Targeting a mechanism involved in energy expenditure in muscles may help treat obesity, according to research published in the Jan. 6 issue of Cell Metabolism.
Alexey E. Alekseev, Ph.D., of the Mayo Clinic in Rochester, Minn., and colleagues analyzed data from KATP channel-deficient mice. These ATP-sensitive potassium channels play a role in regulating cardiac and skeletal muscle action potentials.
The researchers found that mature knockout mice lacking the KATP channels demonstrated lower body weight and fat storage than wild-type mice, but grew to a similar length. Evidence suggested that knockout mice had greater energy expenditure and a higher rate of carbohydrate consumption. These mice also were resistant to becoming obese while on a high-fat diet, compared to wild-type mice, which did become obese. However, the knockout mice also had decreased workload endurance...
Monday, January 18, 2010
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