Titre
Endothelial nitric oxide synthase (eNOS) knockout mice have defective mitochondrial beta-oxidation
Type
article
Institution
UNIL/CHUV/Unisanté + institutions partenaires
Périodique
Auteur(s)
Le Gouill, E.
Auteure/Auteur
Jimenez, M.
Auteure/Auteur
Binnert, C.
Auteure/Auteur
Jayet, P. Y.
Auteure/Auteur
Thalmann, S.
Auteure/Auteur
Nicod, P.
Auteure/Auteur
Scherrer, U.
Auteure/Auteur
Vollenweider, P.
Auteure/Auteur
Liens vers les personnes
Liens vers les unités
ISSN
1939-327X
Statut éditorial
Publié
Date de publication
2007-11
Volume
56
Numéro
11
Première page
2690
Dernière page/numéro d’article
6
Notes
Journal Article
Research Support, Non-U.S. Gov't --- Old month value: Nov
Research Support, Non-U.S. Gov't --- Old month value: Nov
Résumé
OBJECTIVE: Recent observations indicate that the delivery of nitric oxide by endothelial nitric oxide synthase (eNOS) is not only critical for metabolic homeostasis, but could also be important for mitochondrial biogenesis, a key organelle for free fatty acid (FFA) oxidation and energy production. Because mice deficient for the gene of eNOS (eNOS(-/-)) have increased triglycerides and FFA levels, in addition to hypertension and insulin resistance, we hypothesized that these knockout mice may have decreased energy expenditure and defective beta-oxidation. RESEARCH DESIGN AND METHODS: Several markers of mitochondrial activity were assessed in C57BL/6J wild-type or eNOS(-/-) mice including the energy expenditure and oxygen consumption by indirect calorimetry, in vitro beta-oxidation in isolated mitochondria from skeletal muscle, and expression of genes involved in fatty acid oxidation. RESULTS: eNOS(-/-) mice had markedly lower energy expenditure (-10%, P < 0.05) and oxygen consumption (-15%, P < 0.05) than control mice. This was associated with a roughly 30% decrease of the mitochondria content (P < 0.05) and, most importantly, with mitochondrial dysfunction, as evidenced by a markedly lower beta-oxidation of subsarcolemmal mitochondria in skeletal muscle (-30%, P < 0.05). Finally, impaired mitochondrial beta-oxidation was associated with a significant increase of the intramyocellular lipid content (30%, P < 0.05) in gastrocnemius muscle. CONCLUSIONS: These data indicate that elevated FFA and triglyceride in eNOS(-/-) mice result in defective mitochondrial beta-oxidation in muscle cells.
PID Serval
serval:BIB_CF2D92A4279E
PMID
Open Access
Oui
Date de création
2008-01-25T13:00:20.983Z
Date de création dans IRIS
2025-05-21T00:21:34Z