Spread of misfolded proteins could trigger type 2 diabetes
Type 2 diabetes and prion disease seem like an odd couple, but they have something in common: clumps of misfolded, damaging proteins.
Now new research finds that a dose of corrupted pancreas proteins induces normal ones to misfold and clump. This raises the possibility that, like prion disease, type 2 diabetes could be triggered by these deformed proteins spreading between cells or even individuals, the researchers say.
When the deformed pancreas proteins were injected into mice without type 2 diabetes, the animals developed symptoms of the disease, including overly high blood sugar levels, the researchers report online August 1 in the Journal of Experimental Medicine.
“It is interesting, albeit not super-surprising” that the deformed proteins could jump-start the process in other mice, says Bruce Verchere, a diabetes researcher at the University of British Columbia in Vancouver. But “before you could say anything about transmissibility of type 2 diabetes, there’s a lot more that needs to be done.”
Beta cells in the pancreas make the glucose-regulating hormone insulin. The cells also produce a hormone called islet amyloid polypeptide, or IAPP. This protein can clump together and damage cells, although how it first goes bad is not clear. The vast majority of people with type 2 diabetes accumulate deposits of misfolded IAPP in the pancreas, and the clumps are implicated in the death of beta cells.
Deposits of misfolded proteins are a hallmark of such neurodegenerative diseases as Alzheimer’s and Parkinson’s as well as prion disorders like Creutzfeldt-Jakob disea Continue reading