People with diabetes do not make enough insulin to maintain normal glucose levels. Reasons for this are not obvious and remain the subject of much research.
Because insulin is made by the beta cells of the pancreas, it was initially believed that beta cell death was the cause of reduced insulin production in both type 1 diabetes (T1D) and type 2 diabetes (T2D). Specifically, scientists believed that in T1D, the body’s immune cells mistakenly attack and kill its own beta cells. In T2D, they reasoned that increased insulin demand causes beta cells to become overworked and exhausted, which led to their death. Recent research suggests that this may not be the whole story. Rather than dying, a large proportion of stressed beta cells may lose their specialized identity and retreat into a dormant, non-functional state. This beta cell process is called dedifferentiation and has been seen in both T1D and T2D.
In T1D, there is evidence that the beta cells dedifferentiate as a way of hiding or protecting themselves from the immune system which is looking for beta cells to attack. In T2D, this process may protect the cells by stopping them from making insulin and therefore reducing the amount of work that they need to do.
Understanding how beta cells dedifferentiate may identify new ways of reversing this process. If this can be achieved it may lead to new therapies for both T1D (assuming that the immune attack can also be stopped) and for T2D.
About the author
Liam Stanley
Liam is a graduate student at the University of Saskatchewan researching the role of the pancreatic lymphatics in type 2 diabetes. He studies the changes that occur to the lymphatics around the islets to determine if they contribute to disease progression.