Faculty Collaboration Database

Glucose transporters (GLUT1, 2, & 4) in fat, muscle and liver in a rat model of endotoxic shock. Biochem Biophys Res Commun 1994 Feb 15;198(3):923-7

Date

02/15/1994

Pubmed ID

8117297

DOI

10.1006/bbrc.1994.1131

Scopus ID

2-s2.0-0028225080 (requires institutional sign-in at Scopus site)   8 Citations

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 (123 +/- 35% and 101 +/- 23%, respectively). Septic shock induced hypoglycemia cannot be directly explained by changes in total glucose transporter protein levels.

Author List

Zeller WP, Goto M, Parker J, Cava JR, Gottschalk ME, Filkins JP, Hofmann C

Author

Joseph R. Cava MD, PhD Associate Professor in the Pediatrics department at Medical College of Wisconsin

MESH terms used to index this publication - Major topics in bold

Adipose Tissue
Animals
Blotting, Western
Cell Membrane
Disease Models, Animal
Endotoxins
Glucose Transporter Type 1
Glucose Transporter Type 2
Glucose Transporter Type 4
Liver
Male
Monosaccharide Transport Proteins
Muscle Proteins
Muscles
Rats
Rats, Sprague-Dawley
Salmonella enteritidis
Shock, Septic