An omega-3 fatty acid-enriched diet prevents skeletal muscle lesions in a hamster model of dystrophy.

Currently, despite well-known mutational causes, a universal treatment for neuromuscular disorders is still lacking, and current therapeutic efforts are mainly restricted to symptomatic treatments. In the present study, delta-sarcoglycan–null dystrophic hamsters were fed a diet enriched in flaxseed-derived omega3 alpha-linolenic fatty acid from weaning until death. alpha-linolenic fatty acid precluded the dystrophic degeneration of muscle morphology and function. In fact, in dystrophic animals fed flaxseed-derived alpha-linolenic fatty acid, the histological appearance of the muscular tissue was improved, the proliferation of interstitial cells was decreased, and the myogenic differentiation originated new myocytes to repair the injured muscle. In addition, muscle myofibers were larger and cell membrane integrity was preserved, as witnessed by the correct localization of alpha-, beta-, and gamma-sarcoglycans and alpha-dystroglycan. Furthermore, the cytoplasmic accumulation of both beta-catenin and caveolin-3 was abolished in dystrophic hamster muscle fed alpha-linolenic fatty acid versus control animals fed standard diet , while alpha-myosin heavy chain was expressed at nearly physiological levels. These findings, obtained by dietary intervention only, introduce a novel concept that provides evidence that the modulation of the plasmalemma lipid profile could represent an efficacious strategy to ameliorate human muscular dystrophy.