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Diabetes Researching

Could There Be More than One Form of Type 1 Diabetes?

Researchers know that there are significant differences between type 1 diabetes (T1D) and type 2 diabetes (T2D), but now they are digging a little deeper. When it comes to T1D, the disease may not affect everyone in the same way. According to a recent study, there may be more than one endotype, and a major differentiator could be age of diagnosis.

The study looked at a small sample of 19 children diagnosed with T1D within the past two years and compared age of diagnosis against amount of beta cell destruction and levels of proinsulin and C-peptides. They also compared these ratios in a group of 171 adults with T1D based on their age of diagnosis. Their results showed that children who were diagnosed before the age of 7 had much higher levels of proinsulin-insulin co-localization than those diagnosed after age 13. Individuals between ages 7 and 13 were divided and fell into one group or the other.

The researchers also compared results against CD20Hi and CD20Lo immune profile designations for each participant. Children age 7 or younger tended to be CD20Hi, while those age 13 or older were CD20Lo, and the children in between were aligned with their respective groups based on whether they were CD20Hi or CD20Lo.

These differences in proinsulin and C-peptide concentrations demonstrate a distinction in how individuals are impacted by T1D, leading to at least two separate endotypes. Understanding whether an individual has T1D endotype 1 (T1DE1) or T1D endotype 2 (T1DE2) could enable more targeted and effective treatment of the disease based on how each group responds. Individuals with T1DE1 are identified as having higher levels of beta cell loss, therefore may have more difficulty regulating blood glucose. Those with T1DE2 may retain more beta cells, and determining ways to activate and protect these cells could support improved natural insulin production.

Recognizing that T1D affects people differently is a step in the right direction toward more personalized medicine and targeted therapies. Therapeutic trials could be aimed at groups depending on age of diagnosis and specific endotype in the future as larger studies are conducted to determine the significance of these findings.

Diabetes Research Connection (DRC) is committed to supporting advances in research around type 1 diabetes and provides early-career scientists with critical funding for their studies. Research is focused on preventing and curing type 1 diabetes, minimizing complications, and improving quality of life for those living with the disease. Learn more and support these efforts by visiting https://diabetesresearchconnection.org.

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Role of the integrated stress response in type 1 diabetes pathogenesis
In individuals with type 1 diabetes (T1D), the insulin-producing beta cells are spontaneously destroyed by their own immune system. The trigger that provokes the immune system to destroy the beta cells is unknown. However, accumulating evidence suggest that signals are perhaps first sent out by the stressed beta cells that eventually attracts the immune cells. Stressed cells adapt different stress mitigation systems as an adaptive response. However, when these adaptive responses go awry, it results in cell death. One of the stress response mechanisms, namely the integrated stress response (ISR) is activated under a variety of stressful stimuli to promote cell survival. However, when ISR is chronically activated, it can be damaging to the cells and can lead to cell death. The role of the ISR in the context of T1D is unknown. Therefore, in this DRC funded study, we propose to study the ISR in the beta cells to determine its role in propagating T1D.
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Validating the Hypothesis to Cure T1D by Eliminating the Rejection of Cells From Another Person by Farming Beta Cells From a Patient’s Own Stem Cells
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Taming a Particularly Lethal Category of Cells May Reduce/Eliminate the Onset of T1D
JRDwyer 2022 Lab 1
Can the Inhibition of One Specific Body Gene Prevent Type 1 Diabetes?
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Is Cholesterol Exacerbating T1D by Reducing the Functionality and Regeneration Ability of Residual Beta Cells?
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A Call to Question… Is T1D Caused by Dysfunctionality of Two Pancreatic Cells (β and α)?
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Novel therapy initiative with potential path to preventing T1D by targeting TWO components of T1D development (autoimmune response and beta-cell survival)
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