These tools will no longer be maintained as of December 31, 2024. Archived website can be found here. PubMed4Hh GitHub repository can be found here. Contact NLM Customer Service if you have questions.


Pubmed for Handhelds

PUBMED FOR HANDHELDS

Search MEDLINE/PubMed

  • Title: Response of hepatic mitochondrial and peroxisomal beta-oxidation to increasing palmitate concentrations in piglets.
    Author: Yu XX, Drackley JK, Odle J, Lin X.
    Journal: Biol Neonate; 1997; 72(5):284-92. PubMed ID: 9395839.
    Abstract:
    Responses of total, mitochondrial, and peroxisomal beta-oxidation to increasing [1-14C]-palmitate concentrations (0.02-1.0 mM) were measured in liver homogenates from neonatal pigs. Incubations were conducted in the absence (total beta-oxidation) or presence (peroxisomal beta-oxidation) of antimycin A and rotenone; mitochondrial beta-oxidation was calculated as total minus peroxisomal oxidation. Total and mitochondrial beta-oxidations were maximized at a palmitate concentration of 0.05 mM, whereas peroxisomal beta-oxidation was maximized at 0.50 mM palmitate. Across concentrations, peroxisomal beta-oxidation contributed 40-47% of total beta-oxidation. An increased rate of CO2 production and a greater ratio of CO2 production to total mitochondrial beta-oxidation as palmitate concentration increased suggested that the limited capacity for mitochondrial beta-oxidation was attributable primarily to limited ketogenic capacity. Comparative observations in liver from adult rats showed that peroxisomal beta-oxidation was maximized at 0.1 mM palmitate, but total and mitochondrial beta-oxidation rates were not maximized even at 1 mM palmitate. At 1 mM palmitate, peroxisomal beta-oxidation was 20% of total beta-oxidation in adult rats and 37% in adult pigs. Therefore, the contribution of peroxisomal beta-oxidation to total beta-oxidation is highly dependent on substrate concentration and appears to be greater in adult pigs than in adult rats. The greater proportional contribution of peroxisomal beta-oxidation in piglet liver might act as a compensatory mechanism for piglets to oxidize milk fatty acids.
    [Abstract] [Full Text] [Related] [New Search]