St. Louis, Dec. 5, 2007 Metabolism researchers at Washington University School of Medicine in St. Louis have found that although it does not extend maximum lifespan in mice, activating a protein in muscle tissue increases average lifespan and prevents some age-related diseases. The researchers believe a similar approach may someday help people avoid age-related problems such as atherosclerosis, diabetes, hypertension and even some cancers.
In a series of experiments, the research team bred large numbers of mice, fed them a normal chow diet and followed each mouse until its natural death. Half were genetically engineered to make more of a protein in their muscle tissue called uncoupling protein-1. Their littermates did not make excess uncoupling protein. In muscle tissue, uncoupling protein-1 converts the energy from food into heat and mimics the effects of exercise.
Past research conducted in the laboratory of Clay F. Semenkovich, M.D., the Herbert S. Gasser Professor and chief of the Division of Endocrinology, Metabolism and Lipid Research, had found that mice with extra uncoupling protein-1 in muscle tissue are protected from diabetes and obesity.
Because the experiments took so long for this study and involved the breeding and following of so many mice, Semenkovich was joined on the paper by three first authors: Alison C. Gates, Ph.D., a former postdoctoral fellow in the lab now studying at Southern Illinois University Edwardsville; Carlos Bernal-Mazrachi, M.D., assistant professor of medicine and of cell biology and physiology; and Sharon L. Chinault, Ph.D., former postdoctoral fellow and now assistant professor of biology at MacMurray College in Illinois. The findings are published in the December issue of the journal Cell Metabolism.
"Uncoupling basically means generating inefficient metabolism," says Semenkovich. "We knew years ago that when mice manufactured uncoupling protein in muscle, they didn't become obese. Th
|Contact: Jim Dryden|
Washington University School of Medicine