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.
D000818:Animals; D003545:Cysteine / Q000494:pharmacology; D005260:Female; D005943:Gluconeogenesis / Q000187:drug effects*; D008099:Liver / Q000187:drug effects / Q000378:metabolism*; D008112:Liver Glycogen / Q000378:metabolism*; D009539:Nicotinic Acids / Q000494:pharmacology*; D010729:Phosphoenolpyruvate Carboxykinase (GTP) / Q000378:metabolism; D011770:Pyruvate Kinase / Q000378:metabolism*; D051381:Rats; D013217:Starvation
D008112:Liver Glycogen; D009539:Nicotinic Acids; D011770:Pyruvate Kinase; D010729:Phosphoenolpyruvate Carboxykinase (GTP); D003545:Cysteine