Duchenne muscular dystrophy (DMD) is a monogenic disorder caused by the lack of the integral structural protein, dystrophin, which results in severe muscle wasting and cardiomyopathy in affected boys. Indeed, cardiorespiratory complications are the predominant cause for mortality in DMD patients. We have recently shown that circadian rhythm is disrupted in dystrophic mice as a direct result of the lack of dystrophin protein. It is well reported that disruption of circadian rhythmicity leads to perturbed metabolism and an array of disorders including obesity, diabetes and cardiovascular disease. Disturbed cardiac metabolism in DMD patients and dystrophic mice is also well described, and thus it would be interesting to learn whether pertinent metabolic genes which are known to be circadianly regulated, are disrupted in dystrophic mice. Here we show for the first time, significant changes in the differential expression patterns of multiple genes involved in free fatty acid and glucose metabolism, in 2 mouse models of DMD compared to control mice. These findings provide the foundation for further research to better understand the metabolic/circadian milieu and its effect on dystrophic heart, so that we may devise strategies to augment cardiac metabolism, in an effort to halt the deterioration in cardiac phenotype.
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