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Endothelial nitric oxide synthase (NOS) deficiency affects energy metabolism pattern in murine oxidative skeletal muscle.
Biochem J. 2002 Nov 15; 368(Pt 1):341-7.BJ

Abstract

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.

Authors+Show Affiliations

Cardiologie Cellulaire et Moléculaire U-446 INSERM, Faculté de Pharmacie, Université Paris-Sud, Châtenay-Malabry, 92296, France.No affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

12123418

Citation

Momken, Iman, et al. "Endothelial Nitric Oxide Synthase (NOS) Deficiency Affects Energy Metabolism Pattern in Murine Oxidative Skeletal Muscle." The Biochemical Journal, vol. 368, no. Pt 1, 2002, pp. 341-7.
Momken I, Fortin D, Serrurier B, et al. Endothelial nitric oxide synthase (NOS) deficiency affects energy metabolism pattern in murine oxidative skeletal muscle. Biochem J. 2002;368(Pt 1):341-7.
Momken, I., Fortin, D., Serrurier, B., Bigard, X., Ventura-Clapier, R., & Veksler, V. (2002). Endothelial nitric oxide synthase (NOS) deficiency affects energy metabolism pattern in murine oxidative skeletal muscle. The Biochemical Journal, 368(Pt 1), 341-7.
Momken I, et al. Endothelial Nitric Oxide Synthase (NOS) Deficiency Affects Energy Metabolism Pattern in Murine Oxidative Skeletal Muscle. Biochem J. 2002 Nov 15;368(Pt 1):341-7. PubMed PMID: 12123418.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Endothelial nitric oxide synthase (NOS) deficiency affects energy metabolism pattern in murine oxidative skeletal muscle. AU - Momken,Iman, AU - Fortin,Dominique, AU - Serrurier,Bernard, AU - Bigard,Xavier, AU - Ventura-Clapier,Renée, AU - Veksler,Vladimir, PY - 2002/07/17/accepted PY - 2002/07/17/revised PY - 2002/04/15/received PY - 2002/7/19/pubmed PY - 2002/12/28/medline PY - 2002/7/19/entrez SP - 341 EP - 7 JF - The Biochemical journal JO - Biochem J VL - 368 IS - Pt 1 N2 - 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. SN - 0264-6021 UR - https://www.unboundmedicine.com/medline/citation/12123418/Endothelial_nitric_oxide_synthase__NOS__deficiency_affects_energy_metabolism_pattern_in_murine_oxidative_skeletal_muscle_ L2 - https://portlandpress.com/biochemj/article-lookup/doi/10.1042/BJ20020591 DB - PRIME DP - Unbound Medicine ER -