Diabetes affects almost 400 million people worldwide.
One of the hallmarks of this disease is a loss of pancreatic β cells, which secrete insulin.
In many patients the reduction of β cells is associated with an accumulation of a toxic form of a protein produced by β cells, known as islet amyloid polypeptide.
There are no therapies or treatment available to restore the β cell populations or function.
Three new studies in Journal of Clinical Investigation identify a pathway that protects β cells from the toxic form of islet amyloid polypeptide.
Using animal models, all three groups found that a functional autophagy system, which acts to degrade dysfunctional cellular components, prevents toxic accumulation of islet amyloid polypeptide. Animals that expressed the human form of islet amyloid polypeptide, but produced β cells that were autophagy deficient, developed overt diabetes.
In the accompanying Commentary, Dhananjay Gupta and Jack L. Leahy suggest that enhancing autophagy in pre-diabetic patients has potential to prevent or delay the onset of diabetes.
Accompanying Commentary Title: Islet amyloid and type 2 diabetes: overproduction or inadequate clearance and detoxification?