Recent publications from our team have shown that notoriously mild models of muscular dystrophy can show profound exacerbation when their lipid metabolism is altered by apolipoprotein E gene activation.  However, apolipoprotein E is known to modulate adipocyte and lipoprotein metabolism along with whole-body energy storage.  The current project explores new avenues to humanize disease severity in dysferlin-deficient mice without interfering with normal apolipoprotein E expression.