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Carper, D.* ; Lac, M.* ; Coue, M.* ; Labour, A.* ; Märtens, A.* ; Banda, J.A.A.* ; Mazeyrie, L.* ; Mechta, M.* ; Ingerslev, L.R.* ; Elhadad, M.A. ; Petit, J.V.* ; Maslo, C.* ; Monbrun, L.* ; Del Carmine, P.* ; Sainte-Marie, Y.* ; Bourlier, V.* ; Laurens, C.* ; Mithieux, G.* ; Joanisse, D.R.* ; Coudray, C.* ; Feillet-Coudray, C.* ; Montastier, E.* ; Viguerie, N.* ; Tavernier, G.* ; Waldenberger, M. ; Peters, A. ; Wang-Sattler, R. ; Adamski, J. ; Suhre, K.* ; Gieger, C. ; Kastenmüller, G. ; Illig, T.* ; Lichtinghagen, R.* ; Seissler, J.* ; Mounier, R.* ; Hiller, K.* ; Jordan, J.* ; Barrès, R.* ; Kuhn, M.* ; Pesta, D.* ; Moro, C.*

Loss of atrial natriuretic peptide signaling causes insulin resistance, mitochondrial dysfunction, and low endurance capacity.

Sci. Adv. 10:eadl4374 (2024)
Verlagsversion DOI PMC
Open Access Gold
Creative Commons Lizenzvertrag
Type 2 diabetes (T2D) and obesity are strongly associated with low natriuretic peptide (NP) plasma levels and a down-regulation of NP guanylyl cyclase receptor-A (GCA) in skeletal muscle and adipose tissue. However, no study has so far provided evidence for a causal link between atrial NP (ANP)/GCA deficiency and T2D pathogenesis. Here, we show that both systemic and skeletal muscle ANP/GCA deficiencies in mice promote metabolic disturbances and prediabetes. Skeletal muscle insulin resistance is further associated with altered mitochondrial function and impaired endurance running capacity. ANP/GCA-deficient mice exhibit increased proton leak and reduced content of mitochondrial oxidative phosphorylation proteins. We further show that GCA is related to several metabolic traits in T2D and positively correlates with markers of oxidative capacity in human skeletal muscle. Together, these results indicate that ANP/GCA signaling controls muscle mitochondrial integrity and oxidative capacity in vivo and plays a causal role in the development of prediabetes.
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Publikationstyp Artikel: Journalartikel
Dokumenttyp Wissenschaftlicher Artikel
Korrespondenzautor
ISSN (print) / ISBN 2375-2548
e-ISSN 2375-2548
Zeitschrift Science Advances
Quellenangaben Band: 10, Heft: 41, Seiten: , Artikelnummer: eadl4374 Supplement: ,
Verlag American Association for the Advancement of Science (AAAS)
Verlagsort Washington, DC [u.a.]
Nichtpatentliteratur Publikationen
Begutachtungsstatus Peer reviewed
Institut(e) Institute of Epidemiology II (EPI2)
Institute of Experimental Genetics (IEG)
Institute of Computational Biology (ICB)