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PUBLIC RELEASE DATE:
16-Dec-2013

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Tweaking energy consumption to combat muscle wasting and obesity

IMAGE: Thermal images show that KATP channels control energy consumption in muscles during low-level activity. Mice without muscle KATP channel function (right) showed excessive body heat production (red) after light exercise...

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Using a new technique to evaluate working muscles in mice, researchers have uncovered physiological mechanisms that could lead to new strategies for combating metabolism-related disorders like muscle wasting and obesity. The study appears in The Journal of General Physiology.

ATP-sensitive potassium (KATP) channels, which link membrane excitability to cell metabolism, are abundant in skeletal muscle and play an important role in regulating muscle function and energy consumption. However, it is not clear how KATP activation affects muscles under physiological conditions and how this translates to energy use.

Researchers from the University of Iowa Carver College of Medicine developed a technique to evaluate muscle function in the tibialis anterior leg muscle of living mice. They found that, during low-level exercise, which triggered the opening of KATP channels, muscles with disrupted KATP function had higher peak force, calcium release, and heat production-- which is associated with increased energy consumption-- than muscles with normal KATP function.

The results show how KATP channels control energy use even during mundane, low-intensity activity. Modulating KATP channel activity could therefore provide a new strategy to combat metabolic disorders like muscle wasting and cachexia, when the goal is to conserve energy, or obesity, when increasing energy consumption is desired.

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Zhu, Z., et al. 2014. J. Gen. Physiol. doi:10.1085/jgp.201311063

About The Journal of General Physiology

Founded in 1918, The Journal of General Physiology (JGP) is published by The Rockefeller University Press. All editorial decisions on manuscripts submitted are made by active scientists in conjunction with our in-house scientific editor. JGP content is posted to PubMed Central, where it is available to the public for free six months after publication. Authors retain copyright of their published works and third parties may reuse the content for non-commercial purposes under a creative commons license. For more information, please visit http://www.jgp.org.

Research reported in the press release was supported by the National Institutes of Health.



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