By making the skeletal muscles of mice use energy less efficiently, researchers report in the December issue of Cell Metabolism, a publication of Cell Press, that they have delayed the animals deaths and their development of age-related diseases, including vascular disease, obesity, and one form of cancer. Those health benefits, driven by an increased metabolic rate, appear to come without any direct influence on the aging process itself, according to the researchers.
The mitochondria powering the mouse muscles were made inefficient by increasing the activity of so-called uncoupling protein 1 (UCP1). UCP1 disrupts the transfer of electrons from food to oxygen, a process known as mitochondrial respiration, which normally yields the energy transport molecule ATP. Instead, the energy is lost as heat.
When you make the mitochondria inefficient, the muscles burn more calories, a metabolic increase that could be at least a partial substitute for exercise, said Clay Semenkovich of Washington University School of Medicine in St. Louis. There are a couple of ways to treat obesity and related diseases, he continued. You can eat less, but thats unpopular, or you could eat what you want as these animals did and introduce an altered physiology. Its a fundamentally different way of addressing the problem.
Atherosclerosis, diabetes, hypertension, and cancer occur more frequently with increasing age, the researchers explained. These age-related diseases are distinct from the process of aging, a physiological decline that includes decreases in muscle strength, cardiopulmonary function, vision, and hearing as well as wrinkled skin and graying hair. Thus, the researchers added, aging and age-related disease are associated but may not share the same mechanisms.
Given the difficulty of validating strategies to increase life span in humans and the possible dissociation between aging and age-related diseases, the researchers said, identifying a s
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