Korean J Obes.
2005 Mar;14(1):9-15.
Mechanism of Elevated Oxygen Consumption by Intralipid and Heparin Injection: Increased Skeletal Muscle Fat Oxidation and UCP3 Expression
- Affiliations
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- 1Department of Internal Medicine, Daegu Fatima Hospital, Korea.
- 2Department of Physiology, College of Medicine, Yeungnam University, Korea. ywkim@med.yu.ac.kr
Abstract
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BACKGROUND: Energy homeostasis is maintained by the balance between energy uptake and expenditure. When energy uptake exceeds expenditure, surplus energy is accumulated to fat. Exercise and thermogenesis utilize energy substrate and the brown adipose tissue(BAT) and skeletal muscle are known to be responsible for the thermogenesis. However, it is still uncertain which is the main tissue responsible for energy consumption when fat is overloaded.
METHODS
To evaluate which tissue utilizes overloaded fatty acid, fatty acid oxidation capacity was measured following intralipid plus heparin or saline injection in male Sprague-Dawley rats. UCP1, UCP3, leptin, and adiponectin mRNA expression were also analyzed in BAT, soleus muscle, and white adipose tissue(WAT).
RESULTS
The oxygen consumption was increased by intralipid injection and maintained for 3 hours compared to saline injected rats. The palmitate oxidation was increased by intralipid injection in soleus muscle, however, there was no significant change in BAT. UCP3 mRNA expression in soleus was increased by intralipid injection but UCP1 and 3 mRNA expression were not increased in BAT by intralipid injection. There were no significant changes in leptin and adiponectin expression in WAT between saline and intralipid injected rats.
CONCLUSION
These results suggest that the main mechanism responsible for increased oxygen consumption following intralipid injection is the elevated fat oxidation capacity and UCP3 mRNA expression in skeletal muscle.
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