Shutting down an energy-controlling mechanism in mice left them leaner than normal mice and could be a new way to fight obesity in humans, US researchers said in a study published Tuesday.
And the finding is big news in the United States, where around a third of the adult population is considered obese, meaning they have a body mass index (BMI) greater than 30, according to the American Obesity Association.
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The researchers found that by switching off potassium channels which are sensitive to adenosine triphosphate (ATP), a molecule in cells that stores the energy we need to do just about everything, made mice burn more energy and left them leaner than normal mice.
The effect was evident even when the mice were fed high-fat "Western" diets and was long-lasting, too, with the mice remaining slim throughout their lives, scientists from the Mayo Clinic, University of Iowa, University of Connecticut and New York University reported in the journal Cell Metabolism.
The channels, called KATP, sense pools of ATP molecules in cells and regulate heart and muscle performance according to what they find.
Usually the KATP channels would spring into action to limit the duration or amplitude of heart and muscle actions, to prevent energy depletion.
By shutting off the mechanism in mice, the researchers got them to burn more stored energy by giving off more heat, both at rest or when active.
"While mechanisms that preserve energy are naturally protective, in times of food shortage or environmental stress, they promote obesity in a sedentary, modern society," said the Mayo Clinic's Alexey Alekseev, lead author of the study.
"Our findings suggest that therapeutic targeting of the KATP channel function, specifically in muscle, could offer a new option for obese patients with lower capacity for exercise," he said.
One finding was that mice in whom the KATP channel had been switched off burned more glycogen, the form in which carbohydrates are stored in the body and the primary source of energy for endurance athletes, and stored body fat than ordinary mice.
That means that achieving greater leanness by deactivating KATP channels comes at the cost of reduced endurance.
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