Type 2 diabetes may be transmissible, ground-breaking study suggests

by Barbara Hewitt on August 4, 2017

It is possible that type 2 diabetes may be transmissible but scientist say more work is needed to find out if it really can be induced by a pancreatic protein that has gone wrong.

Very early findings from a research project in the United States suggest it is worth looking at how a misfolding protein may drive the disease and further studies could change the way that the medical establishment view the condition.

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It is well documented that type 2 diabetes is more commonly the result of being overweight and leading a sedentary lifestyle and studies have proved it can be helped and even reversed by a strict diet and exercise regime.

But preliminary findings by scientists at the McGovern Medical School, part of the University of Texas, suggest that type 2 diabetes may be transmissible in a way that is similar to prion disorders such as Creutzfeldt-Jakob disease or bovine spongiform encephalopathy, commonly known as mad cow disease.

The study looked at the possibility that type 2 diabetes might be caused by a misfolding of islet amyloid polypeptide protein (IAPP). ‘Considering the experimental nature of the models and conditions utilised in this study, the results should not be extrapolated to conclude that type 2 diabetes is a transmissible disease in humans without additional studies,’ warned Claudio Soto, lead researcher and professor of neurology.

Although the disease has been linked to a variety of genetic and environmental risk factors, what causes type 2 diabetes is still not completely understood. More than 90% of type 2 diabetes patients show abnormal protein deposits in their pancreatic islets that are aggregates of IAPP.

The precise role of these IAPP aggregates in type 2 diabetes is still unclear, but they may damage and kill the pancreatic beta cells that secrete insulin in response to elevated blood glucose levels.

‘Our data therefore opens up an entirely new area of research with profound implications for public health. This prion like mechanism may play a key role in the spreading of the pathology from cell to cell or islet to islet during the progression of type 2 diabetes,’ Soto explained.

He pointed out that a key feature of diseases like Creutzfeldt-Jakob is that a small number of misfolded protein aggregates can serve as seeds that induce the misfolding of additional proteins until they form large aggregates capable of damaging the cells. In the case of prion diseases, these seeds can even be transmitted from one individual to another but Soto said they don’t know yet if that is the case in diabetes.

The research found that injecting small amounts of misfolded IAPP aggregates induced the formation of protein deposits in the pancreases of mice expressing human IAPP. Within weeks, these mice developed several symptoms associated with type 2 diabetes, including a loss of pancreatic beta cells and elevated blood glucose levels.

Small amounts of misfolded IAPP could also induce the formation and accumulation of large IAPP aggregates in pancreatic islets isolated from healthy human donors. Misfolded IAPP can therefore induce protein aggregation and disease similarly to infectious prion proteins.

‘Perhaps more important than a putative inter-individual transmission, the prion-like mechanism may play a key role in the spreading of the pathology from cell to cell or islet to islet during the progression of type 2 diabetes,’ Soto added.


The opinions expressed in this article do not necessarily reflect the views of the DiabetesForum.com Community and should not be interpreted as medical advice. Please see your doctor before making any changes to your diabetes management plan.

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