Research published in the Proceedings of the National Academy of Sciences shows how a newly identified protein in fat cells regulates the activity of a key gene responsible for stimulating thermogenesis; an effect that ensures better fat metabolism.
Thermogenesis is an increase in the metabolism which in turn promotes a greater utilization of fat for energy. Finding new compounds to increase thermogenesis is an ongoing endeavor in both nutritional and pharmaceutical research. A newly identified protein called RIP140 blocks the expression of uncoupling protein 1 (UCP1) and causes the body to burn more fat for energy.
A team of British scientists from Imperial College in London made the discovery in mice. They found that mice without RIP140 remained lean despite the consumption of a high-fat diet.
The results showed that on average, mice without RIP140 accumulated between 50 and 70% less fat when compared with mice with RIP140, even though their food intake was similar.
This finding will prove crucial in future research on fat metabolism in humans. It appears that by reducing the levels of RIP140, it is possible to increase the activity of the UCP1 gene. As I’ve reported previously, UCP1 plays a key role in regulating energy balance in the body. Increasing the activity of UCP1 can accelerate fat loss simply by increasing energy expenditure.
Compounds such as EGCG, found in Dymetadrine Xtreme, are shown to enhance thermogenesis and fat metabolism.
