Vav2 catalysis-dependent pathways contribute to skeletal muscle growth and metabolic homeostasis
Sonia Rodríguez-Fdez,
L. Francisco Lorenzo-Martín,
Isabel Fernández-Pisonero,
Begoña Porteiro,
Christelle Veyrat-Durebex,
Daniel Beiroa,
Omar Al-Massadi,
Antonio Abad,
Carlos Diéguez,
Roberto Coppari,
Rubén Nogueiras and
Xosé R. Bustelo ()
Additional contact information
Sonia Rodríguez-Fdez: CSIC-University of Salamanca
L. Francisco Lorenzo-Martín: CSIC-University of Salamanca
Isabel Fernández-Pisonero: CSIC-University of Salamanca
Begoña Porteiro: University of Santiago de Compostela
Christelle Veyrat-Durebex: University of Geneva
Daniel Beiroa: University of Santiago de Compostela
Omar Al-Massadi: University of Santiago de Compostela
Antonio Abad: CSIC-University of Salamanca
Carlos Diéguez: University of Santiago de Compostela
Roberto Coppari: University of Geneva
Rubén Nogueiras: University of Santiago de Compostela
Xosé R. Bustelo: CSIC-University of Salamanca
Nature Communications, 2020, vol. 11, issue 1, 1-26
Abstract:
Abstract Skeletal muscle promotes metabolic balance by regulating glucose uptake and the stimulation of multiple interorgan crosstalk. We show here that the catalytic activity of Vav2, a Rho GTPase activator, modulates the signaling output of the IGF1- and insulin-stimulated phosphatidylinositol 3-kinase pathway in that tissue. Consistent with this, mice bearing a Vav2 protein with decreased catalytic activity exhibit reduced muscle mass, lack of proper insulin responsiveness and, at much later times, a metabolic syndrome-like condition. Conversely, mice expressing a catalytically hyperactive Vav2 develop muscle hypertrophy and increased insulin responsiveness. Of note, while hypoactive Vav2 predisposes to, hyperactive Vav2 protects against high fat diet-induced metabolic imbalance. These data unveil a regulatory layer affecting the signaling output of insulin family factors in muscle.
Date: 2020
References: Add references at CitEc
Citations:
Downloads: (external link)
https://www.nature.com/articles/s41467-020-19489-z Abstract (text/html)
Related works:
This item may be available elsewhere in EconPapers: Search for items with the same title.
Export reference: BibTeX
RIS (EndNote, ProCite, RefMan)
HTML/Text
Persistent link: https://EconPapers.repec.org/RePEc:nat:natcom:v:11:y:2020:i:1:d:10.1038_s41467-020-19489-z
Ordering information: This journal article can be ordered from
https://www.nature.com/ncomms/
DOI: 10.1038/s41467-020-19489-z
Access Statistics for this article
Nature Communications is currently edited by Nathalie Le Bot, Enda Bergin and Fiona Gillespie
More articles in Nature Communications from Nature
Bibliographic data for series maintained by Sonal Shukla () and Springer Nature Abstracting and Indexing ().