Duchenne muscular dystrophy is a devastating progressive disease of muscle destruction resulting in significant disease of both skeletal and cardiac muscles. Patients with Duchenne muscular dystrophy die in their mid- to late 20s. This disease results from the absence of the protein dystrophin. There are several animal models of this disease, with the most commonly used model being the mouse. The disease in this animal has a very mild phenotype, which provides both limitations and promises. Another animal model is the dog. In contrast to the mouse, the loss of dystrophin in the dog results in a very severe phenotype with dogs living only a couple of years. Understanding the processes by which the mouse is mildly affected and the dog is severely affected is of significant clinical interest, as it may reveal pathways that aggravate or compensate for the loss of dystrophin. This work utilizes the Center for Mass Spectrometry and Proteomics, the University of Minnesota Genomics Center, the Nuclear Magnetic Resonance Laboratory, the University Imaging Centers, and many of MSI's software packages for the analysis of NMR spectra, microscopy, and other imaging data.