The regulation of the biosynthesis of ubiquinone in the rat.
The urinary excretion of p-hydroxybenzoate was not altered by ubiquinone feeding, but, although decreased considerably, was not eliminated in protein deficiency. The incorporation of p-hydroxy[U-14C]benzaldehyde into ubiquinone in vivo increased in cold-exposed and p-chlorophenoxyisobutyrate (clofibrate)-fed rats, and these changes were parallel with the changes in the incorporation of [2-14C]mevalonate under these conditions. Starvation, cholesterol feeding and cholic acid feeding resulted in the decreased incorporation of p-hydroxy[U-14C]benzaldehyde into ubiquinone, confirming the decreased ubiquinone synthesis. Feeding exogenous ubiquinone increased the hepatic ubiquinone concentration, but did not cause any decrease in the incorporation of p-hydroxy[U-14C]benzaldehyde into ubiquinone, indicating the absence of a feedback control.
D000818:Animals; D001547:Benzaldehydes / Q000378:metabolism; D002994:Clofibrate / Q000494:pharmacology; D003080:Cold Temperature; D005246:Feedback; D062385:Hydroxybenzoates / Q000652:urine; D066298:In Vitro Techniques; D008099:Liver / Q000378:metabolism; D008297:Male; D008798:Mevalonic Acid / Q000378:metabolism; D011488:Protein Deficiency / Q000378:metabolism; D051381:Rats; D014451:Ubiquinone / Q000096:biosynthesis*
D001547:Benzaldehydes; D062385:Hydroxybenzoates; D014451:Ubiquinone; D002994:Clofibrate; D008798:Mevalonic Acid