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

Marika Bogdani lab photo

Connect For A Cure: November 2019 Newsletter

The word is getting out, we have some exciting new research updates for you.

We had a record number of early-career scientists submit their research project proposals for funding this year. You can view the new projects in early 2020. We continue to see early-career scientists go on to do amazing things. Wendy Yang, Ph.D., was published for a second time, in the US National Library of Medicine National Institute of Health and as a result her DRC funded project is getting more exposure. Peter Thompson, Ph.D., one out of 20 early-career scientists DRC has supported was just given the opportunity to start his own lab in Canada.

Click on the link below to read more about what we’ve been up to and the impact we are making together. It takes a community to connect for a cure!

November 2019 Newsletter

Learn More +
Addiction Bottle Capsule

Rotavirus Vaccine May Reduce Risk of Type 1 Diabetes

There is no single factor that is entirely responsible for the development of type 1 diabetes. Scientists believe that both genetic and environmental factors play a role. One area that they are examining more closely is the impact of enteroviruses. Studies have found that since the introduction of two rotavirus vaccines in 2006 and 2008, the incidence of type 1 diabetes in children has decreased.

A recent study compared data from 2001 to 2017 for nearly 1.5 million infants in the United States. They looked at the incidence rate of type 1 diabetes in those who received the full series of either rotavirus vaccine (pentavalent RotaTeq or monovalent Rotarix), those who received only partial vaccination, and those who were unvaccinated either by parental choice or because the vaccinations had not yet been developed. They also looked at incidence rates among children who received both a rotavirus vaccine and the diphtheria, tetanus, and pertussis (DTaP) vaccines at the same time, and those who received only the DTaP vaccines.

While partial vaccination had no impact on risk of type 1 diabetes, infants who completed the rotavirus vaccine series showed a 33% reduction in risk, with those receiving the pentavalent vaccine experiencing a 37% lower risk. In addition, children who were vaccinated had lower hospital admission rates due to enteroviruses within 60 days of being vaccinated than children who were unvaccinated. According to the study, in terms of type 1 diabetes risk, “Overall, there was a 3.4% decrease in incidence annually in children ages 0-4 in the United States from 2001-2017, which coincides with the vaccine introduction in 2006.”

When the rotavirus and DTaP vaccines were administered together, there was a 56% reduction in risk of developing type 1 diabetes than when DTaP vaccines only were given. This leads scientists to believe that the rotavirus vaccine plays an integral role in risk reduction. While it does not entirely prevent infants from developing type 1 diabetes at some point in their life, it may reduce their risk of the disease.

Previous studies have shown that rotavirus infection may increase the destruction of insulin-producing beta cells in diabetes-prone mice. In addition, children who had multiple rotavirus infections had increased islet antibody levels which may contribute to islet autoimmunity, which in turn is linked to type 1 diabetes risk.

Though more research is necessary including longer longitudinal studies to determine if type 1 diabetes was prevented entirely or only delayed, this study is a step in the right direction toward potentially reducing diabetes risk. Encouraging families to get their children the rotavirus vaccine – which is covered at no cost under most health insurance plans – could be an effective strategy in decreasing risk of type 1 diabetes.

Diabetes Research Connection (DRC) is interested to see how these findings may impact the future of prevention efforts for type 1 diabetes and what additional research will discover. The DRC supports early career scientists in pursing novel research regarding type 1 diabetes including diagnosis, prevention, treatment, and management of the disease. To learn more about current projects and how to support these efforts, visit http://diabetesresearchconnection.org.

Learn More +
Chemistry Equipment Gloves

Exploring C-Peptide Persistence in Type 1 Diabetes

In diagnosing diabetes, be it type 1 or type 2, one of the key factors doctors look for is C-peptide levels. Traditionally, scientists have believed that low C-peptide levels indicated type 1 diabetes as the body is unable to produce an adequate supply (if any) of insulin, while higher C-peptide levels were associated with type 2 diabetes as the body made insulin but was unable to effectively use it.

However, a recent study shows that this may not be entirely accurate. In a large cohort study in Scotland, there was a broad range of variability in C-peptide persistence across individuals of different ages and duration of disease. Individuals who were older when diagnosed and were close to age of diagnosis had higher C-peptide levels than those who were adolescents when diagnosed and had been living with the disease for a longer period of time. Scientists believe this may point toward there being multiple genetic networks that impact diabetes risk.

The findings also showed that similar C-peptide levels may be present in individuals with adult-onset type 1 diabetes who did not immediately require insulin treatment as those who were diagnosed with type 2 diabetes. Many people with higher C-peptide levels also have increased amounts of proinsulin, which is a prohormone precursor to insulin. However, the cells do not respond to primary stimuli which could mean that they are in a stunned state. If this is the case, there is a potential that they could recover and once again play an active role in insulin production.

The ratio of proinsulin to C-peptide may also be influenced by genetic risk of diabetes. Both genetics and environmental factors may come into play regarding damage to beta cells and their ability or inability to produce insulin.

This study challenges previous understanding about the differences in type 1 and type 2 diabetes when it comes to diagnosis and treatment. There may be the potential to stimulate pancreatic beta cell function in individuals with type 1 diabetes depending on their levels of proinsulin, insulin, and C-peptide.

Diabetes Research Connection (DRC) is interested to see how this may impact the future of diagnosis and treatment of diabetes. It could certainly lead the way to more in-depth research opportunities, and the DRC provides critical funding to support these types of initiatives. Early career scientists can receive up to $75K from the DRC to pursue novel research projects focused on type 1 diabetes. To learn more, visit http://diabetesresearchconnection.org.

Learn More +
DRC Diabetes Researching

Could Improving Cell-to-Cell Communication Enhance Cell Replacement Therapy Options for Type 1 Diabetes?

Researchers have been exploring the potential of stem cell therapies for years, however this is a very challenging endeavor because there are many factors that influence cell development, differentiation, and fate. In the case of type 1 diabetes, researchers have been studying methods for preventing the destruction of insulin-producing beta cells, stimulating the generation of new cells, and directing differentiation of stem cells among other strategies.

In a recent study, scientists focused on enhancing cell-to-cell communication in order to influence differentiation of embryonic stem cells. They examined the role of Connexin 43 (Cx43) specifically, which is a gap junction (GJ) channel protein. Scientists found that by using the AAP10 peptide to activate Cx43 GJ channels, they could steer differentiation of cells toward definitive endoderm and primitive gut tube lineages. In turn, with improved communication between cells triggered by the AAP10 peptide, definitive endoderm cells were more likely to become pancreatic progenitors and pancreatic endocrine progenitors.

Pancreatic progenitors (PP) and pancreatic endocrine progenitors (PE) play a role in the development of pancreatic islet cells which produce insulin and glucagon. These are the same cells that the body mistakenly attacks and destroys in individuals with type 1 diabetes. The ability to influence the differentiation of human embryonic stem cells into PPs and PEs may support improved cell replacement therapies for diabetes.

There is still a great deal of research to be done as it is difficult to manipulate the mechanisms of cell communication in order to produce desired results. Scientists are also continuing to investigate whether improved intercellular communication could lead to an increased production of pancreatic islet cells.

Researchers involved in this study include Dr. Wendy Yang, Dr. Laura Crisa, and Dr. Vincenzo Cirulli. Yang’s research is funded by Diabetes Research Connection (DRC) and Crisa and Cirulli are part of the DRC’s scientific review committee. To learn more about the DRC and the funding it provides to support type 1 diabetes research, visit http://diabetesresearchconnection.org.

Learn More +
Biochemistry Biology Blue

Antibody-Drug Conjugate May Help Reduce Allograft Rejection.

Cell transplantation has been an area of focus in developing treatment for type 1 diabetes. Many studies have examined both autologous and allogeneic transplants and the benefits and risks they provide. A major challenge continues to be rejection and the body’s destruction of these cells, whether initially derived from its own cells or not.

However, a recent study found that an anti-CD103 antibody-drug conjugate (M290-MC-MMAF) may reduce pancreatic islet allograft rejection in mice. This drug decreased the amount of CD103+CD8+ effector T cells while at the same time increasing the amount of CD4+CD25+ regulatory T cells. This balance led to improved survival rate of the allograft and supported immunosuppression without causing systemic toxicity. When CD103+CD8+ levels were increased, allograft rejection quickly followed.

While this study has only been conducted in mouse models, it shows potential for pancreatic islet allografts in treating type 1 diabetes. Further research is necessary to determine how this process translates to human cells. M290-MC-MMAF could eventually be used as a therapeutic intervention to reduce risk of allograft rejection in humans.

Diabetes Research Connection (DRC), though not involved in this study, stays abreast of the latest discoveries in the field and supports early career scientists in pursuing novel, peer-reviewed research projects related to type 1 diabetes. Scientists receive funding that is critical to conducting research and improving the diagnosis, treatment, and management of the disease and one day finding a cure. To learn more about current projects and how to support these efforts, visit http://diabetesresearchconnection.org.

Learn More +
Biomarkers

Early Biomarker for Pancreatic Beta Cell Loss Related to Type 1 Diabetes Identified.

For years, researchers have known that pancreatic beta cell death plays a major role in the development of type 1 diabetes. They have been striving to detect this process early on in order to better assess risk for the disease and develop potential treatments to stop progression. When the body destroys insulin-producing beta cells, it is no longer able to effectively manage blood glucose levels resulting in type 1 diabetes (T1D), a condition that currently has no cure.

In a recent study, researchers used diabetic mice and serum samples from individuals with various stages of T1D as well as INS-1 cells and human islets “to detect an early biomarker of T1D-associated beta-cells loss in humans.” The enriched microRNA (miR-204) that they discovered is released by beta cells during cell death and is detectable in human serum. However, it is only present in elevated levels in individuals with T1D and those who are autoantibody positive, not in individuals with type 2 diabetes.

This discovery may play a role in improving early detection of pancreatic beta cell death prior to full onset of T1D. In turn, that may open doors to new research and developments in treatment in order to reduce risk of T1D.

Diabetes Research Connection (DRC) is excited to see what this discovery could mean for the future of T1D diagnoses and prevention efforts. The DRC supports early career scientists in pursuing novel, peer-reviewed research projects focused on the diagnosis, prevention, treatment, and eventual cure of type 1 diabetes. Learn more about current projects and how to support these efforts by visiting http://diabetesresearchconnection.org.

Learn More +

OUR PROJECTS

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
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