Researchers at Stanford and UCSF have identified a molecular signal that plays an important role in directing a certain type of stem cells to mature into fat cells, and their finding could lead to the design of better drugs for type-2 diabetes and other disease associated with obesity. My colleague Erin Digitale explains more in today's Inside Stanford Medicine:
One class of stem cells, the mesenchymal stem cells, gives rise to muscle, fat, cartilage and bone. Mesenchymal cells are considered “adult” stem cells; they are more specialized than embryonic stem cells, which are capable of differentiating into any cell in the body.
The new work suggests that blocking mesenchymal stem cells’ ability to advance to the fat cell fate may redirect the cells to form muscle instead.
“People might be willing to give up some of their fat in favor of developing some muscle,” [Brian Feldman, MD, PhD, an assistant professor of pediatrics] said. “That would be the utopia - that we may be able to borrow some cells destined for the fat cell fate to try and treat disease.”
Feldman is senior author of a paper appearing in the Journal of Biological Chemistry.
