Article ID | Journal | Published Year | Pages | File Type |
---|---|---|---|---|
2051021 | FEBS Letters | 2006 | 5 Pages |
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.
Related Topics
Life Sciences
Agricultural and Biological Sciences
Plant Science
Authors
Ronnie Minnaard, Patrick Schrauwen, Gert Schaart, Matthijs K.C. Hesselink,