Type 1 diabetes is often described as a condition in which the body fails to produce the hormone insulin. New research, however, provides further evidence that not all insulin production is lost with the condition, and this may be down to an anti-inflammatory protein.

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Researchers have found that many patients with type 1 diabetes still produce some insulin.

Researchers from Uppsala University in Sweden found that nearly half of patients who had been living with diabetes for more than 10 years produced some insulin.

What is more, these insulin-producing patients also had higher blood levels of immune cells that produce a protein called interleukin-35 (IL-35), which is believed to suppress the immune system and reduce inflammation.

Study co-author Dr. Daniel Espes, of the Department of Medical Cell Biology at Uppsala University, and colleagues recently reported their findings in the journal Diabetes Care.

Type 1 diabetes is estimated to affect around 1.25 million children and adults in the United States. The condition arises when the immune system mistakingly attacks the insulin-producing cells, or beta cells, of the pancreas.

It was once thought that patients with type 1 diabetes experienced a complete loss of insulin production, but increasingly, studies have indicated that some patients still possess functioning beta cells.

For this latest study, Dr. Espes and colleagues set out to determine whether there are any immunological mechanisms that might explain why some patients with type 1 diabetes still produce some insulin.

The research included 113 patients with type 1 diabetes who were aged 18 and older. All patients had been living with the condition for at least 10 years.

Using the ultra-sensitive ELISA test, the researchers measured the levels of C-peptide in the patients’ blood, which is an indicator of insulin production.

Additionally, the researchers measured levels of circulating cytokines among the patients, including IL-35. Cytokines are proteins secreted by immune cells that play a key role in cell signaling.

The team found that almost half of patients with type 1 diabetes were C-peptide-positive, meaning that they had some level of insulin production.

The results also revealed that patients who were C-peptide-positive had significantly higher levels of IL-35 in their blood, compared with patients who were C-peptide negative – that is, those who had lost all insulin production.

Previous research has suggested that IL-35 can suppress autoimmune disease, so it is possible that in some patients with type 1 diabetes, the protein prevents the immune system from attacking and destroying insulin-producing beta cells.

However, Dr. Espes and colleagues were unable to determine whether C-peptide positive patients had higher IL-35 levels at type 1 diabetes diagnosis, or whether levels of the protein increased over time due to a reduced immune system attack on beta cells.

While further studies are needed to gain a better understanding of how IL-35 might relate to insulin production, the researchers believe that their current findings demonstrate the potential of IL-35 as a drug treatment for type 1 diabetes.

Furthermore, since the findings show that almost half of patients with type 1 diabetes produce some insulin, the team says that it may be possible to encourage regeneration of their remaining beta cells and boost insulin production.

Researchers at Uppsala University Hospital are already testing the feasibility of these strategies.

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