Scientists have discovered a protein that controls the amount of fat stored in the body, offering new clues for obesity treatments. The research, published in this week’s Proceedings of the National Academy of Sciences, shows how the protein regulates the activity of a key gene responsible for maintaining the body’s temperature, called uncoupling protein 1 (UCP1). The new protein, called RIP140, blocks the expression of UCP1, and causes the body to use up more energy and store less fat.From Imperial College:Scientists discover way to regulate the body’s energy expenditure
Scientists have discovered a protein that controls the amount of fat stored in the body, offering new clues for obesity treatments.
The research, published in this week’s Proceedings of the National Academy of Sciences, shows how the protein regulates the activity of a key gene responsible for maintaining the body’s temperature, called uncoupling protein 1 (UCP1).
The new protein, called RIP140, blocks the expression of UCP1, and causes the body to use up more energy and store less fat.
The team of scientists from Imperial College London, Kings College London, University of Cambridge, and Hammersmith Hospital, UK, conducted studies in transgenic mice born without RIP140, and in normal mice with RIP140. They found that mice without RIP140 were lean and showed resistance to high fat diet induced obesity.
On average, mice without RIP140 were 20 per cent lighter compared with normal mice and accumulated between 50 and 70 per cent less fat when compared with mice with RIP140, even though their food intake was similar.
Professor Malcolm Parker from Imperial College London, and based at Hammersmith Hospital, and one of the study’s authors comments: ”This discovery could provide a novel approach to developing new obesity treatments. By reducing the levels of RIP140, it is possible to increase the activity of the UCP1 gene. UCP1 plays a key role in regulating energy balance in the body, and through this we can reduce body weight by increasing energy expenditure.
”Although these are very promising observations we do need to be careful in interpreting the results. The study was carried out in mice, which were born without RIP140, and it will be important to determine the consequences of blocking RIP140 action in adult animals.”
This work was supported by the Wellcome Trust and the Biotechnology and Biological Sciences Research Council. Professor Parker and his team have recently signed a deal with CytRx, a US based biopharmaceutical company, to commercialise the results of this research.
