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Understanding the Relationship between Diabetes and COVID-19

COVID-19 is a relatively new virus, and one that researchers are continuing to learn more about every day. Studies have shown that individuals with underlying health conditions are at increased risk for complications and mortality from COVID-19; this includes diabetes. Healthcare providers have also seen an increase in new-onset diabetes cases and are interested in knowing whether this is related to COVID-19. The virus binds to ACE2 receptors, which are expressed in pancreatic beta cells. This may contribute to the development of ketosis and ketoacidosis in patients with COVID-19 and alter glucose metabolism.

In an effort to gather data and investigate any potential relationship between COVID-19 and diabetes, researchers have established a global registry called the CoviDIAB Registry. This registry will collect data from patients around the world that “includes, but is not limited to, the prolonged effects after the complications of the virus and diabetes subside, whether the new-onset diabetes is a different type of diabetes, and the impact of different phenotypes present at presentation and during recovery.”

The data would then be used to guide future studies and potentially develop more effective treatment methods. There have been multiple cases where individuals have been diagnosed with COVID-19 as well as ketosis or diabetic ketosis. In turn, this developed into ketoacidosis and diabetic ketoacidosis (DKA) in some patients, which can be dangerous to their health if left untreated. Both ketosis and diabetes are linked to longer hospital stays for COVID-19 patients, and ketosis has also been attributed to an increased risk of mortality.

More research is necessary to understand any possible connections between COVID-19 and diabetes, including severity of complications and diagnosis of new-onset diabetes. As more data is collected and analyzed, researchers can help guide appropriate treatment strategies in order to reduce complications and better manage patient health.

Though not involved with this study, the Diabetes Research Connection (DRC) has been involved in advancing diabetes research through providing critical funding to early career scientists. Donations come from individuals, corporations, and foundations, and 100% of these funds go directly to the scientists for their projects. Check out current DRC projects and learn more about how to 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