Endothelial nitric oxide synthase (NOS) deficiency affects energy metabolism pattern in murine oxidative skeletal muscle (original) (raw)
Research Article| November 15 2002
∗Cardiologie Cellulaire et Moléculaire U-446 INSERM, Faculté de Pharmacie, Université Paris-Sud, Châtenay-Malabry, 92296, France,
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∗Cardiologie Cellulaire et Moléculaire U-446 INSERM, Faculté de Pharmacie, Université Paris-Sud, Châtenay-Malabry, 92296, France,
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†Unité de Bioénergétique, CRSSA, La Tronche Cedex, 38702, France
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†Unité de Bioénergétique, CRSSA, La Tronche Cedex, 38702, France
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∗Cardiologie Cellulaire et Moléculaire U-446 INSERM, Faculté de Pharmacie, Université Paris-Sud, Châtenay-Malabry, 92296, France,
Search for other works by this author on:
∗Cardiologie Cellulaire et Moléculaire U-446 INSERM, Faculté de Pharmacie, Université Paris-Sud, Châtenay-Malabry, 92296, France,
Search for other works by this author on:
Publisher: Portland Press Ltd
Received: April 15 2002
Revision Received: July 17 2002
Accepted: July 17 2002
Accepted Manuscript online: July 17 2002
Online ISSN: 1470-8728
Print ISSN: 0264-6021
The Biochemical Society, London ©2002
2002
Biochem J (2002) 368 (1): 341–347.
Revision Received:
July 17 2002
Accepted Manuscript online:
July 17 2002
Oxidative capacity of muscles correlates with capillary density and with microcirculation, which in turn depend on various regulatory factors, including NO generated by endothelial nitric oxide synthase (eNOS). To determine the role of eNOS in patterns of regulation of energy metabolism in various muscles, we studied mitochondrial respiration in situ in saponin-permeabilized fibres as well as the energy metabolism enzyme profile in the cardiac, soleus (oxidative) and gastrocnemius (glycolytic) muscles isolated from mice lacking eNOS (eNOS-/-). In soleus muscle, the absence of eNOS induced a marked decrease in both basal mitochondrial respiration without ADP (-32%; P<0.05) and maximal respiration in the presence of ADP (-29%; P<0.05). Furthermore, the eNOS-/- soleus muscle showed a decrease in total creatine kinase (-29%; P<0.05), citrate synthase (-31%; P<0.01), adenylate kinase (-27%; P<0.05), glyceraldehyde-3-phosphate dehydrogenase (-43%; P<0.01) and pyruvate kinase (-26%; P<0.05) activities. The percentage of myosin heavy chains I (slow isoform) was significantly increased from 24.3±1.5% in control to 30.1±1.1% in eNOS-/- soleus muscle (P<0.05) at the expense of a slight non-significant decrease in the three other (fast) isoforms. Besides, eNOS-/- soleus showed a 28% loss of weight. Interestingly, we did not find differences in any parameters in cardiac and gastrocnemius muscles compared with respective controls. These results show that eNOS knockout has an important effect on muscle oxidative capacity as well on the activities of energy metabolism enzymes in oxidative (soleus) muscle. The absence of such effects in cardiac and glycolytic (gastrocnemius) muscle suggests a specific role for eNOS-produced NO in oxidative skeletal muscle.
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The Biochemical Society, London ©2002
2002
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