The scientific community has long wondered why some people who are obese develop type 2 diabetes while others do not. A team led by Biochemistry Instructor Libin Liu, PhD, and Professor of Biochemistry and Medicine Paul Pilch, PhD, thinks they are closer at finding out the answer.
Their study, which has appeared in eLife Sciences describes on a protein called PTRF (Cavin-1) inside fat cells. Fat cells normally function to store fat a person ingests. By studying animal models and cells, authors Liu and Pilch conclude that PTRF controls the production of new proteins to allow a fat cell to accommodate more fat. Loss of PTRF results in inefficient fat storage, and dietary fat is mis-targeted to other tissues.
The common Western diet is overly rich in nutrients. The body has to respond to incoming waves of fat by storing them. What distinguishes a “healthy obese” individual from a diabetic obese individual may be the ability of their fat cells to make new fat storage proteins. The latter fails to mount an adequate protein production response in the fat cells, and this leads to fat spilling over to liver and muscle, resulting in type 2 diabetes.
Understanding the role of PTRF may help to clarify how the body distributes fat in health and in disease. Such knowledge may bring new opportunities to treat diabetes in humans. Even as more research unfolds, Liu and Pilch agree that diabetes is a complex condition involving many other proteins, and that “Diet and exercise continue to be the first choice for preventing and treating Type 2 diabetes.”
Submitted by Sherry Yan, MD.