DRC & Research News

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

Get the most recent diabetes research news, delivered straight to your inbox

New Preclinical Drug

A New Approach to Treating Diabetes and Its Effects

For decades, researchers have been studying cellular changes in the body that contribute to the development of diabetes. They have created a wide array of treatment options to help manage the effects and minimize complications. As they gain a better understanding of the causes of diabetes, they have also made advancements toward curing or preventing the disease. Each therapeutic modality works slightly differently.

A recent study has found that a new drug may hold promising results when it comes to combatting both type 1 and type 2 diabetes. This drug has been 18 years in the making and still has a way to go, but it has shown great potential in current mouse models as well as isolated human islets.

The drug, SRI-37330, is administered orally and affects both insulin and glucagon production in the pancreas and liver. In individuals with type 1 diabetes, the body does not produce enough insulin to effectively manage blood sugar while releasing too much glucagon which can contribute to hyperglycemia. SRI-37330 may help control hyperglycemia, hyperglucagonemia, excessive glucose production by the liver, and fatty liver, which are all significant issues when it comes to diabetes.

Lead researcher Dr. Anath Shalev and her team have spent nearly two decades studying diabetes and its potential causes. This led them to identify a key protein, TXNIP, which can have detrimental effects on islet function and survival. SRI-37330 has the ability to inhibit TXNIP signaling and expression without negatively impacting other genes or processes.

According to their research, not only did the drug help protect mouse models from developing type 1 diabetes, it controlled blood glucose levels more effectively than metformin and empagliflozin, two oral anti-diabetic drugs commonly used today. SRI-37330 helped to decrease glucagon production and release by pancreatic islets and the liver without having the countereffect of increasing hypoglycemia liability in the mice.

One result that researchers did not anticipate was the ability of SRI-37330 to “dramatically improve the severe fatty liver observed in obese diabetic db/db mice.” This opens the door for more studies to determine whether the drug could be used as a potential treatment for non-alcoholic fatty liver disease as well.

Overall, researchers concluded that SRI-37330 is “orally bioavailable, has a favorable safety profile and inhibits TXNIP expression and signally in mouse and human islets, inhibits glucagon secretion and function, lowers hepatic glucose production and hepatic steatosis, and exhibits strong anti-diabetic effects in mouse models of Type 1 and Type 2 diabetes.”

It is important to note that mouse models do not always translate the same in human models. A drug that is effective at treating induced diabetes in mice may not have the same efficacy in humans. More research is needed to see how SRI-37330 would work in human clinical trials and not just isolated human islets or mouse models. However, this drug is an encouraging finding in the field and one that may hold significant potential.

The Diabetes Research Connection (DRC) is interested to see how this study progresses moving forward and what it could mean for the treatment and prevention of type 1 diabetes in humans. This type of work is critical in advancing understanding of the disease as well as care and treatment options. The DRC supports early-career scientists pursuing novel research related to type 1 diabetes by providing up to $50K in funding. Learn more about current projects and how to donate by visiting http://diabetesresearchconnection.org

Please DONATE NOW so DRC can keep bringing you credible, peer-reviewed T1D news and research.

Thank you

Learn More +


See our approved research projects and campaigns.

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