Hepatic carbon flux after re-feeding in the glycogen-storage-disease (gsd/gsd) rat.
In this study we utilized the phosphorylase b kinase-deficient (gsd/gsd) rat as a model of hepatic substrate utilization where there is a constraint on glycogenesis imposed by the maintenance of high glycogen concentrations. Glucose re-feeding of 48 h-starved gsd/gsd rats led to suppression of hepatic glucose output. In contrast with the situation in normal rats, activation of the pyruvate dehydrogenase complex and lipogenesis was observed. It is suggested that impeding glycogenic flux may divert substrate into lipogenesis, possibly via activation of the pyruvate dehydrogenase complex.
D000818:Animals; D004789:Enzyme Activation; D005230:Fatty Acids, Nonesterified / Q000097:blood; D005260:Female; D005502:Food; D005947:Glucose / Q000378:metabolism*; D006008:Glycogen Storage Disease / Q000378:metabolism*; D007657:Ketone Bodies / Q000097:blood; D008055:Lipids / Q000096:biosynthesis*; D008099:Liver / Q000201:enzymology / Q000378:metabolism*; D008112:Liver Glycogen / Q000096:biosynthesis; D011768:Pyruvate Dehydrogenase Complex / Q000378:metabolism; D051381:Rats; D011919:Rats, Inbred Strains; D013217:Starvation / Q000378:metabolism
D005230:Fatty Acids, Nonesterified; D007657:Ketone Bodies; D008055:Lipids; D008112:Liver Glycogen; D011768:Pyruvate Dehydrogenase Complex; D005947:Glucose