Mechanisms of pathogenesis in Listeria monocytogenes infection. 3. Carbohydrate metabolism.
Several enzymes and metabolites concerned with carbohydrate metabolism were examined in mice infected with Listeria monocytogenes. Liver glycogen and glucose decreased parallel to severity of infection. The concentration of glucose in the blood fell to abnormally low levels with a hypoglycemia being most evident at 72 hr. There was a significant decrease in the activity of hepatic uridine diphosphate glucose-glycogen transglucosylase. This decrease in enzymatic activity correlated with the rate of glycogen depletion. Phosphorylase activity declined in a similar fashion, contraindicating enhanced glycogenolysis as the mechanism responsible for glycogen depletion. Although glucose-6-phosphatase decreased throughout the infection period, it did not appear to be the major metabolic defect causing hypoglycemia in Listeria-infected mice. Further distortion of carbohydrate metabolism was indicated by findings of increased levels of pyruvate and lactate in the blood of infected animals.
D000818:Animals; D001786:Blood Glucose / Q000378:metabolism; D050260:Carbohydrate Metabolism; D005947:Glucose / Q000378:metabolism; D005964:Glucosyltransferases / Q000378:metabolism; D007003:Hypoglycemia / Q000209:etiology; D007773:Lactates / Q000097:blood; D008089:Listeria monocytogenes / Q000472:pathogenicity*; D008099:Liver / Q000378:metabolism; D008112:Liver Glycogen / Q000378:metabolism; D051379:Mice; D010744:Phosphoric Monoester Hydrolases / Q000378:metabolism; D011773:Pyruvates / Q000097:blood
D001786:Blood Glucose; D007773:Lactates; D008112:Liver Glycogen; D011773:Pyruvates; D005964:Glucosyltransferases; D010744:Phosphoric Monoester Hydrolases; D005947:Glucose