Summary
Nicotinic acid administration, which depletes liver glycogen, leads to an increase of both pyruvate kinase L and phosphoenolpyruvate 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.
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Moreno, F.J., Benito, M., Sánchez-Medina, F. et al. Pyruvate kinase activity and gluconeogenesis in RAT liver after glycogen depletion with nicotinic acid. Mol Cell Biochem 13, 89–93 (1976). https://doi.org/10.1007/BF01837058
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DOI: https://doi.org/10.1007/BF01837058