Abstract
To explore the mechanisms for hypoglycemia in our rat model of septic shock, we examined whether changes occur in glucose transporter isoform protein level. Total membrane protein fractions were collected from tissues 6 to 8 hours after endotoxin injection at which time animals exhibited hypoglycemia (7.2 ± 0.5 vs. 2.6 ± 1.2mM) and lactacidemia (1.0 ± 1.0 vs. 5.1 ± 1 .8mM/L) as compared to saline-treated controls. The protein level of glucose transporter isoforms GLUT1 and 4 in fat did not significantly change in septic shock when compared to control animals (126 ± 22% and 114 ± 79%, respectively). Likewise, no change was seen in GLUT1 or 4 in muscle (124 ± 52% and 101 ± 28%, respectively). The protein abundance of isoforms GLUT1 and 2 in liver were not significantly altered (1 23 ± 35% and 101 ± 23%. respectively). Septic shock induced hypoglycemia cannot be directly explained by changes in total glucose transporter protein levels.
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