The discovery of a new molecular pathway could be key in fighting obesity, cardiovascular disease, and type 2 diabetes.

An investigation at McGill University, Montreal, has uncovered evidence as to how a known protein, folliculin, regulates the activity of fat cells.

It was found that inhibiting – or ‘turning off’ – the gene that produces folliculin in mice caused them to burn fat, rather than store it.

The process has to do with converting white fat cells into brown fat cells. These two types of tissue do different jobs, but both use fat. White fat is stored and eventually used for energy, but brown fat tissue uses up fat to produce heat.

A middle ground, inventively known as ‘beige fat’, has recently been discovered. These beige fat cells act like brown fat under certain circumstances, such as being in a cold temperature. The more active these cells are, the less likely we are to accumulate fat deposits around the body.

This could open a new line of treatment for managing obesity. If this effect could be recreated in humans, through an administered treatment, it could help not only reduce obesity, but prevent metabolic diseases like type 2 diabetes.

The research group bred mice that did not produce folliculin, and fed them a high-calorie diet for 14 weeks. When compared to a control group, the folliculin-deficient mice remained slimmer.

Furthermore, the control group experienced higher insulin and triglyceride levels than the folliculin-deficient mice. Overall, the folliculin-deficient group had less white fat, and were more tolerating of cold temperatures, as they were burning off more fat.

“Since that mechanism involves a class of proteins that can be targeted by drugs that are readily absorbed in the body, one implication is that a drug could be developed to stimulate the activity of beige/brown fat cells and thus help manage obesity and other metabolic disorders,” explained Vincent Giguère, study author.

The study appears in the journal Genes and Development.