Microarray analysis of the white muscle transcriptome in feed deprived rainbow trout treated with insulin-like growth factor-I
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ABSTRACT: Treatment with insulin-like growth factor-I (IGF-I) during feed deprivation attenuates the weight loss response in both mammals and fish, therefore the reduction in plasma IGF-I concentrations during fasting likely serves as a signal that contributes to the catabolic response. To better understand the physiological mechanisms responsible for this effect rainbow trout were administered IGF-I during a 2 wk period of feed deprivation and changes in gene expression in white muscle were determined using microarray analysis. Weight loss was reduced by 15% (P<0.05) in IGF-I treated fish. A total of 440 transcripts were identified as differentially regulated (P<0.05) between saline and IGF-I treated fish. Genes related to protein degradation were down-regulated and included protease and peptidase genes and genes involved in ubiquitin-proteasome and cathepsin-mediated proteolytic pathways. IGF-I increased expression of myosin binding protein H and coronin-1C, while decreasing expression of other myofibrillar and cytoskeleton-associated genes like troponin-C and parvalbumin-2. Polyadenylate-binding protein 2, a transcription factor that positively regulates myoD and myogenin expression, was upregulated with IGF-I treatment. Additional genes that were differentially regulated are associated with lipid and carbohydrate metabolism, mitochondrial biogenesis and electron transport, gene transcription, signal transduction and regulation of apoptosis. In summary, these data suggest that IGF-I plays a central role in regulating protein degradation, especially via the ubiquitin-proteasomal pathway, and that reductions in protein degradation and the subsequent effects on other physiological systems are largely responsible for the IGF-I-induced reduction in weight loss.
ORGANISM(S): Salmo salar Oncorhynchus mykiss
PROVIDER: GSE31765 | GEO | 2015/02/01
SECONDARY ACCESSION(S): PRJNA145185
REPOSITORIES: GEO
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