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Diabetes X-Ray

Exploring Protective Factors Against Diabetic Kidney Disease

One of the complications that can stem from living with diabetes is the risk of developing diabetic kidney disease. The kidneys play a critical role in filtering waste and excess water out of the blood and sending it out of the body. Prolonged high blood sugar and/or blood pressure can damage the kidneys and prevent them from functioning effectively. Eventually, individuals may require dialysis or a kidney transplant if damage is too extensive.

However, a recent study from the Joslin Diabetes Center found that some people have biological protective factors that may be effective in reducing risk of diabetic kidney disease. Their bodies have certain enzymes that affect glucose metabolism and protect the kidneys. Researchers studied cohorts of individuals who have been living with type 1 or type 2 diabetes for more than 50 years with minimal or no complications. They are referred to as Joslin Medalists.

One key finding was that the Medalists had increased PKM2, an enzyme in the blood that protects against diabetic kidney disease. There were also other metabolites and proteins that appeared at higher levels as well in their plasma. An interesting discovery was that the presence of an amyloid precursor protein (APP)—which is known to signal increased risk of Alzheimer’s disease—may actually work as a protective factor against diabetic kidney disease.

Scientists need to conduct additional research to further understand these potential protective factors and how they can be used to improve diagnosis and treatment of diabetic kidney disease or diabetes in general. Diabetic kidney disease can be a potentially fatal complication, so the more researchers understand about how it develops and the biological protective factors that can decrease risk, the better they can support individuals living with diabetes and their health.

Though not involved with this study, the Diabetes Research Connection (DRC) stays abreast of the latest research regarding type 1 diabetes and ways to improve diagnosis, treatment, and quality of life for individuals with the disease. Through donations from individuals, corporations, and foundations, the DRC provides critical funding for early career scientists to pursue novel research studies and further understanding of type 1 diabetes.


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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?
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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)
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