Sarcolipin is a protein in humans is encoded by the SLN gene. It’s a small peptide only found in muscles. Researchers at Sanford Burnham Prebys Medical Discovery Institute (SBP) have shown that sarcolipin increases muscle energy expenditure and fat oxidization.
The scientists found sarcolipin forces muscle to use more energy to move calcium by interacting with calcium ion transporter SERCA and making it less efficient. This drives mitochondrial power plants to produce extra energy by burning more fat. This mechanism is intrinsic to muscle and generates heat at the expense of fat burning.
Two factors increase energy expenditure in muscle—exercise and cold. When either happens, muscle cells intensify calcium cycling and recruit SERCA to move calcium ions into the sarcoplasmic reticulum, a structure within muscle cells that balances calcium levels. This process uses a lot of (ATP) energy because SERCA relies on ATP to move calcium. When sarcolipin binds to SERCA, it uncouples SERCA activity. As a result, it allows ATP consumption but not efficient calcium transport, which causes more energy consumption. The net result is more heat and fat burning.
In the study, the team found that animals without sarcolipin had fewer mitochondria and had trouble burning fat, accumulating more in their muscle (called lipotoxicity), which is a common cause of insulin resistance. However, those with more sarcolipin boosted their concentration of mitochondria and showed increased fat oxidation.
Researchers have already shown that extreme obesity reduces sarcolipin function. 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.