Physical deconditioning is associated with the development of chronic diseases, including type 2 diabetes and cardiovascular disease. Exercise training effectively counteracts these developments, but the underlying mechanisms are largely unknown. To gain more insight in these mechanisms, muscular gene expression levels were assessed after physical deconditioning and after exercise training of the lower limbs in humans using gene expression microarrays. In order to exclude systemic effects, we used human models for local physical inactivity (three weeks of unilateral limb suspension) and for local exercise training (six weeks of functional electrical stimulation exercise of the extremely deconditioned legs of individuals with a spinal cord injury). The most interesting subset of genes, those downregulated after deconditioning as well as upregulated after exercise training, contained 18 genes related to both the 'insulin action' and 'adipocytokine signaling' pathway. Of these genes, the three with strongest up/downregulation were the muscular fatty acid binding protein 3 (FABP3), the fatty acid oxidizing enzyme hydroxyacyl-CoA dehydrogenase (HADH), and the mitochondrial fatty acid transporter solute carrier 25 family member A20 (SLC25A20). The expression levels of these genes were confirmed using RT-qPCR. The results of the present study indicate an important role for a decreased transport and metabolism of fatty acids which provides a link between physical activity levels and insulin signaling in relation to physical (in)activity.
- Fatty acid metabolism
- Insulin resistance
- Copyright © 2012, American Journal of Physiology - Endocrinology and Metabolism