Dr. Alekseev and his colleagues suspected that the KATP channel could control energy expenditure. To test the hypothesis, they studied genetically modified mice in which the KATP channel had been inactivated in the whole body or muscle tissues. They compared these mice to normal mice and found that as early as 5 months of age, the modified mice were leaner and stayed that way throughout their life span.

Researchers compared activity patterns, hormone levels, food intake, and respiratory gas exchange while at rest and under moderate exercise. A hallmark of the study was the discovery that activity in the absence of the KATP channel function resulted in increased consumption of carbohydrates and lipids. That, in turn, led to enforced burning of glycogen and stored body fat.

"By sensing cellular energy content, KATP channels continuously, at any activity level, optimize energy use and define the balance between energy availability and consumption," explains Dr. Alekseev. "In principle, a positive energy balance favoring weight gain could be reversed by targeting muscle KATP channels to control obesity in patients with low to moderate exercise capacity imposed by the overweight state."

Source: Mayo Clinic