Scientists from institutions across Europe have identified a new molecule that could be used as a biological ‘marker’ in the early diagnosis of type 1 diabetes and signify whether a treatment is working or not.
The research, published in the journal Diabetologia, shows that the molecule miR-409-3p was reduced both in mice with a type 1-like condition and in people recently diagnosed with type 1 compared to their unaffected counterparts. Found to be involved in regulation of the immune response, levels of the molecule rose when mice with a type 1-like condition were treated with an immunotherapy.
Further work is needed to determine how the molecule is involved in the development of type 1, however it could be used as a marker to both assist in the early diagnosis of type 1 and to signify how well a treatment is working.
Why did they do this research?
Currently, screening for and diagnosing type 1 diabetes is done by measuring blood glucose levels and detecting autoantibodies (proteins that allow the immune system to attack and destroy beta cells). However, these ‘markers’ are often only detected when a person has already lost most of their insulin-producing beta cells.
In this research project, part-funded by JDRF, a team of scientists wanted to find a new marker for type 1 that was present in the very early stages of the condition. This way, a person could be diagnosed and treated much sooner, reducing their risk of complications associated with high blood glucose.
It could also help scientists developing treatments that protect beta cells from the immune system’s attack, by allowing them to intervene sooner to save more beta cells and improve glucose management.
Additionally, a new marker could allow researchers to monitor how well future treatments such as immunotherapy are working in people with type 1.
What did they do?
The team began by measuring the levels of certain molecules in the blood and pancreas of either healthy mice or those with a condition similar to type 1 diabetes. They also investigated the biological importance of the molecules by measuring the effects of a known immunotherapy on levels of the molecules.
Next, they recruited three groups of participants: people who had been very recently diagnosed with type 1, people who didn’t have the condition but had a relative with type 1, and people who didn’t have the condition and didn’t have a relative with type 1.
They then took blood samples from all the participants and looked at levels of the same molecules they looked at in the mice.
What did they find?
The scientists found that levels of a particular protein molecule were lower in both the blood and the areas surrounding the beta cells of mice with a type 1-like condition compared to mice without the condition.
When looking at human blood samples they found that the same molecule was also lower in those with recently-diagnosed type 1 diabetes compared to those without type 1. The molecule, called miR-409-3p, was also found to be involved in regulating certain mechanisms of the immune system.
On further investigation, the team found that levels of miR-409-3p increased in the blood of mice with a type 1-like condition following treatment with an immunotherapy, which works in a similar way as teplizumab (clinical trials of which we highlighted last summer) to slow development of type 1 diabetes.
What does this mean for type 1?
Although in its early stages, this research suggests that miR-409-3p could be a new marker of early type 1 diabetes development, enabling us to diagnose and treat the condition sooner.
Combined with experimental therapies to stop the immune attack, early detection could make it possible to save more beta cells, making it easier for people with type 1 to manage their blood glucose.
Secondly, as miR-409-3p levels rose in mice that were treated with an immunotherapy, the molecule could be used to monitor how effective these treatments are in people with type 1.
Finally, as the team found that miR-409-3p had a role in regulating mechanisms of the immune system, this research could add an important piece to the puzzle of why type 1 diabetes happens – allowing us to get a step closer to stopping it altogether.