PuSH - Publication Server of Helmholtz Zentrum München: Loss of atrial natriuretic peptide signaling causes insulin resistance, mitochondrial dysfunction, and low endurance capacity.

Information

Clues to quality of journals

Open Access Policy of Helmholtz Association 2016

CC Licencences

Publication Metrics

Navigation

Home

Deutsch

EVA: Electronic Publishing

New EVA Application

Research

Advanced Search

Browse by ...

... HMGU-Authors/Consortia

... Organizational Structure

... Journal

... Publication Type

... Research Data

... Arbeitsgruppen

... Publication Year

Publication overview

Statistics

Statistics (last 5 years)

OA Publications

Publish

Submit Publication

Import publication from...

...EVA

Report missing publication

Highlights

Support & Contact

Contact persons

Help

Data protection

Helmholtz Open Science

JANE Journal Estimator

SHERPA/RoMEO

DOAJ

Export:

Text

Endnote (RIS) BIB

BibTeX

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)

Publ. Version/Full Text

DOI

PMC

	Free by publisher

Abstract
Metrics
Extra information

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.

Impact Factor

Scopus SNIP

Altmetric

11.700

0.000