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Expanding Type 1 Diabetes Research Through Marmoset Models

It is not uncommon for researchers to use animal models for initial research before transitioning to human clinical trials. Many animals’ systems are biologically similar in nature to humans and respond in similar ways to various diseases and medications. Often mouse models are used for diabetes research, but other species such as nonhuman primates (NHP) are also advantageous. While various types of monkeys and baboons have been used to study diabetes pathogenesis and treatment, there was previously not a marmoset model.

In a recent study, researchers successfully induced type 1 diabetes mellitus in marmosets. They conducted a partial pancreatectomy and administered streptozotocin (STZ) to decrease and destroy insulin-producing beta cells. This led to the marmosets having higher sustained blood glucose levels (above 200 mg/dL) and the inability to manage their condition through natural insulin production. Instead, they were injected with exogenous human insulin which brought their glucose levels back into the target range. Researchers found that they had a high sensitivity to human insulin making them a valuable NHP model.

Multiple glucose and insulin tolerance tests were conducted to determine how the diabetic marmosets responded compared to normal marmosets and whether they would be suitable candidates for future testing regarding islet transplantation. Continuous glucose monitors (CGM) were used to compare normal marmosets with diabetic marmosets as well, further showing that diabetic marmosets had consistently higher blood glucose levels, especially following meals, much like humans with type 1 diabetes.

While additional research is necessary, researchers believe that marmoset models could play an integral role in type 1 diabetes research and the advancement of preclinical testing. They were able to effectively induce diabetes in the marmosets and control it using human insulin, so the next step would be to move to cell transplantation trials. Eventually these transplant models may translate to human clinical trials and enhance diabetes treatment options.

It is these types of studies and use of animal models that help to advance scientists’ understanding and treatment of type 1 diabetes and allow them to work toward a cure. Diabetes Research Connection (DRC) is interested to see how marmoset models will influence the future of diabetes care.

DRC is committed to supporting early career scientists in pursuing novel, peer-reviewed research regarding type 1 diabetes. Researchers can receive up to $75K in funding for their projects allowing them to move forward with their work. Learn more about current projects and how to help 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.
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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
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Taming a Particularly Lethal Category of Cells May Reduce/Eliminate the Onset of T1D
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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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