An article in Medical New Today caught our eye this week – research recently found that people with type 1 diabetes produced some insulin.
Yeah, yeah, I thought, it’s the newbies again. But apparently not. The Uppsala University in Sweden’s researchers found that nearly half of patients who’d had the condition for more than ten years did produce insulin.
Type 1 diabetes is routinely described as a condition where the body doesn’t make insulin. The researchers found that the insulin-producing patients had higher levels of immune cells that produce a protein called interleukin-35 (IL-35). This is believed to suppress the immune system and reduce inflammation in the body.
The findings were reported by the study’s co-author, Dr Daniel Epses, in Diabetes Care.
Type 1 diabetes happens when the immune system mistakenly attacks insulin-producing cells or beta cells in the pancreas.
This was believed to lead to a complete loss of insulin production in type 1 diabetics, but studies in recent years have shown that some patients still have functioning beta cells.
Dr Epses and his colleagues wanted to work out if there are any immunological mechanisms that could explain why some type 1 diabetics still produce small amounts of insulin.
The study looked at 113 patients aged 18 and over. All of them had been living with diabetes for at least ten years.
Researchers measured the levels of C-peptide in the blood – an indicator of insulin production. They also measured circulating cytokine levels, including IL-35. Cytokines are proteins that are secreted by the immune cells and they play a major role in cell signalling.
The team found that almost half the patients were C-peptide positive – in other words, they had some level of insulin production. The results also showed that patients who were C-peptide positive had significantly higher levels of IL-35 in their blood, compared with the patients who were C-peptide negative (the ones who had lost all insulin production).
Previous research has indicated that IL-35 can suppress auto-immune disease. It is possible that in some type 1 diabetics, the protein prevents the immune system from attacking and destroying beta cells.
Dr Epses and his colleagues, who are based at the Department of Medical Cell Biology at Uppsala University, couldn’t determine if C-peptide positive patients had higher IL-35 levels at type 1 diabetes diagnosis, or whether levels of the protein increased over time because of a reduced immune system attack on insulin-producing beta cells.
More study is needed to gain an understanding of how IL-35 might relate to insulin production. The researchers believe, however, that their findings show the potential of IL-35 as a treatment for type 1 diabetes. As the findings also show that almost half of patients with type 1 diabetes produce some insulin, the team thinks it might be possible to encourage regeneration of their remaining beta cells and so boost insulin production.