In preparation, UCP1 gene was ablated through homologous recombination to give UCP1 (-/-) mice. Acclimatisation of the m
Example 7 Uncoupling protein UCP1 is found to be vital to adaptive nonshivering thermogenesis after UPC1abalation causes poor thermogenesis in mice. Uncoupling protein 1, found in brown adipose tissue, is a major contributor to adaptive nonshivering thermogenesis. This study investigates the possibility of an alternative mechanism, perhaps involving non-brown adipose UPCs. The discovery of such a mechanism would have impacts in bioenergetics, metabolic and obesity research. In preparation, UCP1 gene was ablated through homologous recombination to give UCP1 (-/-) mice. Acclimatisation of the mice was carried out for 3 weeks at 18°C, 24°C and 30°C. Acute cold exposure was at 4°C and body temperature was measured every 30 minutes. Oxygen consumption was measured to give an estimate of thermogenesis. An EMG was used to collect muscle activity data of the 4°C and 30°C acclimated mice in an environment of 4°C and 30°C. The mean rectified value was then used to quantify the raw trace. During acute cold exposure, the 24°C and 30°C acclimated UCP1-ablated mice saw a poor maintenance of body temperature compared to wild-type (donor strain) mice. UCP1-ablated mice had a lower oxygen consumption increase than wild-type mice, indicating thermogenesis was decreased. Muscle activity in 4°C acclimated mice was 3-fold higher in UCP1-ablated mice at 4°C than it was for wild-type mice due to shivering and locomotion. In conclusion, UCP1-ablated mice were poorer at maintaining body temperature and had decreased thermogenesis during acute cold exposure than wild-type mice. UCP1-ablated mice relied upon shivering at 4°C, despite previous acclimation to the cold, whereas the wild-type did not. This suggests that UCP1 is vital to a good adaptive nonshivering thermogenesis response. Count 249 Turnitin report. Result – 0% similarity with examination paper
