Hepatic glycogen synthesis on carbohydrate re-feeding after starvation. A regulatory role for pyruvate dehydrogenase in liver and extrahepatic tissues.
Glucose administration to 48 h-starved rats increased hepatic glucose, lactate, pyruvate and glycogen concentrations and re-activated PDH (pyruvate dehydrogenase complex) in kidney, but not in heart or liver. Dichloroacetate together with glucose re-activated PDH in all three tissues, decreased hepatic lactate and pyruvate concentrations and impaired glycogen resynthesis. Thus on re-feeding, delayed PDH re-activation is important for provision of precursors for hepatic glyconeogenesis.
D000818:Animals; D003999:Dichloroacetic Acid / Q000494:pharmacology; D004040:Dietary Carbohydrates / Q000494:pharmacology*; D005227:Fatty Acids / Q000096:biosynthesis; D005260:Female; D005502:Food; D005943:Gluconeogenesis / Q000187:drug effects; D005947:Glucose / Q000494:pharmacology; D007657:Ketone Bodies / Q000096:biosynthesis; D008099:Liver / Q000187:drug effects / Q000378:metabolism*; D008112:Liver Glycogen / Q000096:biosynthesis*; D011768:Pyruvate Dehydrogenase Complex / Q000378:metabolism*; D051381:Rats; D011919:Rats, Inbred Strains; D013217:Starvation / Q000378:metabolism
D004040:Dietary Carbohydrates; D005227:Fatty Acids; D007657:Ketone Bodies; D008112:Liver Glycogen; D011768:Pyruvate Dehydrogenase Complex; D003999:Dichloroacetic Acid; D005947:Glucose