New Clue to Development of Diabetes
Researchers have discovered a mechanism that can eliminate excess quantities of a harmful protein in people with Type 2 diabetes.
The discovery sheds light on the accumulation of the protein called islet amyloid polypeptide, or IAPP. That accumulation is linked to the loss of pancreatic beta cells that produce insulin.
Researchers from UCLA appear to have found why that happens. They said that autophagy, a process that clears damaged and toxic proteins from cells, may be to blame.
In their study, published in the Journal of Clinical Investigation, the UCLA researchers said that in people who do not have Type 2 diabetes, autophagy prevents the accumulation of toxic forms of IAPP.
But in people who do have Type 2 diabetes, the process appears to malfunction, contributing to the destruction of beta cells. These cells are key in maintaining healthy blood sugar levels.
“Only a few previous studies have reported that autophagy is important for beta cell function and survival,” said Safia Costes, a research scientist and the study’s co-first author. But, Costes added, those studies didn’t address “the role of this process in the regulation of the amyloidogenic protein, which is an important contributor to Type 2 diabetes.”
In reaching their conclusion, the investigators used pancreatic cells from mice, which are similar to the human form of IAPP, as well as cells from humans.
“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.”