Regulation of fatty acid oxidation by adenosine at the level of its extramitochondrial activation
Por:
de Sánchez V.C., Grau P.A., Jiménez B., Villalobos-M R., Piña E.
Publicada:
1 ene 1977
Resumen:
Conditions for the conversion of palmitate into CO2 and acetoacetate by liver homogenates and isolated liver mitochondria are described. In this system, using liver homogenates, adenosine inhibited the conversion of palmitate into CO2 and acetoacetate. The inhibition was not observed if the homogenate was substituted by mitochondria or if palmitate was substituted by palmitoyl CoA or palmitoyl carnitine. Intraperitoneal injection of adenosine produced a marked decrease in the level of acetoacetate and ?-hydroxybutyrate in plasma, without changing the concentration of serum free fatty acids. Thus, the nucleoside depressed in vivo the oxidation of long chain fatty acids in liver by inhibiting the extramitochondrial acyl CoA synthase(s). The paramount importance of the extramitochondrial activation of fatty acids as a key control in their oxidation and in the production of ketone bodies is discussed. © 1977.
Filiaciones:
de Sánchez V.C.:
Departamento de Biología Experimental, Instituto de Biología Universidad Nacional Autónoma de México, México 20, D. F. USA
Grau P.A.:
Departamento de Biología Experimental, Instituto de Biología Universidad Nacional Autónoma de México, México 20, D. F. USA
Jiménez B.:
Departamento de Biología Experimental, Instituto de Biología Universidad Nacional Autónoma de México, México 20, D. F. USA
Villalobos-M R.:
Departamento de Biología Experimental, Instituto de Biología Universidad Nacional Autónoma de México, México 20, D. F. USA
Piña E.:
Departamento de Biología Experimental, Instituto de Biología Universidad Nacional Autónoma de México, México 20, D. F. USA
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