Muscle wasting is associated with
chronic diseases and
cancer. Elucidation of the
biological mechanism involved in the process of muscle mass loss and
cachexia may help identify therapeutic targets. We hypothesized that
l-carnitine treatment may differentially revert muscle fiber
atrophy and other structural alterations in slow- and fast-twitch limb muscles of rats bearing the Yoshida
ascites hepatoma. In soleus and gastrocnemius of
tumor-bearing rats (108 AH-130 Yoshida
ascites hepatoma cells inoculated intraperitoneally) with and without treatment with
l-carnitine (1 g/kg
body weight for 7 days, intragastric), food intake, body and muscle weights, fiber typing and morphometry, morphological features, redox balance, autophagy and proteolytic, and signaling markers were explored. Levels of
carnitine palmitoyl
transferase were also measured in all the study muscles.
l-Carnitine treatment ameliorated the
atrophy of both slow- and fast-twitch fibers (gastrocnemius particularly), muscle structural alterations (both muscles), and attenuated oxidative stress, proteolytic and signaling markers (gastrocnemius). Despite that
carnitine palmitoyl transferase-1 levels increased in both muscle types in a similar fashion,
l-carnitine ameliorated
muscle atrophy and proteolysis in a muscle-specific manner in
cancer-induced
cachexia. These data reveal the need to study muscles of different fiber type composition and function to better understand whereby
l-carnitine exerts its beneficial effects on the myofibers in muscle wasting processes. These findings also have potential clinical implications, since combinations of various exercise and muscle training modalities with
l-carnitine should be specifically targeted for the muscle groups to be trained.