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.
