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 |
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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: |
Male
endocrine system medicine.medical_specialty medicine.drug_class Respiratory chain Medicine (miscellaneous) Adipose tissue Mitochondria Liver Citrate (si)-Synthase Oxidative phosphorylation Mitochondrion Biology and respiratory chain complexes Article Dexamethasone Oxidative Phosphorylation Rats Sprague-Dawley Eating Gastrocnemius muscle Oxygen Consumption Glutamates Internal medicine polycyclic compounds medicine mitochondrion Animals Muscle Skeletal Glucocorticoids Nutrition and Dietetics Body Weight Succinates Organ Size Nutrition Disorders Rats [SDV.AEN] Life Sciences [q-bio]/Food and Nutrition Endocrinology Adipose Tissue Toxicity Corticosteroid glucocorticoid Energy Metabolism hormones hormone substitutes and hormone antagonists medicine.drug |
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 |
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