During development so called master fat determination genes or PPARs govern whether an immature cell commits to becoming a fat cell, explains Dr Fouzia Sadiq of Imperial's Animal Science Research section.

"A further signal, PGC- 1 alpha is then needed to convert immature fat cells into brown fat that expresses UCP-1 rather than normal white fat," she says.

"But what we dont know is the underlying mechanism that regulates the loss of UCP-1 activity after birth. If we can establish this then we will be in a much better position to understand how to switch back on the signals that make immature fat cells develop into brown fat."

To establish whether PPARs and PGC-1 alpha play a role in switching UCP-1 off the researchers looked at expression levels during late pregnancy and over the first month after birth. The results indicate that levels of UCP-1 closely mirror levels of PPARs and PGC-1 alpha, suggesting that they are the key switches that control conversion of immature fat cells into brown rather than white fat.

"Having established the key role of PPARs and PGC-1 alpha were now focusing on what drugs and natural compounds could reverse the process," says Dr Sadiq.

"Already the drug isoprenaline has been shown to increases levels of PGC-1 alpha and PPARs with a subsequent increase UCP-1 after birth. Now were looking at whether synthetic and natural activators of the genes that express PPARs and PGC-1 alpha have the same effect."

The research is funded by the Biotechnology and Biological Sciences Research Council.