It's common knowledge that exercise and weight loss go hand in hand, but what is not so clear is the cellular machinery that underpins that relationship. In response to exercise, scientists have now observed a big spike in levels of a fat hormone previously thought to be unrelated to physical exertion. The discovery sheds new light on the metabolic process and raises new targets for tackling weight loss.
Central to the new discovery is the different types of fat in the human body. While white fat cells store excess energy as lipids and play a key role in obesity, heart disease and diabetes, brown fat, or adipose tissue, is considered a good fat, rich in mitochondria that burns lipids and glucose to generate body heat and keep us warm in cold temperatures.
Until relatively recently, it was thought that only babies possessed brown fat, using it to keep warm until they grew old enough to shiver, then discarding it all together. But a 2009 discovery that the adult body also contains low amounts of brown fat kicked off a whole new area of research looking at how white fat might be converted to brown through a so-called "fat switch," with fish oil and nanoparticles injections just a couple of possible paths forward.
The new research carried out by scientists at the Harvard School of Medicine and Ohio State University Wexner Medical Center is said to be the first to comprehensively look at the activity of fat-controlling molecules known as lipokines during exercise.
This meant enlisting male and female participants across different age groups and activity levels, and measuring lipkine levels before, straight after and then hours after moderate-intensity exercise. Some subjects were made to ride a bike for 40 minutes and others ran on a treadmill for 45 minutes.
"One lipokine just shot right up to the top," says Kristin Stanford, a researcher at Ohio State University Wexner Medical Center.
That lipokine, bearing the catchy name 12, 13-diHOME, had previously only been linked to exposure to cold temperatures, leading the researchers to suspect that it was coming from brown fat rather than white. They explored this theory by carrying out another study on mice.
As these animals exercised, the researchers found that 12, 13-diHOME activity was heightened. They then surgically removed the brown fat stores from the mice and checked again. They found no signs of increased 12, 13-diHOME activity during exercise, suggesting their earlier suspicions were on the money. This intrigued the scientists for a couple of reasons. One is that previous research had shown exercise to dampen the activity of brown fat cells in humans and rodents, while cold exposure gives it a boost.
"Most data have suggested that cold and exercise have opposite effects on BAT (brown adipose tissue), so to see that 12,13-diHOME was released from BAT after both exercise and cold exposure was unexpected," says Stanford.
The other reason it piqued their interest is that in follow-up experiments on mice, 12,13-diHOME appeared to act as signal for the brown fats to burn fatty acids as fuels, which again runs counter to earlier research.
"It's fascinating that rather than burning calories during exercise – which is what occurs with cold exposure – brown fat is functioning to signal the muscle to take up more fatty acids to use as fuel," says Laurie Goodyear of Harvard Medical School and study co-author. "During exercise, all the different metabolic tissues, surprisingly including fat tissues, 'talk' to each other, which enables the muscles to use energy, contract and perform."
From here, the team hopes to learn more about how the lipokine 12,13-diHOME works and eventually, that the findings can provide the basis for advanced drugs that replicate the effects of exercise to boost muscle function and weight loss.
"The more knowledge we have about exercise and how it works, the better we can understand how to combat metabolic disease," says Goodyear.
The research was published in the journal Cell Metabolism.
Sources: Ohio State University, Harvard Medical School
