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Beta Cells

Enhancing Protection of Insulin-Producing Beta-Cells

Enhancing Protection of Insulin-Producing Beta-Cells

Insulin-producing beta-cells play a critical role in managing blood sugar by automatically releasing insulin in response to increased blood glucose levels. In individuals with type 1 diabetes, the immune system mistakenly attacks and destroys these cells, leaving blood sugar unchecked. Since the body no longer produces insulin on its own, individuals must regulate this process, often with the help of continuous glucose monitors, insulin pumps, and other devices.

For years, researchers have been trying to better understand why the immune system attacks these beta-cells and how they can prevent this process from occurring. A recent study found that the enzyme renalase may play a role. Stress is a key factor in cell destruction, and by inhibiting renalase, cells have greater protection against the effects of endoplasmic reticulum (ER) stress. This inhibiting may help enhance the survival of transplanted pancreatic beta-cells in the treatment of type 1 diabetes, and it may have the ability to help slow progression of the disease at its onset.

Researchers tested these processes on non-obese diabetic (NOD) mouse models as well as human cells. In the mice, the beta-cells that had the functionality of renalase disabled survived better against immune system attacks than fully functional beta-cells. In addition, certain T-cells were less likely to attack the pancreatic beta-cells without renalase function. The same results held true for human cells; they were better protected against ER stress.

Furthermore, the researchers found that there was already an FDA-approved drug that targets an enzyme similar to renalase and is used to treat hypertension called pargyline. They tested pargyline in a small clinical trial to evaluate its effects on pancreatic beta-cells and whether or not it could protect them against ER stress. Their results showed that it had a protective effect on both mouse models and human cells. The next step is to test the drug in human clinical trials.

More research and testing are needed to determine whether this drug could be used to protect against or slow the progression of type 1 diabetes or be used as the starting block for developing a new drug that specifically targets renalase. However, this is a step in the right direction toward improving prevention methods for type 1 diabetes.

Many studies are focused on treatment or potential cures for type 1 diabetes, but more funding is necessary for prevention efforts like the one above. The Diabetes Research Connection, though not involved with this study, supports research across all aspects of type 1 diabetes, including prevention. There are several current projects led by early-career scientists focused on disrupting the onset of T1Dblocking processes that contribute to the development of the disease, and preserving insulin secretion, which can potentially impact prevention efforts if fully funded. Learn more about these projects and how to help 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.
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