Skeletal Muscle Oxidative Capacity in Cachectic Mice
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abstract
Cachexia is often defined as a complex metabolic syndrome associated with underlying illness and characterized by the loss of muscle with or without loss of fat mass. These changes are often attributed to chronic inflammation that can enhance protein degradation in skeletal muscle and lypolysis in adipose tissue. The purpose of this study was to examine if the enhanced metabolic demands during cachexia alter oxidative capacity in red and white portions of the gastrocnemius muscle from cachectic ApcMin/+ mice. Twenty week ApcMin/+ mice were stratified by cachexia severity determined by body weight, muscle, and fat mass. The gastrocnemius muscle was separated into red and white portions to determine phenotype specific changes. Muscle mitochondrial content and succinate dehydrogenase activity were significantly reduced in mice with severe cachexia. Gene expression related to mitochondrial fission and fusion were quantified in the muscle. In glycolytic muscle there was a significant decrease in mfn1 and mfn2 expression, and an increase in fis1 mRNA expression. Nitrotyrosine expression, a marker of oxidative stress was significantly decreased in both oxidative and glycolytic muscle from severely cachectic mice. These results suggest that during severe cachexia skeletal muscle mitochondria number and function are altered in red and white portions of rapidly wasting skeletal muscle. RO1CA12124901A2
