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

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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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Author notes

  1. Fermín Sánchez-Medina

    Present address: Departamento de Bioquimica, Universidad de Granada, Rector López Argueta 4, Granada, Spain

Authors and Affiliations

  1. Departamento de Bioquimica y Biologia Molecular, Facultad de Ciencias, Universidad Autónoma de Madrid, Canto Blanco, Madrid-34, Spain

    Francisco J. Moreno, Manuel Benito, Fermín Sánchez-Medina, José M. Medina & Federico Mayor

Authors
  1. Francisco J. Moreno
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  2. Manuel Benito
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  3. Fermín Sánchez-Medina
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  4. José M. Medina
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  5. Federico Mayor
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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

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