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Islet amyloid and type 2 diabetes: overproduction or inadequate clearance and detoxification?
Dhananjay Gupta, Jack L. Leahy
Dhananjay Gupta, Jack L. Leahy
Published July 18, 2014
Citation Information: J Clin Invest. 2014;124(8):3292-3294. https://doi.org/10.1172/JCI77506.
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Commentary

Islet amyloid and type 2 diabetes: overproduction or inadequate clearance and detoxification?

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Abstract

A hallmark of type 2 diabetes is the reduction of pancreatic islet β cell mass through induction of apoptosis and lack of regeneration. In most patients, β cell dysfunction is associated with the presence of extracellular amyloid plaques adjacent to β cells and intracellular toxic oligomers that are comprised of islet amyloid polypeptide (IAPP). In this issue of the JCI, three independent research groups reveal that a functional autophagy system normally prevents the accumulation of toxic IAPP oligomers in human IAPP–expressing murine models. Furthermore, mice expressing human IAPP but deficient for β cell autophagy through genetic deletion of the autophagy initiator ATG7 developed β cell apoptosis and overt diabetes. Together, these studies indicate that autophagy protects β cells from the accumulation of toxic IAPP oligomers and suggest that enhancing autophagy may be a novel target for prevention of type 2 diabetes.

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Dhananjay Gupta, Jack L. Leahy

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