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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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Long acting insulin

Long Acting Insulin Versus Immediate Acting Insulin for Type 1 Diabetes Patients Compared in Review

For many people Long acting insulinwith type 1 diabetes, daily treatment and management of the condition is a big part of their life. But is one form of treatment better than others?

A new review explored long-acting insulin in the treatment of type 1 diabetes. The researchers found evidence that this treatment method was more effective at controlling type 1 diabetes than immediate-acting insulin. They also found that long-acting insulin was tied to fewer safety concerns, including weight gain and severe diabetic episodes.

In type 1 diabetes, which is often diagnosed during youth, the body doesn’t produce insulin — a hormone that helps turn sugar into energy — causing issues with blood sugar levels. Because the body of type 1 diabetes patients doesn’t produce insulin, insulin therapy is required.

According to the authors of this study, which was led by Andrea C. Tricco, PhD, of the Li Ka Shing Knowledge Institute at St. Michael’s Hospital in Ontario, Canada, some have suggested that newer, long-acting insulin treatments (like glargine and detemir) might be better than immediate-acting versions of insulin therapy (like Neutral Protamine Hagedorn).

To explore the topic, Dr. Tricco and team identified 39 studies comparing the two insulin therapy methods in 7,496 adult type 1 diabetes patients.

In reviewing the studies, the researchers found that long-acting methods were slightly more effective at reducing glycosylated hemoglobin (A1C) levels — a measure of average blood sugar levels over several months.

The patients on long-acting insulin also gained less weight and were less likely to experience severe hypoglycemia — when blood sugar drops so low that medical attention is required.

When looking at cost-effectiveness, the majority of studies found that long-acting insulin was more expensive, but more effective.

“Patients and their physicians should tailor their choice of insulin according to preference, cost and accessibility,” wrote the review authors.

It is important to note that these findings were based on a review of previous studies. Dr. Tricco and team noted that further research comparing long-acting and immediate-acting insulin treatment options is needed.

This study was published October 1 in The BMJ.

Funding for the study was provided by the Canadian Institutes for Health Research/Drug Safety and Effectiveness Network (CIHR/DSEN). No conflicts of interest were reported.

 

Citation: 

The BMJ, “Safety, effectiveness, and cost-effectiveness of long-acting versus intermediate-acting insulin for patients with type 1 diabetes: a systematic review and network meta-analysis”

Last Updated:

October 1, 2014

Source:

dailyrx.com

 

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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.
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A Potential Second Cure for T1D by Re-Educating the Patient’s Immune System
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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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