Glycolytic enzyme activities in normal and diabetic dog livers during endotoxic shock
- 1 January 1981
- journal article
- research article
- Published by American Physiological Society in American Journal of Physiology-Regulatory, Integrative and Comparative Physiology
- Vol. 240 (1) , R10-R15
- https://doi.org/10.1152/ajpregu.1981.240.1.r10
Abstract
The influences of Escherichia coli endotoxin administration on the levels of key glycolytic enzymes in the normal and alloxan-diabetic dog liver were studied, and the results were correlated with changes in plasma glucose concentrations. Plasma glucose concentrations in normal dogs were increased at 1 h followed by a decrease at 2 h (and thereafter) following endotoxin administration. In diabetic dogs, plasma glucose levels remained elevated (> 250 mg/100 ml) during the 4-h period after endotoxin injection. Glucokinase activity was decreased by 46-32% at 2-4 h following endotoxin injection in normal dogs. In diabetic dogs, glucokinase activity was decreased by 55% and it was not affected by endotoxin administration. Hexokinase activity was increased by 126% at 2 h postendotoxin in normal dogs. Hexokinase activity was also stimulated in diabetic postendotoxic dogs (diabetes alone had no effect on hexokinase activity). Phosphofructokinase activity was decreased by 66-43% at 2-4 h following endotoxin injection. In diabetic dogs, phosphofructokinase activity was decreased by 56% and it was not affected by endotoxin injection. Pyruvate kinase activity was stimulated by 132% at 2 h and returned to the control value 4 h postendotoxin. The stimulatory effect of endotoxin on pyruvate kinase was of longer duration in diabetic postendotoxic dogs (diabetes alone had no effect on the enzyme activity). The specific effects of endotoxin on hepatic key glycolytic enzymes apparently are not mediated by certain substrates and hormones. However, it is possible that combinations of changes in substrates and hormones may be associated with the effects of endotoxin.This publication has 10 references indexed in Scilit:
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