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Pancreatic Islet Cells

Advances in Pancreatic Islet Cell Transplantation

Currently, the most effective method for managing type 1 diabetes is regularly testing blood sugar levels and administering insulin. However, this can be hard on patients and on their bodies, and it does not control type 1 diabetes (T1D) as well as the pancreas does naturally on its own. But in individuals with T1D, the immune system mistakenly attacks and destroys insulin-producing beta cells produced by the pancreas, which is why insulin injections are necessary.

Researchers have been testing methods of transplanting pancreatic islet cells into patients with T1D in an effort to replicate or restimulate the body’s natural process for managing blood sugar. One of the challenges that they have faced is keeping transplanted cells alive and functioning for more than a few days or possibly weeks. They often do not establish the proper vascularization or oxygenation necessary for survival. In some cases, they are once again attacked and destroyed by the immune system.

A recent study shows encouraging results when it comes to islet cell transplantation, however. Rather than transplanting the cells into or near the liver, scientists placed them under the skin. The islets were encapsulated in a collagen-based matrix that provided a layer of protection while also improving the amount of oxygen the cells received. Scientists are not entirely sure why this process works, but it has shown positive results in mouse models.

One hundred mice whose pancreases had been removed were transplanted with collagen-encased islet cells from mice, pigs, and humans. Results showed that the mice did not require insulin injections to control blood sugar levels for up to 100 days. It is important to note that tests in mouse models do not always translate exactly the same in human models. Scientists do not yet know if humans would experience the same response to this approach. More testing is needed.

But it is a step in the right direction toward improving diabetes management and stimulating a more natural and effective process. Though not involved with this particular study, the Diabetes Research Connection (DRC) is committed to advancing understanding and treatment of the disease by providing critical funding to early career scientists. One hundred percent of donations go directly to researchers and their projects. Learn more and find out 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
zhang
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?
Melanie
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