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 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.
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