Researchers have figured out why people burn fat when they exercise or are cold: A small protein only found in muscles that heat up.
Sarcolipin, the small peptide in muscles, boosts muscle energy expenditure and fat oxidization during exercise and cold exposure, according to researchers at the nonprofit Sanford Burnham Prebys Medical Discovery Institute in Orlando, Fla., who published their findings Tuesday in the journal Cell Report.
Although skeletal muscle represents 40 percent to 50 percent of body mass, it consumes most of the glucose and fatty acids. “It has the ability to increase its energy expenditure 20- to 30-fold during intense exercise by stimulating insulin-independent glucose uptake and by switching to higher fatty acid uptake and oxidation,” the authors wrote.
“When you exercise, your muscle makes more mitochondria and oxidizes more fat,” Dr. Muthu Periasamy, a professor at SBP Lake Nona, said in a press release.
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The mechanism is unique to muscle, and generates heat at the expense of fat burning, Periasamy said, and “sarcolipin is the missing link.”
Muscle cells intensify calcium cycling and get SERCA to pump calcium ions into the sarcoplasmic reticulum, where muscle cells balance calcium levels. A lot of adenosine triphosphate is consumed because SERCA relies on it to move calcium.
SERCA activity is uncoupled when sarcolipin binds to it. Because it allows ATP consumption but not the efficient transportation of calcium, more energy is consumed. Hence more heat and fat burning.
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The researchers found that animals without sarcolipin had fewer mitochondria and it was difficult for them to burn fat. By accumulating more fat in their muscle, it becomes insulin resistant.
“When we feed mice with more sarcolipin a high-fat diet, they don’t accumulate any fat in their muscle, and they don’t develop insulin resistance and type 2 diabetes,” said first author Dr. Santosh Maurya, a staff scientist at SBP Lake Nona.
Sarcolipin conceivably could be used to treat people with obesity, type 2 diabetes or both.
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“Researchers have already shown that extreme obesity reduces sarcolipin function,” Periasamy said. “There might be a therapeutic window to increase sarcolipin recruitment to burn more energy. This strategy could help people with metabolic conditions, as well as those who have difficulty exercising.”
Periasamy noted people have an abundance of SERCA pumps.
“Some are bound by sarcolipin, but it only binds around 25 percent of SERCA pumps at any one time,” Periasamy said. “We would need to find drugs that increase efficiency of sarcolipin uncoupling SERCA.”