Many diseases – obesity, Type 2 diabetes, and muscular dystrophy, for example – are associated with fat accumulation in muscle. In essence, fat replacement causes the muscles to weaken and degenerate. Scientists at Wake Forest Baptist Medical Center have discovered the biological mechanism involved in this process, which could point the way to potential therapies. The findings were published online on April 27, 2013 in Stem Cells and Development. The Wake Forest Baptist researchers proved that pericytes, stem cells associated with blood vessels, contain two sub-types with completely different roles: Type 1, which form only fat cells, and Type 2, which form only muscle cells. "We found that Type 1 contributes to fat accumulation in the skeletal muscle under pathogenic conditions, while Type 2 helps in forming muscle," said Osvaldo Delbono, M.D., Ph.D., professor of internal medicine at Wake Forest Baptist and senior author of the study. "This is important because now we have the potential to develop therapies that can block the activity of Type 1 pericytes to form fat or activate Type 2 pericytes to regenerate muscle." In the study, the researchers were able to identify the subtypes through genetic and molecular labeling methods. Using an in vitro model, they showed that Type 1 pericytes form fat while Type 2 pericytes form muscle. To test their theory in an animal model, the scientists first injected Type 2 cells into injured muscle in healthy young mice to determine if the muscle would regenerate to repair the damage; it did. When Type 1 cells were injected, the mice did not form muscle.
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