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Disuse-induced insulin resistance susceptibility coincides with a dysregulated skeletal muscle metabolic transcriptome.

Short-term muscle disuse is characterized by skeletal muscle insulin resistance, though this response is divergent across subjects. The mechanisms regulating inactivity-induced insulin resistance between populations that are more or less susceptibile to disuse-induced insulin resistance are not known. RNA sequencing was conducted on vastus lateralis muscle biopsies from subjects before and after bed rest (n=26) to describe the transcriptome of inactivity-induced insulin resistance. Subjects were separated into Low (n=14) or High (n=12) Susceptibility based on the magnitude of change in insulin sensitivity after 5-days of bed rest. Results: Both groups became insulin resistant after bed rest and there were no differences between groups in non-metabolic characteristics (body mass, BMI, fat mass, and lean mass). The High Susceptibility group had more genes altered >1.5-fold (426 High vs 391 Low) and >2-fold (73 High vs 55 Low). 24 genes were altered >2-fold in High that did not change in Low. 95 gene changes correlated with the changes in insulin sensitivity; 6 of these genes changed >2-fold in the High Susceptibility group. High Susceptibilityparticipants were uniquely characterized with muscle gene responses described by a decrease in pathways responsible for lipid uptake and oxidation, decreased capacity for triglyceride export (APOB), increased lipogenesis (i.e., PFKFB3, FASN), and increased amino acid export (SLC43A1). Conclusion: These transcriptomic data provide a comprehensive examination of pathways and genes that may be useful biomarkers, or novel targets to offset muscle disuse-induced insulin resistance.

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