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This page shares the latest news in T1D research and DRC’s community.

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Diabetes Jigsaw Puzzle

Exploring the Potential Impact of Genetics and Infection on T1D Risk

There is no clear, concise explanation for why some people develop type 1 diabetes (T1D) and others do not, or what puts some people at greater risk for the disease. The origins and triggering factors for T1D are something that scientists have been studying for decades. A recent study looks at the possible relationship between genetic risk variants and viral infections and their impact on T1D development.

In some individuals, enteroviruses may trigger or accelerate disease development. However, in others, these same viruses may stimulate a variety of protective factors. Both genetic and environmental factors come into play, and researchers are exploring how to use these findings to improve treatment and prevention of T1D.

Scientists know that the destruction of insulin-producing beta cells plays a role in disease development. Some individuals present with autoantibodies long before T1D develops, and there are still beta cells present in many people even after living with the disease for many years. Yet they are still unsure about exactly what triggers beta cell destruction.

Studies have shown that around 50 percent of T1D risk is heritable. But just because a person carries this risk, does not necessarily mean they will develop the disease. There are around 60 different loci for single-nucleotide polymorphisms (SNP) that are associated with T1D and may contribute to risk.

Researchers believe that enteroviruses may also play a role. Many links have been found between enterovirus infections and the presence of various autoantibodies.  These infections may trigger beta cell autoimmunity in individuals who already have factors that put them at greater risk of developing T1D. By more effectively identifying individuals who have multiple risk factors, scientists may be able to create targeted antiviral treatments or preventive virus vaccines.

There is still a great deal of research to be done regarding the development of and triggers for T1D. Genetics, environment, and infection may all play a role, but their impact differs from person to person. There is also limited insight into factors such as ethnicity and gender, especially when looking at enteroviral etiology.

Though not involved with this study, the Diabetes Research Connection (DRC) contributes to current bodies of research through providing critical funding for early career scientists pursuing projects related to the diagnosis, prevention, treatment, and eventual cure for T1D. Scientists are learning more about the disease every day. Support these efforts by visiting http://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.
Wearable Skin Fluorescence Imaging Patch for the Detection of Blood Glucose Level on an Engineered Skin Platform
A Potential Second Cure for T1D by Re-Educating the Patient’s Immune System
L Ferreira
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
Han Zhu
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?
Is Cholesterol Exacerbating T1D by Reducing the Functionality and Regeneration Ability of Residual Beta Cells?
Regeneration Ability of Residual Beta Cells
A Call to Question… Is T1D Caused by Dysfunctionality of Two Pancreatic Cells (β and α)?
Xin Tong
Novel therapy initiative with potential path to preventing T1D by targeting TWO components of T1D development (autoimmune response and beta-cell survival)
flavia pecanha