Decreased glycogen mobilization during ochratoxicosis in broiler chickens.
Graded doses of pure ochratoxin A (0, 0.5, 1.0, 2.0, 4.0, and 8.0 microgram of toxin per g of feed) were incorporated into a commercial diet which was fed to chickens from hatching to 3 weeks of age, at which time the experiments were terminated. Liver glycogen levels were elevated significantly (P less than 0.05) by 4.0 and 8.0 microgram/g but not lower doses. Glucagon stimulation of glycogen mobilization was inhibited at the same concentrations. Histopathological examination revealed cytoplasmic but not nuclear deposits of glycogen in cells at the periphery of liver lobes. These data demonstrated that ochratoxin inhibited glycogenolysis. Impaired ability to generate glucose from glycogen could account for the increased susceptibility to cold stress previously reported to occur in ochratoxicosis. Based on present and prior observations, it seems possible that ochratoxin induces a syndrome which mimics the glycogen storage disease of type X which is caused by a deficiency in the cyclic AMP-dependent enzyme of the glycogenolytic enzymatic cascade.
D000818:Animals; D001786:Blood Glucose / Q000378:metabolism; D001831:Body Temperature; D002645:Chickens; D003624:Darkness; D005934:Glucagon / Q000494:pharmacology; D008099:Liver / Q000187:drug effects / Q000378:metabolism; D008112:Liver Glycogen / Q000378:metabolism*; D008297:Male; D009793:Ochratoxins / Q000506:poisoning*; D013390:Succinylcholine / Q000494:pharmacology
D001786:Blood Glucose; D008112:Liver Glycogen; D009793:Ochratoxins; D005934:Glucagon; D013390:Succinylcholine