Summary
Acetate, at a concentration of 5 or 10 mM, stimulated gluconeogenesis from lactate (10 mM) to the extent of 40% in the perfused, 24-hr. fasted rat liver. The rate of acetoacetate production was increased three-fold when acetate was present alone at a concentration of 5 or 10 mM. This increased ketogenesis was completely suppressed by lactate.
No increase in liver acetyl-CoA was observed during acetate-, oleate- or glucagon-stimulated gluconeogenesis. These data indicate that acetyl-CoA activation of pyruvic carboxylase can play no major role in the increased gluconeogenesis or ketogenesis under fasting conditions. By using lactate as substrate, one can exclude a „sparing effect“ as a possible reason for the observed effects. Since an increase in medium β-hydroxybutyrate/acetoacetate ratio occurs during oleate- and glucagon-stimulated gluconeogenesis, an increase in NADH provision for the triose phosphate dehydrogenase reaction can be a possible explanation for the observed stimulation.
Supported by the Deutsche Forschungsgemeinschaft, Bad Godesberg, Germany.
NATO Postdoctoral Fellow 1966–1967.
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Menahan, L.A., Ross, B.D., Wieland, O. (1968). Studies on the Mechanism of Fatty Acid and Glucagon Stimulated Gluconeogenesis in the Perfused Rat Liver. In: Staib, W., Scholz, R. (eds) Stoffwechsel der isoliert perfundierten Leber. Springer, Berlin, Heidelberg. https://doi.org/10.1007/978-3-662-39856-2_12
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