A new study has identified what is happening inside insulin-producing pancreatic cells that can develop into a neonatal form of non-autoimmune type 1 diabetes, and which could also be a key factor in type 2 diabetes . Researchers have found a potential target that could be used by medication aimed at protecting the normally functioning proteins essential for producing insulin .
The study, from the University of Michiga, revealed that specific insulin gene mutations that are involved in neonatal diabetes could be responsible for the misfolding of a part of the proinsulin proteins in the pancreas’ beta cells . Proinsulin proteins, which are the precursors of insulin, help to regulate the body’s blood sugar levels .
The research, which was published in the journal PLoS One, found that the misfolded mutant proteins cause normal proinsulin proteins in beta cells to misfold as well. Peter Arva, the study’s senior author, said “Once the ‘good’ proinsulin turns ‘bad,’ it cannot be made into insulin and so the beta cells, and then the whole animal, become insulin deficient . The insulin deficiency causes diabetes and from there, things get worse and worse.”
As beta cells don’t perform to the level needed in diabetes, it may be that the beta cell failure of type 2 diabetes also has a critical protein-folding component. Arvan added “The question is, can you reach a point in ordinary diabetes where misfolding causes the problem we have identified?”
Protein folding is thought to play a role in several common diseases. The scientists also found that protein-misfolding events could first block insulin production and cause insulin deficiency, which leads to diabetes.

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