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Chronic stress inhibits growth and induces proteolytic mechanisms through two different nonoverlapping pathways in the skeletal muscle of a teleost fish

Journal article
Authors C. A. Valenzuela
R. Zuloaga
L. Mercado
Ingibjörg Einarsdottir
Björn Thrandur Björnsson
J. A. Valdes
A. Molina
Published in American Journal of Physiology-Regulatory Integrative and Comparative Physiology
Volume 314
Issue 1
Pages R102-R113
ISSN 0363-6119
Publication year 2018
Published at Department of Biological and Environmental Sciences
Pages R102-R113
Language en
Keywords muscle growth, stress, apoptosis, ubiquitin-proteasome, autophagy, different nutritional statuses, trout oncorhynchus-mykiss, fine, flounder, rainbow-trout, in-vivo, glucocorticoid-receptor, signaling, pathways, gene-expression, hormone, autophagy, Physiology
Subject categories Physiology


Chronic stress detrimentally affects animal health and homeostasis, with somatic growth, and thus skeletal muscle, being particularly affected. A detailed understanding of the underlying endocrine and molecular mechanisms of how chronic stress affects skeletal muscle growth remains lacking. To address this issue, the present study assessed primary (plasma cortisol), secondary (key components of the GH/IGF system, muscular proteolytic pathways, and apoptosis), and tertiary (growth performance) stress responses in fine flounder (Paralichthys adspersus) exposed to crowding chronic stress. Levels of plasma cortisol, glucocorticoid receptor 2 (gr2), and its target genes (klf15 and redd1) mRNA increased significantly only at 4 wk of crowding (P < 0.05). The components of the GH/IGF system, including ligands, receptors, and their signaling pathways, were significantly downregulated at 7 wk of crowding (P < 0.05). Interestingly, chronic stress upregulated the ubiquitin-proteasome pathway and the intrinsic apoptosis pathways at 4wk (P < 0.01), whereas autophagy was only significantly activated at 7 wk (P < 0.05), and meanwhile the ubiquitin-proteasome and the apoptosis pathways returned to control levels. Overall growth was inhibited in fish in the 7-wk chronic stress trial (P < 0.05). In conclusion, chronic stress directly affects muscle growth and downregulates the GH/IGF system, an action through which muscular catabolic mechanisms are promoted by two different and nonoverlapping proteolytic pathways. These findings provide new information on molecular mechanisms involved in the negative effects that chronic stress has on muscle anabolic/catabolic signaling balance.

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