The body contains both white fat, which stores energy, and brown fat, which burns it up. Fat cells can convert between these two states, with their state determined by the brain’s response to the presence or absence of insulin. However, according to new research on mice, the switch responsible can malfunction, permanently keeping cells in the white state and triggering obesity. Finding a way to supress this activity could provide a path to address the rise in obesity.

Our body responds to food consumption by producing insulin, which has long been known to trigger effects in the brain. However, recent research has revealed additional complexity to these responses. Professor Tony Tiganis of Monash University reports in Cell Metoblism on one of these pathways, as observed in mice.

Tiganis’ mice responded to fasting by producing TCPTP, a protein that leads brown fat cells to whiten, storing what little food energy they have. When fed a high-fat diet, the TCPTP degraded and production was suppressed. The fat cells turned brown, releasing the stored energy as heat.

The production of TCPTP is controlled by what Tiganis calls a “brain switch”, but this malfunctions in some mice. "What happens in the context of obesity is that the switch stays on all the time – it doesn't turn off during feeding," Tiganis said in a statement. "As a consequence, browning is turned off all the time and energy expenditure is decreased all the time, so when you eat, you don't see a commensurate increase in energy expenditure – and that promotes weight gain."

While smaller mammals rely on brown fat to keep warm, clothes and warm environments for humans have removed this evolutionary imperative. Genes that leave the switch on nearly permanently may have survived, ready to become a problem when our diets allowed.

Although the team are yet to confirm that the operation of the switch works the same way in humans as mice, Tiganis told IFLScience that many aspects of the process are known to be the same. “We can say in humans that when we overeat we expend more energy, and when we fast we expend less, so fasting is counterproductive. We also know obese people have decreased energy expenditure,” he said.

Assuming our biology turns out to match mice this way, Tiganis told IFLScience that interventions might not target TCPTP directly. TCPTP’s release is induced through glucocorticoids, a class of hormones that can be blocked by a number of known drugs, including the morning after pill.

Tiganis told IFLScience there are already clinical trials underway to tackle obesity using glucocorticoid antagonists, but no one had thought the mechanism of their success would be through the controlling of fat browning.