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Preserving Endogenous Insulin Production

Preserving Endogenous Insulin Production in Newly Diagnosed Type 1 Diabetes Patients

A hallmark of type 1 diabetes is the body loses its ability to naturally produce enough (or any) insulin to effectively manage blood glucose levels. This is due to the mistaken destruction of insulin-producing beta cells by the immune system, a process that researchers are continually learning more about. In many cases, when type 1 diabetes (T1D) is first diagnosed, there is a short window of time (up to about six months) where the body still creates insulin, but not enough to meet demand.

A recent study explored a new way to try to preserve endogenous insulin production and reduce the amount of insulin newly diagnosed patients required. The study involved 84 patients ages 6 to 21 who had been diagnosed with T1D within 100 days of the start of the trial. Approximately two-thirds of participants were given the drug golimumab, while the other one-third received a placebo. Golimumab is an anti-tumor-necrosis-factor (TNF) therapy that is already approved by the Food and Drug Administration (FDA) for the treatment of rheumatoid arthritis, ulcerative colitis, and other autoimmune conditions. It has not yet been approved for use in patients with T1D.

The patients who received golimumab self-administered the drug via injection every two weeks. Results showed that these patients achieved markedly better glycemic control that patients receiving the placebo. After 52 weeks of treatment, “41.4% of participants receiving golimumab had an increase or less than 5% decrease in C-peptide compared to only 10.7% in the placebo group.”

Furthermore, patients who were still in the “honeymoon phase” of their diabetes, or the first 3-6 months after diagnosis where there is still some endogenous insulin production and not as much injected insulin is needed, also showed improvement once transitioning out this phase and continuing to take golimumab. Those patients showed a smaller increase in injected insulin than the placebo group requiring just 0.07 units per kilogram more per day versus 0.24 units per kilogram per day respectively. Another notable improvement is that patients between the ages of 6 and 18 experienced 36% fewer episodes of level 2 hypoglycemia, a condition that can be potentially life-threatening and negatively impact the quality of life.

Since golimumab is already FDA-approved for other conditions, these phase 2 study results play an important role in moving the process forward to show that it may be an effective treatment for T1D as well. This therapy may be able to help newly diagnosed patients retain some of their body’s natural insulin-producing abilities and decrease the amount of injected insulin needed to maintain good glycemic control.

Golimumab may become another option for patients with type 1 diabetes in the future and change how the disease is managed when caught and treated early on. It is encouraging to see new ways to preserve beta-cell function. Diabetes Research Connection (DRC) is interested to see how this study unfolds and whether golimumab is approved for the treatment of type 1 diabetes.

Although not involved in this study, DRC supports early-career scientists in pursuing studies like these and other projects related to preventing and curing T1D as well as minimizing complications and improving the quality of life for individuals living with the disease. Scientists can receive up to $50K in funding to advance their research. Click to learn more about current projects and provide support.

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DNA Strands

Recapping Current Research Regarding Type 1 Diabetes Development and Cardiovascular Risks

Our bodies are formed from an innumerable number of cells and molecules. Both DNA and RNA play a role in determining cells’ function and purpose. At a conference of the National Congress of the Spanish Diabetes Society, researchers revealed new studies regarding the potential role of long non-coding RNAs (lncRNAs) in the development of type 1 diabetes, as well as the risk of cardiovascular problems in individuals with the disease.

A recent study found that lncRNA, which are use in transcriptional and post-transcriptional regulation of cells and are not translated into proteins, may be involved in the destruction of insulin-producing beta cells. There may be some forms of lncRNAs that affect inflammation and cell death, which are factors in the development of type 1 diabetes.

Dr. Izortze Santín Gómez, a professor at the University of the Basque Country and a researcher at the Biocruces Bizkaia Research Institute is studying the fundamental characteristics of the lncRNAs and how they may affect pancreatic beta cells on a genetic-molecular level. Once this is better understood, researchers could begin modifying the lncRNAs to create a targeted therapy that increases survival rate and viability of the pancreatic beta cells.

Another study that was presented at the conference involved cardiovascular risk for individuals with type 1 diabetes. Joseph Ribalta, a professor at the Rovira i Vigili University of Reus, found that “more than 30% of heart attacks occur in people with apparently normal LDL cholesterol.” High cholesterol is a key risk factor for heart attacks. His findings have revealed that individuals with T1D may be at greater risk because “LDL particles are more numerous and smaller, that their HDLs work less effectively and/or that there are some lipoproteins (remnants) that the body has trouble eliminating.”

Identifying these potential risk factors and knowing how to test for or treat them could help reduce hidden cardiovascular risk in individuals with T1D. For instance, focusing on triglycerides rather than cholesterol may be beneficial for patients who meet certain criteria.

There is a lot of interesting work coming out of laboratories and universities around the world regarding type 1 diabetes. Researchers are constantly improving and refining their understanding of the disease and possible ways to prevent, treat, or cure it. Diabetes Research Connection (DRC) is committed to contributing to this wealth of knowledge by providing critical funding to early-career scientists pursuing novel research studies focused on type 1 diabetes. Click to learn more about current projects and provide support.

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Diabetes Researching

Increasing Cell Protection Against Immune System Attacks

One of the challenges researchers have faced with using cell therapy to treat type 1 diabetes is that the body’s immune system may still attack and destroy transplanted cells. This process may be slightly delayed depending on the approach used, but it often still occurs. That means that patients may still need to rely on immune suppression medications in conjunction with cell therapy. However, immunosuppression can increase risk of infection or other complications.

A recent study found that targeting highly durable cells that have the ability to escape immune attacks and survive may be key in developing a more effective treatment for type 1 diabetes. Dr. Judith Agudo has identified stem cells with this “immune privilege” and is working to determine exactly what contributes to this level of protection and how to replicate it with beta cells. Dr. Agudo is an assistant professor in the department of immunology at Harvard Medical School and in the department of cancer immunology and virology at the Dana-Farber Cancer Institute.

If scientists can engineer insulin-producing beta cells that have the ability to avoid attacks from the immune system while still performing their intended functions, this could be a huge step forward in potentially treating type 1 diabetes. The beta cells would be able to stimulate insulin production without requiring the patient to take immune suppression medications, meaning their immune system could continue to function as normal and fend off infection.

Once Dr. Agudo is able to develop these durable beta cells, they will be tested in animal models, followed by humans a few years later. It is important to conduct thorough testing to ensure this method is both safe and effective. If it is, the goal would be to eventually make it available to anyone who requires the use of insulin.

Diabetes Research Connection (DRC) is excited to see how this study evolves and what it could mean for the future of diabetes treatment. While not involved in this study, the DRC plays an integral role in providing critical funding for early career scientists focused on research for type 1 diabetes. Scientists continue to advance understanding of the disease and potential approaches to improve diagnosis, treatment, management, and quality of life for individuals living with type 1 diabetes. Click to learn more about current projects and provide support.

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Diabetes Researching

Generating Pancreatic Islet Organoids to Treat Type 1 Diabetes

In individuals with type 1 diabetes, the immune system mistakenly attacks and destroys insulin-producing beta cells. Without a naturally occurring supply of insulin to manage glucose, blood-glucose levels can quickly spiral out of control leading to hypo- or hyperglycemia. If left untreated, this can become potentially fatal.

A recent study found a way to generate an abundance of pancreatic islet organoids that are glucose-responsive and insulin-secreting. As such, they can help with management and potential reversal of type 1 diabetes. Researchers identified a cluster of protein C receptor positive (Procr+) cells in the pancreas of adult mice. These cells have the ability to differentiate into alpha, beta, omega, and pancreatic polypeptide (PP) cells, with beta cells being the most abundant.

The Procr+ islet cells can then be cultured to generate a multitude of islet-like organoids. When the organoids were then be transplanted into adult diabetic mice, they were found to reverse type 1 diabetes. More research is necessary to determine if human pancreatic islets contain these same Procr+ endocrine progenitors and a similar process could be used to treat type 1 diabetes in humans.

As scientists delve deeper into the cellular impact of the disease and how different cells respond and can be manipulated, it opens new doors to potential treatments or cures for type 1 diabetes. Though not involved in this study, this is the type of cutting-edge research that the Diabetes Research Connection (DRC) is committed to supporting. Early-career scientists can receive up to $50,000 in funding through DRC for novel, peer-reviewed research aimed at preventing and curing type 1 diabetes, minimizing complications, and improving the quality of life for individuals living with the disease. To learn more and support these efforts, visit https://diabetesresearchconnection.org.

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Diabetes Researching

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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Beta Cells

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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Diabetes Research

Exploring the Impact of Environment on Type 1 Diabetes Risk

While researchers know that type 1 diabetes is caused by the destruction of insulin-producing beta cells, what they are still uncertain about are the exact causes of this process. They know that genetics play a role, yet there is not a single gene responsible for the disease; there are several genes that are believed to contribute. Furthermore, they are not convinced that the disease is entirely genetic, and have reason to believe that environmental factors are to blame as well. But once again, there is not a single environmental risk that has a significantly greater impact than others.

A recent study examined several environmental risk factors such as “air pollution, diet, childhood obesity, the duration of breastfeeding, the introduction of cow’s milk, infections, and many others” and yet researchers still do not have any definitive answers. What they do know is that the incidence of type 1 diabetes has increased over the past 30 years by 3 percent year over year, and this change is too significant to be caused by genetics alone.

Using a variety of modeling, they evaluated the impact of specific environmental factors over time. But the simulated data did not pinpoint one factor that stood out above the others and had a stronger impact on diabetes risk. It is likely that a combination of environmental factors is at play in conjunction with genetic risk. More research is needed to further investigate potential risks and protective factors when it comes to type 1 diabetes.

These findings may inspire other researchers to dig more deeply into environmental factors and their impact on disease development and progression. Diabetes Research Connection (DRC), though not involved with this study, provides critical funding for early-career scientists to pursue novel research studies related to type 1 diabetes to enhance understanding as well as prevention, treatment, and management of the disease. The goal is ultimately to find a cure. Learn more about current projects and how to help by visiting https://diabetesresearchconnection.org.

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Stem Cells

Scientists Found a Way to Generate Insulin-Producing Beta Cells

More than one million people in the United States are living with type 1 diabetes according to statistics from the Centers for Disease Control and Prevention. There is a strong push to improve management of the disease and find a cure. The more researchers learn about T1D, the more precise their prevention and treatment methods become.

A recent study reveals that improvements in stem cell therapy have reversed T1D in mice for at least nine months and, in some cases, for more than a year. One of the challenges that scientists have faced with using human pluripotent stem cells (hPSCs) is that it can be difficult to zero differentiation in one specific type of cell. Often multiple types of pancreatic cells are produced. While there may be an abundance of cells that scientists want, the infiltration of excess cells that are not needed diminishes their impact (even though they are not harmful).

Scientists at the Washington University School of Medicine in St. Louis have found a way to generate insulin-producing beta cells without creating as many irrelevant cells. Their approach focuses on the cell’s cytoskeleton, which is its inner framework. Through this process, they were able to produce vast amounts of beta cells that are able to normalize blood glucose levels.

When transplanted into severely diabetic mice (blood glucose levels above 500 mg/dL), the cells effectively reversed the effects of diabetes and brought blood sugar levels down into target range within two weeks. Normoglycemia was maintained for at least nine months.

This is a major step forward in stem cell therapy and the use of hPSCs to potentially cure diabetes one day. There is still more testing and research that needs to be done before this approach is applied to human trials.

Ongoing research is essential for finding a cure for T1D. Diabetes Research Connection supports these efforts by providing critical funding to early-career scientists pursuing novel research studies on the disease. By giving them the means to complete their projects, these researchers can continue to advance knowledge and treatment options. Learn more about current studies and how to help by visiting https://diabetesresearchconnection.org.

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Person Putting a Drop on Test Tube

Improved Beta Cell Function of Transplanted Islet Cells in T1D

One of the major challenges of using transplanted islet cells in the treatment of type 1 diabetes is cell death. Due to cellular stressors, poor oxygenation or vascularization, autoimmune response, and other factors, not all transplanted cells survive, and this can make treatment less effective. The body needs functional insulin-producing islet cells in order to effectively regulate blood sugar levels.

A recent study found that coculturing allogeneic islet beta cells with mesenchymal stromal cells (MSCs) may improve not only cell survival, but function as well. After donor cells are procured, they must be cultured and tested before being transplanted. This can generate significant cellular stress including hypoxia or low oxygenation, which can in turn lead to cell death. However, researchers found that MSCs support islet cells during this culture period by improving oxygenation and insulin secretion.

They also found that in response to these stressors, MSCs actually initiate mitochondria transfer to the islet beta cells.  This may improve mitochondrial ATP generation which plays an integral role in controlling insulin secretion. As a result, as glucose levels around the beta cells increased, so did their production and secretion of insulin.

Researchers experimented with this coculturing process with both mouse cells and human cells and found that human cells have a greater response and higher level of MSC-mediated mitochondria transfer that occurs. Though more extensive testing is necessary, these results show that MSCs may be an essential part of clinical islet transplantation and improved efficacy of beta cell function in treating individuals with type 1 diabetes.

Diabetes Research Connection (DRC) is interested to see how this study evolves moving forward and what it may mean for future therapeutic treatments for the disease. The DRC, though not involved in this study, provides critical funding for early career scientists pursuing novel, peer-reviewed research projects for type 1 diabetes. Click to learn more about current projects and provide support.

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T1D Vaccine

Type 1 Diabetes Vaccine Shows Positive Results

In an effort to prevent or delay the onset of type 1 diabetes, researchers have been striving to create an effective vaccine. One of the challenges is that there are many different subgroups of type 1 diabetes, meaning not all patients respond the same. A recent study found that patients who had a specific human leukocyte antigen (HLA) showed a “positive and statistically significant dose-dependent treatment response” to the Diamyd vaccine, especially when given four doses rather than two.

Compared to patients who received a placebo, those who received a higher number of doses of the Diamyd vaccine had a “statistically significant treatment effect of approximately 60%” within 15 months. These findings may help to advance the development of antigen-specific immunotherapy options for individuals with type 1 diabetes leading to improved treatment or management of the disease.

Diabetes Research Connection (DRC) is interested to see how this vaccine continues to evolve moving forward and what it could mean for the prevention of type 1 diabetes in the future. Though not involved with this study, the DRC provides early career scientists with funding necessary to conduct novel, peer-reviewed research projects around type 1 diabetes in an effort to improve understanding, prevention, treatment, and management of the disease. To learn more or donate to a current project, visit https://diabetesresearchconnection.org.

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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