Abstract
Summary
An in vitro model employing homogenates of mouse liver was developed to study the effects of endotoxin from Sal-monella typhimurium on glycogen metabolism. Studies with this model showed that endotoxin can act directly and that the accelerated loss of glycogen was not related to an increased release of epinephrine. These results indicated that endotoxin acts on the glycogenolytic enzymes.
Endotoxin from Serratia marcescens also caused a rapid loss of glycogen in the in vitro model but was not as effective as the typhimurium endotoxin. Potassium methylate treatment of the S. marcescens endotoxin did not eliminate the ability of the endotoxin to deplete glycogen.
This research was supported by National Science Foundation Grant GB-8363. Peter Zwadyk was the recipient of an NDEA IV fellowship.
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