A diet high in a certain type of fat may actually boost metabolism and help you shed flab, according to new research.
After studying genetically modified mice, the discovery by Texas Tech University nutrition scientists could lead to supplements and a diet regime that will increase metabolism and decrease muscle fatigue in humans.
Researcher Chad Paton and colleagues were curious why skeletal muscles of obese people contained a certain type of enzyme that breaks down saturated fats.
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"We used a transgenic mouse model, and we took the gene that makes the enzyme that's not normally expressed and took away it's regulation to make it active all the time," Paton said.
"What we found in those animals is they had a hypermetabolic rate compared to the wild mice, increased energy consumption and greatly increased these animals' exercise capacity, said Paton.
The enzyme, called SCD1, converts saturated fat into monounsaturated fat, which is easier to metabolise. The liver will produce this enzyme depending on the fat content of the food consumed, he said.
Fatty adipose tissue produces it all the time as a way of regulating itself.
Only in heavily exercised muscle tissue or in the case of obesity does skeletal muscle produce the enzyme, he said.
After looking at skeletal muscles of the genetically modified mice compared to that of the wild mice, Paton and his team discovered higher levels of polyunsaturated fats, particularly linoleic acid, gotten only through diet.
Higher levels of linoleic acid could only mean one thing - the modified mice were eating more food. But Paton's team found that the modified mice weighed less than the wild mice. On top of that, their ability to exercise increased.
"We found in the genetically modified animals that they had a hypermetabolic rate," he said.
"They were increasing their energy consumption, and they experienced greatly increased exercise capacity. For example, on the exercise wheels, normal mice fatigue after 7 to 10 minutes.
The study was published in the The Journal of Lipid Research.