Submitted to: Comparative Biochemistry and Physiology
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: February 25, 2002
Publication Date: September 9, 2002
Citation: Comparative Biochemistry & Physiology 133(2):345.
Interpretive Summary: This study further characterizes an uncoupling protein (UCP) found in chickens and other avian species such as turkeys, ducks, and hummingbirds. We provide evidence that this UCP is probably UCP 3. Originally this uncoupling protein was thought to have a role in adaptive thermogenesis, but we now report it also is modulated by increased fatty acid oxidation and movement of these fatty acids out of the bloodstream and into muscle. Chicken UCP gene expression in muscle is increased after 24 to 48 hours of feed deprivation, when plasma levels of free fatty acids are also elevated. We report clear evidence that the metabolic adaptation to feed deprivation in chickens leads to an increase in skeletal muscle UCP, and that this increase in UCP is highly correlated with plasma triglyceride, and free fatty acid concentrations. Chronic exogenous leptin exposure reduces adipose tissue mass and increases energy expenditure in mammals. Recombinant human leptin had no effect on UCP expression in skeletal muscle in birds, either in the feed- deprived or the fed state. Although the exact biochemical role or mechanism of action of this UCP is currently unknown, it is likely that avian UCP is involved in regulating, or is regulated by fatty acid oxidation, especially under times of nutritional stress.
An avian uncoupling protein (UCP) gene homolog was recently sequenced from skeletal muscle and proposed to have a role in thermogenesis in chickens, ducks, and hummingbirds. Since mammalian UCP 2 and UCP 3 also appear to have functions associated with energy and substrate partitioning and body weight regulation, the purpose of this study was to further characterize chicken UCP under conditions of nutritional stress and/or leptin administration. Three-week-old male chickens were starved for 24 or 48 hours and then half of each group were refed for an additional 24 hours. In a follow-up experiment, chickens were fed or starved for 48 hours with or without leptin administration. Feed deprivation increased UCP mRNA expression in skeletal muscle by up to 260 %, and in a time-dependent manner in pectoralis muscle. Refeeding for 24 hours normalized muscle UCP mRNA levels. Leptin administration had no effect on muscle UCP. Chicken muscle UCP mRNA levels were highly correlated with plasma triglyceride and NEFA concentrations, and with circulating levels of insulin, IGF-I and IGF-II. These results suggest that, as in mammals, avian UCP is up-regulated during starvation and is highly correlated with increased fatty acid oxidation and flux into skeletal muscle.