Journal
JOURNAL OF CLINICAL INVESTIGATION
Volume 122, Issue 12, Pages 4675-4679Publisher
AMER SOC CLINICAL INVESTIGATION INC
DOI: 10.1172/JCI64526
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Funding
- National Research Agency [ANR-09-JCJC-0019-01, ANR-09-GENO-0018-01]
- European Federation for the Study of Diabetes/Novo Nordisk
- Inserm DHOS Recherche Translationnelle
- Glaxo Smith Kline
- Deutsche Forschungsgemeinschaft [Bl 1292/4-1]
- German Hypertension League
- European Commission (SICA-HF) [FP7 241558]
- [AOL-0816302 Hopitaux de Toulouse]
- [JO 284/5-2]
- Agence Nationale de la Recherche (ANR) [ANR-09-JCJC-0019, ANR-09-GENO-0018] Funding Source: Agence Nationale de la Recherche (ANR)
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Cardiac natriuretic peptides (NP) are major activators of human fat cell lipolysis and have recently been shown to control brown fat thermogenesis. Here, we investigated the physiological role of NP on the oxidative metabolism of human skeletal muscle. NP receptor type A (NPRA) gene expression was positively correlated to mRNA levels of PPAR gamma coactivator-1 alpha (PGC1A) and several oxidative phosphorylation (OXPHOS) genes in human skeletal muscle. Further, the expression of NPRA, PGC1A, and OXPHOS genes was coordinately upregulated in response to aerobic exercise training in human skeletal muscle. In human myotubes, NP induced PGC-1 alpha and mitochondrial OXPHOS gene expression in a cyclic GMP-dependent manner. NP treatment increased OXPHOS protein expression, fat oxidation, and maximal respiration independent of substantial changes in mitochondrial proliferation and mass. Treatment of myotubes with NP recapitulated the effect of exercise training on muscle fat oxidative capacity in vivo. Collectively, these data show that activation of NP signaling in human skeletal muscle enhances mitochondrial oxidative metabolism and fat oxidation. We propose that NP could contribute to exercise training-induced improvement in skeletal muscle fat oxidative capacity in humans.
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