Peroxisomal beta-oxidation from endogenous substrates. Demonstration through H2O2 production in the unanaesthetized mouse.
A system was developed in which it is possible to detect in vivo changes in hepatic H2O2 production, using a combination of the catalase inhibitor, 3-amino-1,2,4-triazole and methanol. In mice, starvation significantly increases hepatic H2O2 production and plasma non-esterified fatty acid concentrations. Short-term refeeding after a 24 h starvation period brings H2O2 production and plasma non-esterified fatty acid concentration back to normal in 3h. Administration of insulin 24 h after the onset of starvation normalizes H2O2 production in less than 2h and decreases non-esterified fatty acid concentration below normal values. The suppression by insulin of H2O2 production, as well as its coherence with plasma non-esterified fatty acid concentration, indicate that increased H2O2 production in starved mice reflects peroxisomal beta-oxidation.
D000640:Amitrole / Q000494:pharmacology; D000818:Animals; D002374:Catalase / Q000378:metabolism; D005230:Fatty Acids, Nonesterified / Q000097:blood; D006861:Hydrogen Peroxide / Q000378:metabolism*; D007328:Insulin / Q000494:pharmacology; D008099:Liver / Q000187:drug effects / Q000378:metabolism*; D008297:Male; D000432:Methanol / Q000494:pharmacology; D051379:Mice; D008807:Mice, Inbred BALB C; D008830:Microbodies / Q000187:drug effects / Q000378:metabolism*; D010084:Oxidation-Reduction; D013217:Starvation / Q000378:metabolism
D005230:Fatty Acids, Nonesterified; D007328:Insulin; D006861:Hydrogen Peroxide; D002374:Catalase; D000432:Methanol; D000640:Amitrole