 30 min. [3H]2-Deoxyglucose uptake was measured for 5 min of incubation. Data are mean ± SEM (n = 8 for each bar). **P < 0.01 versus 1.2 mM sevoflurane-stimulated glucose uptake.

 
Increased PKC activity can stimulate glucose transport, and PKC is mediated by tyrosine kinase and intracellular Ca2+ concentrations. Staurosporine 100 nM alone had no significant effect on basal glucose uptake. Staurosporine 100 nM significantly decreased sevo-flurane-stimulated glucose uptake, from 32.1 ± 1.8 pmol · h-1 · mg protein-1 to 26.1 ± 1.5 pmol · h-1 · mg protein-1 (Fig. 4).



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  		Figure 4. Effects of staurosporine (a protein kinase C antagonist) on sevoflurane-stimulated glucose uptake. Staurosporine 10 and 100 nM were incubated for 30 min before exposure to 1.2 mM sevoflurane. [3H]2-Deoxyglucose uptake into cardiomyocytes was measured for 5 min of incubation. Data are mean ± SEM (n = 8) for each bar. *P < 0.01 versus 1.2 mM sevoflurane-stimulated glucose uptake.

 
Wortmannin 100 nM alone had no significant effect on basal glucose uptake. Wortmannin 10 and 100 nM did not significantly block sevoflurane-induced glucose uptake (Fig. 5).



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  		Figure 5. Effects of wortmannin (a phosphatidylinositol 3-kinase antagonist) on sevoflurane-stimulated glucose uptake; 10 and 100 nM wortmannin were incubated for 30 min before exposure to 1.2 mM sevoflurane. [3 H]2-Deoxyglucose uptake into cardiomyocytes was measured for 5 min of incubation. Data are mean ± SEM (n = 8 for each bar).

 

   Discussion
Top
 Abstract
 Introduction
 Methods
 Results
 Discussion
References
 
This study demonstrated that sevoflurane stimulated glucose uptake in skeletal muscle cells in a dose-dependent manner. The sevoflurane-stimulated glucose uptake was inhibited by inhibitors of tyrosine kinase at small concentrations. Activation of tyrosine kinase is associated with stimulation of glucose trans- port. We previously reported that sevoflurane stimulated IP3 production through an activation of tyrosine kinase in skeletal muscle cells (4). Therefore, sevo-flurane-stimulated glucose uptake appears to act via activation of tyrosine kinase.

Our data showed that sevoflurane-stimulated glucose uptake was blocked by intracellular Ca2+ antagonists. Increases of intracellular Ca2+ can stimulate glucose transport. Westfall and Sayeed (9) found that a Ca2+-channel agonist with BAY K 8644 could increase the basal glucose transport and that the effect could be blocked by Ca2+-channel blockers with nifedipine and diltiazem. Youn et al. (6) also found that W7, which induces Ca2+ release from the sarcoplasmic reticulum (SR), caused an increase in glucose transport and that the effect was inhibited by dantrolene, which blocks Ca2+ release from the SR. Halothane increases intracellular Ca2+, and approximately 50% of this increase is released from the SR in skeletal muscle cells (10). The TMB-8 used in this study inhibited the release of Ca2+ from the SR. A major effect of TMB-8 on cellular Ca2+ metabolism is to prevent intracellular Ca2+ mobilization by inhibiting the IP3-induced Ca2+ release (11). We reported that sevoflurane stimulated IP3 production in skeletal muscle cells (4). IP3 increases intracellular Ca2+ concentration and plays a role in the modulation of the excitation-contraction coupling process and in the pathophysiology of muscle disease, such as malignant hyperthermia, in the skeletal muscle. Tyrosine kinase has a role in the regulation of intracellular Ca2+. Activation of tyrosine kinase requires an increase of intracellular Ca2+ (12). Thus, the fact that an intracellular Ca2+ blocker inhibited sevoflurane-stimulated glucose uptake appears to partly support the contention that increased Ca2+ levels are necessary for activation of tyrosine kinase.

PKC is important in the stimulation of glucose transport regulation (5). Phorbol-12-myristate-13-acetate, which is a PKC agonist, stimulates glucose transport, and the PKC inhibitor with staurosporine inhibits the glucose transport (5). The PKC-induced glucose uptake may occur via different mechanisms from insulin-induced glucose uptake (13). In this study, staurosporine inhibited sevoflurane-stimulated glucose uptake. The activation of PKC appears to be partly associated with sevoflurane-stimulated glucose uptake. Three mechanisms of the activation of PKC are considered. The first mechanism is directly sevoflurane-induced PKC activation. PKC is reported to modulate the effect of halothane on the Na channel in skeletal muscle (14). However, the effect of inhaled anesthetics on PKC in skeletal muscle has not been adequately evaluated. The second mechanism is activation of PKC by IP3-induced Ca2+ mobilization. We reported that sevoflurane stimulates IP3 production in skeletal muscle cells (4). The third mechanism is activation of PKC by tyrosine phosphorylation (15). In this study, sevoflurane-stimulated glucose uptake was inhibited by inhibitors of tyrosine kinase.

Wortmannin, a PI3-kinase inhibitor, is a potent and selective inhibitor of PI3-kinase and inhibits insulin-stimulated glucose transport (16). In this study, wortmannin could not block sevoflurane-induced glucose uptake, although the same concentration of wortmannin significantly blocked insulin-induced glucose uptake. Sevoflurane-induced glucose uptake seems to act via a different pathway from PI3-kinase.

We showed in Figure 6 the mechanism of sevo-flurane-stimulated glucose uptake in skeletal muscle cells. Sevoflurane stimulates tyrosine kinase receptors and increases intracellular Ca2+ from the SR through activation of PLC. The increase of intracellular Ca2+ and the activation of tyrosine kinase and PLC activate PKC. The activation of PKC results in stimulation of glucose uptake.



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  		Figure 6. Mechanism of sevoflurane-stimulated glucose uptake in skeletal muscle cells. Sevoflurane stimulates tyrosine kinase receptors and increases intracellular Ca2+ from the sarcoplasmic reticulum through activation of phospholipase C (PLC). The increase of intracellular Ca2+ and the activation of tyrosine kinase and PLC activate protein kinase C (PKC). The activation of PKC results in stimulation of glucose uptake. IP3 = inositol 1,4,5-triphosphate.

 
Sevoflurane has an inhibitory effect on insulin secretion (2). However, sevoflurane stimulated glucose uptake in skeletal muscle cells through another pathway than the process mediated by insulin. Sevoflurane 0.4 mM, which corresponds to 1.3% in the vapor phase, increased the glucose uptake by 22%. Thus, intracellular glucose metabolism during sevoflurane anesthesia appears to be preserved. In this study, exposure of sevoflurane was for 10 minutes. The increase of intracellular Ca2+ by IP3 persisted for only approximately 10 minutes after stimulation. The effect of sevoflurane on glucose uptake in a longer exposure of sevoflurane remains unclear. Wortmannin, staurosporine, TMB-8, genistein, and tyrphostin A-23 have been used for many years as pharmacologic tools. Wortmannin has been proven to be a potent and selective inhibitor of PI3-kinase. Because the concentration required for the half-maximal inhibition was 10 nmol or less when the inhibitor was added directly (16), the dose used in this study was adequate for the inhibition of PI3-kinase. Staurosporine is used as a PKC antagonist. We used 100 nM staurosporine for preventing several actions at a large concentration. The doses of TMB-8 were determined according to the study of Northover (17). He suggested that exposure of 2 µM TMB-8 for 15 minutes significantly decreased the concentration of intracellular Ca2+. Because large concentrations of TMB-8 provide several actions, including depression of PKC and tyrosine kinase (11), the culture was exposed for 30 minutes to concentrations of 100 nM and 1 µM TMB-8 in this study. Genistein interferes competitively with the adenosine triphosphate-binding site of tyrosine kinase (18). However, tyrphostin is another type of tyrosine kinase inhibitor that competes for the substrate binding site of specific tyrosine kinases. Tyrphostin can inhibit PLC activity (19); however, genistein did not inhibit PLC or PKC activity and appears to be specific for tyrosine kinase (18).

We have previously reported that halothane and sevoflurane decreased norepinephrine-stimulated glucose uptake through a decrease in intracellular Ca2+ in cardiomyocytes (20). Karon et al. (21) showed that halothane activated Ca-adenosine triphosphatase in skeletal SR but inhibited the Ca-adenosine triphosphatase in cardiac SR. Thus, regulation of intracellular Ca2+ between heart and skeletal muscle may be different. Ca2+ is released from the SR by a ryanodine receptor, which is triggered by L-type Ca2+ channels or dihydropyridine receptors. Skeletal muscle, but not cardiac muscle, has a direct interaction between ryanodine receptors and dihydropyridine receptors (22). The effect of inhaled anesthetics on PKC may also be different between heart and skeletal muscle. Isoflurane has no significant effect on PKC of cardiac cells (23). However, PKC is involved in the modulation of the cellular effects of halothane in skeletal muscle (14). Additional investigations are required to further confirm the dissociation of glucose uptake between skeletal and cardiac muscle.

We conclude that sevoflurane stimulates glucose uptake through activation of tyrosine kinase. The stimulation is associated with an increase in intracellular Ca2+. A positive feedback loop may play a role in sevoflurane-stimulated glucose uptake through tyrosine kinase, PKC, and increases in intracellular Ca2+.


   Acknowledgments
 
The authors thank Professor E. G. Erdos (Department of Pharmacology, University of Illinois College of Medicine at Chicago) and Dr. S. F. Rabito (Department of Anesthesiology and Pain Management, Cook County Hospital, Chicago) for their support of this research and for their critical comments and Dr. Paul Hollister for correction of English grammar and syntax.


   References
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 Abstract
 Introduction
 Methods
 Results
 Discussion
 References
 

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Accepted for publication February 27, 2002.




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Lippincott, Williams & Wilkins Anesthesia & Analgesia® is published for the International Anesthesia Research Society® by Lippincott Williams & Wilkins with the assistance of Stanford University Libraries' HighWire Press®. Copyright 2006 by the International Anesthesia Research Society. Online ISSN: 1526-7598   Print ISSN: 0003-2999 HighWire Press