Glucose Transporters (GLUT1, 2, and 4) in Fat, Muscle and Liver in a Rat Model of Endotoxic Shock

• Published in: Biochemical and biophysical research communications Vol. 198; no. 3; pp. 923 - 927
• Main Authors: Zeller, W.P., Goto, M., Parker, J., Cava, J.R., Gottschalk, M.E., Filkins, J.P., Hofmann, C.
• Format: Journal Article
• Language: English
• Published: San Diego, CA Elsevier Inc 15.02.1994; Elsevier
• Subjects: Adipose Tissue - metabolism; Animals; Bacterial diseases; Biological and medical sciences; Blotting, Western; Cell Membrane - drug effects; Cell Membrane - metabolism; Disease Models, Animal; Endotoxins - toxicity; Experimental bacterial diseases and models; Glucose Transporter Type 1; Glucose Transporter Type 2; Glucose Transporter Type 4; Infectious diseases; Liver - metabolism; Male; Medical sciences; Monosaccharide Transport Proteins - biosynthesis; Monosaccharide Transport Proteins - isolation & purification; Muscle Proteins; Muscles - metabolism; Rats; Rats, Sprague-Dawley; Salmonella enteritidis; Shock, Septic - metabolism; Shock; Animal model; Molecular form; Rat; Rodentia; Biosynthesis; Glucose; Hypoglycemia; Endotoxin; Infection; Vertebrata; Experimental disease; Mammalia; Etiology; Animal; Carrier protein; Quantitative analysis
• ISSN: 0006-291X; 1090-2104
• DOI: 10.1006/bbrc.1994.1131

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.