Harmful proteins linked to the development of Type 2 diabetes.

proteinsResearchers have demonstrated that people with type 2 diabetes have an abundance of a protein call islet amyloid polypeptide (IAPP). The protein is correlated to the loss of insulin-producing beta cells. Pancreatic beta cells play a key role in maintaining healthy blood sugar levels by producing insulin. Diabetes and Alzheimer’s show similarities as both are impacted by accumulation of amyloid proteins.

The research findings were published in the Journal of Clinical Investigation and reveals that the accumulation of IAPP is due to the failure of toxic proteins being cleared from the cell. The process is called autophagy and in people diagnosed with type 2 diabetes the cellular protein removal process appears to be impaired contributing to the destruction of beta cells. The researchers confirmed the results by developing a novel mouse model that was deficient in the autophage process, revealing elevated levels of accumulated IAPP, leading to the death of beta cells.

“Only a few previous studies have reported that autophagy is important for beta cell function and survival,” said Safia Costes, a research scientist at the Hillblom Center and the study’s co-first author. “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.”

“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. “This would aid the development of the next generation of treatments as well as combination therapies for Type 2 diabetes.”


Jacqueline F. Rivera, Safia Costes, Tatyana Gurlo, Charles G. Glabe, Peter C. Butler. Autophagy defends pancreatic β cells from human islet amyloid polypeptide-induced toxicity. Journal of Clinical Investigation, 2014; DOI: 10.1172/JCI71981

Be Sociable, Share!

    Leave a Reply

    Your email address will not be published.