Pyruvate kinase activity and gluconeogenesis in rat liver after glycogen depletion with nicotinic acid

Nicotinic acid administration, which depletes liver glycogen, leads to an increase of both pyruvate kinase L and phosphoenolypyruvate carboxykinase in liver by a factor of nearly two. The former is not prevented by either cycloheximide or actinomycin D. L-Cysteine, an allosteric inhibitor of pyruvate kinase L, favors gluconeogenesis from lactate in both nicotinic acid treated and starved animals.