A new breakthrough in cellular biology has revealed a biological “fat switch” that could help in the fight against the worldwide obesity epidemic, according to a study published by scientists at the Dana Farber Cancer Institute last week.
The “switch”—a channel-shaped protein that sits in the outer membrane of human fat cells—can help prevent insulin resistance and obesity when it is blocked.
Senior author Bruce Spiegelman, a professor of cell biology at Harvard Medical School, said the implications of this research are far-extending.
“The fact that there is a pathway [...]that is potentially druggable that controls these aspects of biology opens up a pretty clear possibility to develop therapeutics,” he said.
According to co-author Jun Wu, an instructor at Dana Farber Cancer Institute, one-third of the world’s population suffers from obesity, but there are still no effective drugs in the United States capable of helping reduce metabolic rates.
In any animal, a high calorie diet can lead to obesity or insulin resistance–and commonly both. The diseases, especially when coupled, lead to greatly increased risk of coronary heart disease, type II diabetes and stroke.
The fat switch protein these scientists studied is predominately found in “brown fat cells”—a type of fat cell that is especially good at using chemical energy to generate and dissipate heat. This heat dissipation functions to prevent insulin resistance, distinguishing it as a “good” fat cell, according to Wu.
Through five years of experimentation, Spiegelman, Wu and their colleagues found that mice who had blocked fat switch proteins in their brown cells had an increase in their energy expenditure and decrease in insulin resistance compared to mice that did not have this block, even without putting the mice on a low-calorie diet.
Spiegelman said that the fat switch protein is from the same family of proteins as capsaicin, a protein that can be blocked by drugs to prevent the taste of spice—evidence that the fat switch could be manipulated to produce an effect in humans in a similar way.
The “druggable” potential for the fat switch, Spiegelman added, was one of the most exiciting finds of his work.