DRC & Research News

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

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Could Vitamin D Help Protect Against Type 1 Diabetes?

One trend that researchers have noticed in type 1 diabetes (T1D) is that individuals with this disease tend to have some level of vitamin D deficiency. This impacts vitamin D receptor (VDR) expression, which may contribute to the development of diabetes.

A recent study found that higher levels of VDR may actually protect insulin-producing pancreatic beta cells and preserve some of their mass and function. They also found that as circulating glucose levels decreased, so did VDR levels. Maintaining a stable level of vitamin D may help counteract the disease.

Researchers are investigating the potential effectiveness of using vitamin D supplements as a prevention and treatment strategy for type 1 diabetes, and it may be beneficial for type 2 diabetes as well. They need to develop a clearer understanding of the negative regulation of VDR in individuals with the disease and how to improve VDR levels to a point where they would be more protective.

This study was conducted on mouse models, so it would need to be tested in humans as well to see if the same findings are true. However, this could be a step toward proactively reducing risk of T1D and protecting insulin-producing beta-cell function and mass. Researchers are continuing to learn more about VDR expression and its relationship to diabetes.

Diabetes Research Connection, though not involved with this study, is committed to supporting early-career scientists pursuing novel research on type 1 diabetes in order to expand the body of knowledge and help prevent or cure the disease in addition to reducing complications and improving quality of life for those living with the disease. Scientists are learning more every day. To support these efforts and find out more about current projects, visit https://diabetesresearchconnection.org.

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Could Insulin-Producing Beta Cells Play a Role in Triggering Onset of Type 1 Diabetes?

Researchers know that type 1 diabetes (T1D) occurs when the immune system mistakenly attacks and destroys insulin-producing beta cells. This leaves the body unable to self-regulate blood glucose levels because it produces little or no insulin on its own. What scientists have been striving to understand is what causes the body to destroy these cells in the first place.

A recent study found that the beta cells themselves may play a role in signaling the attack. The insulin-producing cells may be sending out signals that increase M1 macrophages that cause inflammation and the resulting cell destruction. The M2 macrophages that reduce inflammation and help repair tissue are not as heavily expressed.

The researchers looked specifically at Ca2+-independent phospholipase A2beta (iPLA2beta) enzymes and the resulting iPLA2beta-derived lipids (idles) and how they are activated by beta cells.  The idols either stimulate M1 macrophages or M2 macrophages depending on the active signaling pathways.

The study involved two sets of mice – one group that had no iPLA2beta expression (knockout mice), and one group with overexpression of iPLA2beta.  Researchers found that even when M1 macrophage activation was induced, the knockout mice experienced an increase in M2 macrophages and a reduced inflammatory state. The mice that had overexpression of iPLA2beta, on the other hand, experience an increase in M1 macrophages and inflammatory eicosanoids.

According to Sasanka Ramanadham, Ph.D., research co-lead, “To our knowledge, this is the first demonstration of lipid signaling generated by beta cells having an impact on an immune cell that elicits inflammatory consequences. We think lipids generated by beta cells can cause the cells’ own death.”

As scientists continue to learn more about lipid signaling and the potential role it plays in the development of type 1 diabetes, this could lead to improved methods of delaying or preventing onset or progression of the disease. This is yet another approach that researchers are taking to understand as much as they can about how and why T1D develops and how to better manage the disease.

It is this type of research that opens doors to advancements toward preventing or curing type 1 diabetes. Diabetes Research Connection (DRC) supports early-career scientists pursuing novel, peer-reviewed research studies focused on improving diagnosis, treatment, and prevention of T1D as well as improving quality of life for individuals living with the disease and one day finding a cure. Ensuring researchers receive necessary funding for their projects is critical. To learn more about current projects and support these efforts, visit https://diabetesresearchconnection.org.

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Redifferentiating Beta Cells to Treat Type 1 Diabetes

All cells serve a specific purpose, and each one plays an integral role in the function and survival of the human body. However, in individuals with type 1 diabetes, insulin-producing beta cells are destroyed leaving the body unable to self-manage glucose levels. Scientists have been trying to determine exactly why this occurs, and how to stop, prevent, or reverse it for years. Each day they learn a little more.

A recent study out of Germany examines dedifferentiation of beta cells as a potential cause for type 1 diabetes.  Researchers believe that insulin-producing beta cells may lose their identity, which in turns causes a regression in function.  They sought to target the affected cells using diabetic mouse models to see if they could redifferentiate the beta cells back to normal function, or at least preserve existing function if regression is caught early.

To do this, they invoked diabetes in mice using streptozotocin but left some functional beta cells. Then, they administered a combination of Glucagon-like peptide-1 (GLP-1) and estrogen in conjunction with long-acting insulin.  The drug was directed to the dedifferentiated beta cells, and results showed that this combination treatment helped to “normalize glycemia, glucose tolerance, to increase pancreatic insulin content and to increase the number of beta cells.”  They also found that when GLP-1/estrogen was used together, rather than each substance on its own, human beta cells also showed improved function.

The mice in the study showed no signs of systemic toxicity even when high doses of the drug were administered.  This could help to ease the way when the treatment is ready to be used in human trials. Researchers want to further explore whether this treatment could be used as a form of regenerative therapy to redifferentiate dedifferentiated beta cells and stimulate insulin production. If type 1 diabetes was detected early on, the therapy could potentially be used to slow or stop cell regression.

This study could change the way that some researchers approach their work and inspire new studies aimed at treating or curing type 1 diabetes. Diabetes Research Connection (DRC) supports early-career scientists in pursuing this type of work by providing necessary financial resources. With proper funding, scientists can move forward with their projects and improve not only understanding of the disease, but also treatment options.  The goal is to one day discover a cure. To learn more about current projects and how to help, visit https://diabetesresearchconnection.org.

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Understanding the Impact of GABA on Insulin Secretion and Regulation

In order to manage blood glucose levels, pancreatic beta cells release insulin in pulses. These bursts of insulin help the body to regulate and stabilize blood sugar. In individuals with type 1 diabetes, however, the pancreatic beta cells that normally secrete insulin are mistakenly destroyed by the body. This leaves the body unable to effectively regulate blood sugar on its own. Understanding the interaction between insulin-producing beta cells and other processes in the body may help researchers improve treatment and prevention options when it comes to diabetes.

A recent study examined the different roles gamma amino-butyric acid (GABA) plays in cell activity. In the brain, GABA is released from nerve cell vesicles each time a nerve impulse occurs. The GABA prepares cells for subsequent impulses by working as a calming agent. Researchers previously believed that this process worked in much the same way in the pancreas.

However, in the pancreas, GABA is evenly distributed throughout the beta cells rather than contained within small vesicles, and it is transported via the volume regulatory anion channel. This is the same channel that helps stabilize pressure inside and outside of cells so that they maintain their shape. Furthermore, research showed that GABA is released in a similar pattern and frequency as pulsatile in vivo insulin secretion. Just like in the brain, GABA plays an integral role in preparing and calming cells to make them more receptive to subsequent insulin pulses.

Scientists are interested in learning more about how GABA signaling can support the regulation of insulin secretion and potentially protect cells from autoimmune activity. This opens new doors for biomedical research that has the ability to impact diabetes care.

It is encouraging to see different types of researchers all coming together and learning from and building upon one another’s work in order to advance understanding, prevention, and treatment of various diseases, including diabetes.

Diabetes Research Connection stays abreast of the latest discoveries in the field and supports early career scientists in contributing to this body of work by providing critical funding for their projects. It is essential that scientists have the resources to pursue novel research in order to develop improved prevention, treatment, and management options for type 1 diabetes. Learn more and support current projects by visiting https://diabetesresearchconnection.org.

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Could Higher-Dose and Lower-Dose Insulin Glargine be Equally Effective in Managing Type 1 Diabetes?

In an effort to maintain greater blood-glucose stability throughout the day and minimize highs and lows, some individuals with type 1 diabetes use insulin glargine, which is a once-a-day, long-acting insulin. It is an analogue, or laboratory-created, insulin which has been modified to act more uniformly in managing glucose levels.

Insulin glargine comes in varying strengths, and a recent study found that there were no significant differences in safety or effectiveness between insulin glargine 100 U/mL and insulin glargine 300 U/mL when administered in children and adolescents. Data from 463 EDITION JUNIOR study participants between the ages of 6 and 17 were compared over 26 weeks. Of those participants, 233 were randomly assigned to insulin glargine 300 U/mL, and 228 were randomly assigned to insulin glargine 100 U/mL. Both groups continued to follow their normal routine for mealtime insulin but injected insulin glargine once per day.

Results showed that all participants experienced a reduction in HbA1c levels over the 26 weeks. However, there were fewer instances of severe hypoglycemia among participants using the insulin glargine 300 U/mL, though overall, results were comparable between groups. Both insulins were effective in achieving target study endpoints and did not demonstrate any unexpected safety concerns.

In comparing insulin glargine 100 U/mL and insulin glargine 300 U/mL, researchers may be able to use insulin glargine 300 U/mL as yet another treatment option for children and adolescents with type 1 diabetes. It is currently under review by the FDA, and researchers are evaluating data from a six-month safety follow-up.

It is encouraging to see that more options are being explored to meet the needs of individuals living with type 1 diabetes in order to maintain target glucose levels with fewer fluctuations. Diabetes Research Connection (DRC) will continue to follow these types of studies to see how they impact the future of diabetes management and accessibility to care.

DRC provides critical funding for early career scientists pursuing novel, peer-reviewed research studies for type 1 diabetes. Projects aim to improve prevention and treatment of the disease, as well as enhance quality of life and eventually find a cure. To learn more about current studies and support these efforts, visit http://diabetesresearchconnection.org.

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Controlling Beta Cell Proliferation and Apoptosis to Manage Type 1 Diabetes

A key indicator of type 1 diabetes is lack of insulin-producing beta cells in the pancreas. These cells are mistakenly attacked and destroyed by the immune system leaving individuals unable to naturally manage their blood sugar. With little to no production of insulin, the body cannot effectively process sugars and use them as fuel. Instead, individuals must constantly monitor their blood glucose levels and administer insulin as needed.

However, a recent study uncovered how an FDA-approved drug for treating breast cancer may also be effective in diabetes care. Neratinib is a dual inhibitor of HER2 and EGFR kinases, but researchers have also found that it is incredibly effective at blocking mammalian sterile 20-like kinase 1 (MST1) as well. MST1 plays a key role in regulating beta cell proliferation and apoptosis. By inhibiting MST1 expression, insulin-producing beta cells may be protected from this process leading to greater beta cell survival and improved function.

In addition, when mouse models and human islets were treated with neratinib, they showed a marked improvement in glucose control and maintained lower overall glucose levels. The drug also restored expression of specific transcription factors such as PDX1 that contribute to glucose metabolism and insulin production.

Neratinib is an FDA-approved cancer treatment drug currently being used for breast cancer, but its effectiveness in treating other forms of cancer is being explored as well. Now researchers are examining whether its indications could be expanded to include diabetes.  While it has been proven safe in cancer treatment, scientists are looking at ways to decrease its toxicity and improve specificity for diabetes.

In its current form, neratinib does not only target MST1 – it inhibits other kinases as well. Furthermore, there is concern that an extreme decrease in beta cell apoptosis could lead to increased expression of other cell types which could impact health. However, researchers can use this study as a foundation for exploring ways in which to refine the drug and improve beta-cell protection and function while minimizing other effects.

Diabetes Research Connection (DRC) is interested to see how this study impacts future treatment and prevention efforts in regard to type 1 diabetes. The DRC provides critical funding to early career scientists pursuing novel, peer-reviewed research projects focused on prevention, treatment, and improvement of quality of life for individuals living with the disease. This support can lead to scientific breakthroughs and have a significant impact on understanding of type 1 diabetes. To learn more about current projects and how to support these efforts, visit http://diabetesresearchconnection.org.

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Leveraging the Power of Light to Manage Type 1 Diabetes

A common problem in managing type 1 diabetes is maintaining relatively stable blood glucose levels. By the time a person realizes their blood sugar is rising or falling and begins to treat it, they may already experience spikes. This can be tough on the body and lead to over- or undertreatment in an effort to curb the highs or lows. Though technology has made it faster and easier to track blood glucose levels and more accurately administer insulin, it’s still not a perfect system.

A recent study reveals that researchers may have come up with a way to manage blood sugar without manually administering insulin. They engineered pancreatic beta cells to be responsive to exposure to blue light. By introducing a photoactivatable adenylate cyclase (PAC) enzyme into the cells, they produce a molecule that increases insulin production in response to high levels of glucose in the blood.

The molecule is turned on or off by blue light and can generate two to three times the typical amount of insulin produced by cells. However, it does not boost production when glucose levels in the blood are low. Furthermore, the cells do not require more oxygen than normal cells, which helps alleviate the common issue of oxygen starvation in transplanted cells.

The study was conducted on diabetic mice, so more research is needed to determine whether the process will be as effective in humans. If it is, this could mean that individuals with type 1 diabetes may have an option for controlling blood sugar levels without pharmacological intervention. When paired with a continuous glucose monitor (CGM) or other device as well as a source of blue light, it could create a closed loop model of managing the disease by functioning as a bioartificial pancreas.

This could be potentially life changing for individuals living with type 1 diabetes, and Diabetes Research Connection (DRC) is excited to see how the study progresses. Though not involved with this project, the DRC supports advancement of type 1 diabetes research and treatment options by providing critical funding for early career scientists pursuing novel research projects. Learn more by visiting http://diabetesresearchconnection.org.

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Improving Vascularization of Transplanted Islet Cells

One option that researchers have explored for treating type 1 diabetes is cell transplantation. By introducing new pancreatic islet cells, they aim to better control glucose levels and insulin production. However, there are still many challenges surrounding this approach including cell death due to poor vascularization.

Pancreatic islet cells are highly vascularized in order to quickly and easily transport insulin. If they are not able to establish blood vessel connections following transplantation, they cannot work as effectively and may not survive long-term. A recent study has found an improved method for promoting vascularization and enabling more effective cell transplantation.

A multidisciplinary team of researchers developed a biomimetic microvascular mesh that maintained its shape and promoted the survival of transplanted cells by stimulating revascularization. When transplanted into diabetic mouse models, they were able to maintain normoglycemia for up to three months.

The researchers created micropillars to improve anchoring of the microvascular mesh and decrease risk of shrinkage as cells matured. They had success using both human umbilical vein endothelial cells (HUVECs) and human induced pluripotent stem cell-derived endothelial cells (iPSC-ECs) in the meshes. Compared to a mesh without these cells, the mesh with the cells showed both anastomoses and vascular remodeling which are essential in vascularization during cell replacement therapy.

Though they have only been tested in mouse models, biomimetic microvascular mesh could one day be used to improve cell replacement therapy for humans with type 1 diabetes in order to improve glycemic control. This study opens doors for additional research and further refining islet transplantation methods.

Though not involved with this study, Diabetes Research Connection (DRC) supports novel research projects that strive to advance treatment for type 1 diabetes and one day find a cure. Early career scientists can receive up to $75K in funding from donations by individuals, corporations, and foundations to support their research. Learn more by visiting http://diabetesresearchconnection.org.

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