PuSH - Publication Server of Helmholtz Zentrum München

Engeli, S.* ; Birkenfeld, A.L.* ; Badin, P.M.* ; Bourlier, V.* ; Louche, K.* ; Viguerie, N.* ; Thalamas, C.* ; Montastier, E.* ; Larrouy, D.* ; Harant, I.* ; de Glisezinski, I.* ; Lieske, S.* ; Reinke, J.* ; Beckmann, B.* ; Langin, D.* ; Jordan, J.* ; Moro, C.*

Natriuretic peptides enhance the oxidative capacity of human skeletal muscle.

J. Clin. Invest. 122, 4675-4679 (2012)
DOI PMC
Open Access Gold as soon as Publ. Version/Full Text is submitted to ZB.
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 PPARγ coactivator-1α (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-1α 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.
Impact Factor
Scopus SNIP
Scopus
Cited By
Altmetric
0.000
3.368
109
Tags
Annotations
Special Publikation
Hide on homepage

Edit extra information
Edit own tags
Private
Edit own annotation
Private
Hide on publication lists
on hompage
Mark as special
publikation
Publication type Article: Journal article
Document type Scientific Article
Language english
Publication Year 2012
HGF-reported in Year 0
ISSN (print) / ISBN 0021-9738
e-ISSN 1558-8238
Quellenangaben Volume: 122, Issue: 12, Pages: 4675-4679 Article Number: , Supplement: ,
Publisher American Society of Clinical Investigation
Reviewing status Peer reviewed
Institute(s) Institute of Pancreatic Islet Research (IPI)
PubMed ID 23114600
Erfassungsdatum 2012-12-31