Published on January 8, 2013 at 12:21 AM
When functioning normally, TRIP-Br2 restricts the amount of fat that cells burn as energy. But when TRIP-Br2 is absent, a fat-burning fury seems to occur in fat cells. Although other proteins have been linked to the storage and release of fat in cells, TRIP-Br2 is unique in that it regulates how cells burn fat in a few different ways, Hsu said. When TRIP-Br2 is absent, fat cells dramatically increase the release of free fatty acids and also burn fat to produce the molecular fuel called ATP that powers mitochondria - the cell's energy source. In addition, cells free from the influence of TRIP-Br2 start using free fatty acids to generate thermal energy, which protects the body from exposure to cold.
"TRIP-Br2 is important for the accumulation of fat," said Rohit N. Kulkarni, M.D., Ph.D., also a senior author of the paper and an associate professor of medicine at Harvard Medical School and the Joslin Diabetes Center. "When an animal lacks TRIP-Br2, it can't accumulate fat."
Because the studies were done mostly in mice, additional studies are still needed to see if the findings translate to humans.
"We are very optimistic about the translational promise of our findings because we showed that only human subjects who had the kind of fat (visceral) that becomes insulin-resistant also had high protein levels of TRIP-Br2," Hsu said.
"Imagine you are able to develop drugs that pharmacologically mimic the complete absence of TRIP-Br2," Hsu said. "If a patient started off fat, he or she would burn the weight off. If people are at risk of obesity and its associated conditions, such as type 2 diabetes, it would help keep them lean regardless of how much fat they ate. That is the ideal anti-obesity drug, one that prevents obesity and helps people burn off excess weight."
Source: University of Florida