<<http://www.eurekalert.org/pub_releases/2004-05/bpl-cmh052804.php>>
Could mice hold the secret to longer life? Scientists from the University of Aberdeen, the Aberdeen-based Rowett Research Institute and the Medical Research Council (MRC) in Cambridge have made a major breakthrough in understanding how metabolism affects lifespan. In a seven-year study of mice they found that those with the highest metabolic rate lived the longest, raising the prospect that the effect could be mimicked in humans. Scientists have long thought that a high metabolic rate was linked to a shortened life-span. The present discovery turns this century old belief on its head and changes dramatically our understanding of the regulation of life-span. Metabolism is the means by which nutrients are broken down to smaller building blocks and chemical energy, which are used to make new body materials and to do work. The researchers discovered that the most metabolically active 25% of the mice studied, far from having shorter life-spans, in fact lived 36% longer than the least active. If the same effects are mimicked in humans then the finding would imply that a higher metabolic rate could add an extra 27 years to the average human lifespan. When the muscles of the most metabolically active mice were examined, they were found to contain factors that increased their metabolism by making it less efficient. Although the scientists do not yet fully understand how these factors work, it is suspected that while the make the metabolism less efficient, on the positive side they reduce the generation of toxic by-products called "oxygen free radicals". ---- <<http://www.eurekalert.org/pub_releases/2004-05/src-rmf052704.php>> Reduced mitochondrial function important mechanism in aging Scientists at the Karolinska Institute have found that changes in the "powerhouse" of cells, the mitochondria, play a key role in aging. The findings are being published in this week's issue of the journal Nature. Mitochondria, which provide energy to cells, have their own set of DNA. Mutations of mitochondrial DNA increase with age, but until now no one knew whether this is a result of aging or a cause of aging. New research findings now indicate that the latter is the case. Mice with a deficient capacity to correct mutations in mitochondrial DNA acquired an increased number of mutations and proved to age considerably earlier than normal. They lived an average of 10 to 12 months compared with the normal 2 or 3 years. These mice also developed several typical signs of premature aging, such as osteoporosis, weight loss, hair loss, anemia, reduced fertility, and heart muscle disorders. The findings reveal fundamental biological mechanisms that lie behind the aging process. This knowledge paves the way for the possibility of slowing down aging and treating pathological changes that arise in connection with aging by protecting mitochondrial DNA from damage.
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