A new type 1 diabetes medication could prevent the disease by inhibiting a gene associated with the onset of the disease, according to the University of Helsinki.
A drug based on this mechanism has already been approved for the treatment of psoriasis, another autoimmune disease, in the United States. This may accelerate the development of drug therapies for diabetes.
Cases of type 1 diabetes are higher in Finland than in any other country in the world. Hundreds of underlying genes that may cause the disease have been identified, however, most of the mechanisms in action in these genes are not understood by scientists.
This means that people at high risk of developing diabetes can be identified, but there is no effective way of preventing the disease’s progression without risking adverse effects.
Led by Professor Timo Otonkoski, the researchers at the University of Helsinki investigated the mechanisms in the genes associated with type 1 diabetes risk. The researchers were aiming to find novel methods for the prevention of the disease.
“We focused on a gene known as TYK2, as its mutations are known to protect against type 1 diabetes,” said Otonkoski.
The results have been published in the journal Nature Communications.
Neutralising white blood cells
The researchers hypothesised that inhibiting the expression of the TYK2 gene could reduce the destruction of pancreatic beta cells that are known to cause the onset of type 1 diabetes.
These cells produce vital insulin for the body; patients with diabetes need to compensate for these cells with regular insulin injections.
The researcher’s hypothesis was confirmed in the study, and the destruction of beta cells was successfully neutralised by inhibiting TYK2 expression.
“The destruction of beta cells is the result of an autoimmune reaction where white blood cells activated by the body’s immune system attack their own tissues. Using the TYK2 inhibitor, the havoc wreaked by the white blood cells was markedly reduced,” confirmed Otonkoski.
The study also found that eliminating the effect of the TYK2 gene resulted in a reduction of the differentiation of pancreatic islet cells and a reduction in beta cell production.
“However, this adverse effect was only observed in the earlier stages of beta-cell development. Inhibiting TYK2 expression did not affect the functioning of mature beta cells,” said Dr Vikash Chandra, the first author of the paper.
The development of the new type 1 diabetes medication could begin soon
Previous research from Otonkoski’s team successfully developed fully functional pancreatic beta cells from stem cells. These cells can be used to restore insulin production in the body. These findings show that a TYK2 inhibitor could make a promising candidate for a new preventative type 1 diabetes medication.
“We utilised not only cells from which the TYK2 gene had been removed but also a chemical TYK2 inhibitor. This drug molecule has already been approved in the United States for the treatment of psoriasis,” said Otonkoski.
The researchers say the effect of TYK2 inhibitors as type 1 diabetes medication needs to be investigated carefully in an animal model. If the results are positive the team will explore clinical trials.
