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UCLA researchers find way to clear excess IAPP from insulin-producing beta cells

Monday July 28, 2014
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People with type 2 diabetes have an excess of a protein called islet amyloid polypeptide, or IAPP, and the accumulation of this protein is linked to the loss of insulin-producing pancreatic beta cells, according to a study by UCLA researchers.

What causes this accumulation of IAPP in pancreatic beta cells of people with diabetes has remained a mystery, according to an article on the UCLA website. But a team of researchers from the Larry L. Hillblom Islet Research Center led by Peter Butler, MD, professor of medicine at UCLA, may have found an answer in autophagy, a process that clears damaged and toxic proteins from cells.

In a study published online July 18 in the Journal of Clinical Investigation, the UCLA researchers suggest autophagy prevents the accumulation of toxic forms of IAPP in people who do not have type 2 diabetes. In people with type 2 diabetes, the process appears to not work properly, contributing to the destruction of beta cells. As the body’s insulin producers, beta cells play a key role in maintaining healthy blood sugar levels.

“Only a few previous studies have reported that autophagy is important for beta cell function and survival,” Safia Costes PhD, a research scientist at the Hillblom Center and the study’s co-first author, said in the article. “Those studies, however, were not conducted to address the role of this process in the regulation of the amyloidogenic protein, which is an important contributor to type 2 diabetes.”

Investigators found that autophagy plays a role in clearing IAPP from pancreatic beta cells using three experimental models: pancreatic beta cells, isolated pancreatic islets from mice that express the human form of IAPP and human islets.

To corroborate the findings, the researchers also developed a mouse model that was deficient for autophagy specifically in beta cells with expression of the human form of islet amyloid polypeptide. They found that mice that had beta cells in which autophagy didn’t work properly showed elevated levels of toxic IAPP, which led to the death of the beta cells. As a result, those mice developed diabetes.

“The goal of our work is to understand the cellular mechanisms responsible for beta cell destruction so that we can identify the best targets for beta cell protection,” Costes said in the article. “This would aid the development of the next generation of treatments as well as combination therapies for
type 2 diabetes.”

The research was supported by grants from National Institute of Diabetes and Digestive and Kidney Diseases, the National Institutes of Health, the Larry L. Hillblom Foundation and the Esther B
O’Keeffe Foundation.


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