作者: Tomoki Abe , Ahmad Mujahid , Kan Sato , Yukio Akiba , Masaaki Toyomizu
DOI: 10.1016/J.FEBSLET.2006.07.070
关键词: Skeletal muscle 、 Beta oxidation 、 Fatty acid 、 Thermogenin 、 Acyl CoA dehydrogenase 、 Internal medicine 、 Endocrinology 、 Uncoupling protein 、 UCP3 、 Mitochondrion 、 Biology
摘要: Little is known about the precise physiological roles of uncoupling protein 1 (UCP1) homologs (UCP2, UCP3, avian UCP) whose levels are up-regulated during fasting. UCPs in skeletal muscle thought to play a role regulation lipids as fuel substrates, and/or controlling production reactive oxygen species (ROS). The aim this investigation, using from fasted chickens, was examine alterations expression genes encoding for UCP and key enzymes relevant lipid flux across mitochondrial β-oxidation pathway. We also clarified whether an increase avUCP content could be associated with altered ROS by mitochondria. Transcription CPT-I were increased 7.7- 9.5-fold after 24 h fast slightly diminished but remained 5.0- 7.7-fold higher than baseline levels, respectively, 48 In contrast, members pathway, LCAD 3HADH, gradually 12 This suggests that processes involved transfer oxidation fatty acids differently initial stage Analysis lucigenin-derived chemiluminescence showed FFA-sensitive portion carboxyatractyloside-upregulated greater mitochondria h-fasted chickens compared control, which leads us postulate potentially down-regulated UCP. possible involvement backlog acid oxidation, observed fast, transmembrane gradient free non-oxidized discussed.