FRIDAY, Jan. 15 (HealthDay News) -- 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.
"In summary, this study demonstrates that sarcolemmal KATP channels not only respond to metabolic stress but continuously control energy use by cardiac and skeletal muscles, thereby promoting body energy conservation. Positive energy balance favoring obesity would be therefore moderated by tissue-specific interruption of KATP channel-driven optimization of energy use, offering a paradigm in weight control," the authors conclude.
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