UCP3 in muscle wasting, a role in modulating lipotoxicity?

Abstract
UCP3 has been postulated to function in the defense against lipid‐induced oxidative muscle damage (lipotoxicity). We explored this hypothesis during cachexia in rats (zymosan‐induced sepsis), a condition characterized by increased oxidative stress and supply of fatty acids to the muscle. Muscle UCP3 protein content was increased 2, 6 and 11 days after zymosan injection. Plasma FFA levels were increased at day 2, but dropped below control levels on days 6 and 11. Muscular levels of the lipid peroxidation byproduct 4‐hydroxy‐2‐nonenal (4‐HNE) were increased at days 6 and 11 in zymosan‐treated rats, supporting a role for UCP3 in modulating lipotoxicity during cachexia.