Mitochondrial energy metabolism in a model of undernutrition induced by dexamethasone

Autor: Patrick Ritz, Gilles Simard, Jean-François Dumas, Damien Roussel, Olivier Douay, Françoise Foussard, Yves Malthièry
Přispěvatelé: Expression des gènes des phosphorylations oxydatives mitochondriales. Maintenance de l'ADN MT, Institut National de la Santé et de la Recherche Médicale (INSERM), Financement Mairie d'Angers, Dumas, Jean-François
Rok vydání: 2003
Předmět:
Zdroj: Br J Nutr
Br J Nutr, 2003, 90 (5), pp.969-77
ISSN: 1475-2662
0007-1145
DOI: 10.1079/bjn2003980
Popis: The present investigation was undertaken to evaluate whether mitochondrial energy metabolism is altered in a model of malnutrition induced by dexamethasone (DEX) treatment (1·5mg/kg per d for 5d). The gastrocnemius and liver mitochondria were isolated from DEX-treated, pair-fed (PF) and control (CON) rats. Body weight was reduced significantly more in the DEX-treated group (−16%) than in the PF group (−9%). DEX treatment increased liver mass (+59%v.PF, +23%v. CON) and decreased gastrocnemius mass. Moreover, in DEX-treated rats, liver mitochondria had an increased rate of non-phosphorylative O2consumption with all substrates (approximately +42%). There was no difference in enzymatic complex activities in liver mitochondria between rat groups. Collectively, these results suggest an increased proton leak and/or redox slipping in the liver mitochondria of DEX-treated rats. In addition, DEX decreased the thermodynamic coupling and efficiency of oxidative phosphorylation. We therefore suggest that this increase in the proton leak and/or redox slip in the liver is responsible for the decrease in the thermodynamic efficiency of energy conversion. In contrast, none of the variables of energy metabolism determined in gastrocnemius mitochondria was altered by DEX treatment. Therefore, it appears that DEX specifically affects mitochondrial energy metabolism in the liver.
Databáze: OpenAIRE