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Senior Woman Checking Her Blood Sugar Level

Research suggests that diabetes could be due to failure of beta cell ‘hubs’

Original article published by University of Birmingham on July 21, 2016. Click here to read the original article.

The significant role of beta cell ‘hubs’ in the pancreas has been demonstrated for the first time, suggesting that diabetes may due to the failure of a privileged few cells, rather than the behaviour of all cells.

Researchers used optogenetic and photopharmacological targeting to precisely map the role of the cells required for the secretion of insulin.

The team believe that the findings, published in Cell Metabolism, could pave the way for therapies that target the ‘hubs’.

Dr David Hodson, from the University of Birmingham, explained, “It has long been suspected that ‘not all cells are equal’ when it comes to insulin secretion. These findings provide a revised blueprint for how our pancreatic islets function, whereby these hubs dictate the behaviour of other cells in response to glucose.”

According to the NHS, there are currently 3.9 million people living with diabetes in the UK, with 90% of those affected having type 2 diabetes.

Type 2 diabetes occurs when the pancreas fails to produce enough insulin to function properly, meaning that glucose stays in the blood rather than being converted into energy.

Beta cells (β cells) make up around 65-80% of the cells in the islets of the pancreas. Their primary function is to store and release insulin and, when functioning correctly, can respond quickly to fluctuations in blood glucose concentrations by secreting some of their stored insulin.

These findings show that just 1-10% of beta cells control islet responses to glucose.

Dr Hodson, who is supported by Diabetes UK RD Lawrence and EFSD/Novo Nordisk Rising Star Fellowships, continued, “These specialised beta cells appear to serve as pacemakers for insulin secretion. We found that when their activity was silenced, islets were no longer able to properly respond to glucose. “

Prof Guy Rutter, who co-led the study at Imperial College London, added “This study is interesting as it suggests that failure of a handful of cells may lead to diabetes”.

Studies were conducted on islet samples from both murine and human models.

The team noted that, though the findings present a significant step forward in understanding the cell mechanisms, the experiments therefore may not be reflected in vivo, where blood flow direction and other molecule dynamics may influence the role of the hubs and insulin secretion.

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Berries in wooden spoons

Fruity, Diabetic-Friendly Double Berry Pie Squares

There’s something special about eating a cool, sweet treat in the summer.

For those with type 1 diabetes, though, typical “summery” desserts such as ice cream can signal trouble, as they are often full of sugar, fat and artificial ingredients. Opting for a more nutritional option such as fruit is a great way to stay on track and keep your body healthy.

Make this summer just a little sweeter with these diabetic-friendly double berry pie squares. Consider bringing this healthy, fruity summer treat to your next cookout, pool party or family gathering.

Recipe: Double Berry Pie Squares

Taken from Diabetic Living.

Makes: 9 servings

Serving Size: 1 square and 1/2 tablespoon dessert topping
Carb Grams Per Serving: 25


  • 1/3 cup sugar or sugar substitute* equivalent to 1/3 cup sugar
  • 1 envelope unflavored gelatin
  • 1 pound fresh strawberries, hulled and diced
  • 1 12 – ounce package frozen raspberries, thawed
  • Nonstick cooking spray
  • 2/3 cup finely crushed graham crackers
  • 2 tablespoons sugar or sugar substitute* equivalent to 2 tablespoons sugar
  • 2 tablespoons butter, melted
  • 1/3 cup frozen sugar-free whipped dessert topping, thawed


  1. For filling: In a large saucepan, combine the 1/3 cup sugar and the gelatin; add strawberries and raspberries. Cook and stir over medium-high heat until gelatin is dissolved and mixture is simmering.
  2. Transfer berry mixture to a shallow bowl. Chill about 45 minutes or until mixture begins to set up around the edges, stirring occasionally.
  3. For crust: Lightly coat a 2-quart square baking dish with cooking spray. In a medium bowl, stir together finely crushed graham crackers, the 2 tablespoons sugar, and the melted butter. Press graham cracker mixture evenly over the bottom of the prepared baking dish. Place in freezer while chilling filling.
  4. Carefully pour filling over the crust. Chill about 3 hours or until filling is completely set.
  5. Cut into squares to serve. Top with whipped dessert topping. Makes 9 servings (1 square and 1/2 tablespoon dessert topping per serving)


  • *Sugar Substitute: Choose from Splenda® Granular or Sweet’N Low® bulk or packets. Follow package directions to use product amount equivalent to 1/3 cup and 2 tablespoons sugar.
  • *Sugar Substitute: PER SERVING WITH SUBSTITUTE: same as above, except 103 cal., 16 g carb. Exchanges: 0 other carb. Carb Choices: 1.

Nutrition Facts Per Serving:

Servings Per Recipe: 9

PER SERVING: 138 cal., 4 g total fat (2 g sat. fat), 7 mg chol., 80 mg sodium, 25 g carb. (4 g fiber, 15 g sugars), 2 g pro.

Diabetic Exchanges

Fruit (d.e): 1; Other Carb (d.e): 0.5; Fat (d.e): 1

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Laboratory Equipment - microscope

New Approach for Regenerative Therapy

Original article published by HelmholtzZentrum munchen on June 12, 2016. Click here to read the original article.

Neuherberg, June 12, 2016. The marker Flattop subdivides the insulin-producing beta cells of the pancreas into those that maintain glucose metabolism and into immature cells that divide more frequently and adapt to metabolic changes. This could provide a starting point for regenerative diabetes therapies, as scientists of Helmholtz Zentrum München, in collaboration with colleagues of the Technical University of Munich and the German Center for Diabetes Research (DZD), report in the journal ‘Nature’.

The beta cells of the pancreas produce the metabolic hormone insulin when blood glucose levels rise, in order to keep glucose levels in equilibrium. If the beta cells are destroyed or lose their function, this can lead to serious diseases such as diabetes. However, not all beta cells are identical. “It has long been known that there are different subpopulations of beta cells,” said Professor Heiko Lickert, director of the Institute of Diabetes and Regeneration Research at Helmholtz Zentrum München. “But until now, the underlying molecular mechanisms have remained elusive.”

Flattop is a marker for mature beta cells

In the current study, the researchers led by Lickert searched for molecular markers subdividing the respective subgroups. One molecule, in particular, captivated their attention: the protein Flattop.* It was present in about 80 percent of all beta cells. These cells effectively determined the glucose concentration of their environment and secreted the corresponding amount of insulin, thus showing the metabolic properties of mature beta cells.

Cells without Flattop proliferate more frequently

Conversely, the team of researchers observed that beta cells in which no Flattop was measurable showed a particularly high rate of proliferation. “In our experimental model, these cells proliferated up to four times more often than the Flattop-positive cells,” said study leader Lickert.

A type of precursor cells?

To pursue the hypothesis that the actively dividing cells (without Flattop) could be precursors of metabolically active cells, the scientists made use of a genetic trick to map the fate of single cells. This so called lineage tracing revealed that the proliferative progenitor cells were able to develop into mature beta cells with metabolic properties. This was also the case, when the scientists placed them in an artificial mini-organ-like 3D environment. Moreover, genetic analyses confirmed that in beta cells without Flattop, primarily genes responsible for sensing the environment were expressed, while in cells with Flattop primarily classic metabolic programs took place.

“Our results suggest that the Flattop-negative cells are a kind of immature reserve pool, which constantly renews itself and can replenish the mature beta cells,” Lickert said. According to the study leader this new possibility of subdividing these two subgroups allows a comprehensive analysis of the signaling pathways involved. The results of the researchers raise hopes for the development of regenerative therapies: “The heterogeneity of the beta cells has been studied for more than 50 years, now with enabling technologies it looks like we are beginning to understand how the cells behave,“ said Lickert.

In the future, the scientist will focus on two major aspects: on the one hand in terms of regenerative therapy their goal would be to regenerate endogenous beta cells in a targeted manner to replace dysfunctional or lost cells in patients. On the other hand the findings are a milestone in the generation of functional beta cells from stem cells in cell culture for cell replacement therapy, which was not possible so far.

Further Information

* Flattop is part of the Wnt signaling pathway, which in particular regulates the development of tissues and cell functions.

**Lineage tracing is a method to map the fate of single cells. It is based on gene variants emitting a color signal upon induction of the respective gene. In this particular case cells without Flattop were colored in red and turned into green upon Flattop induction.

Original Publication:
Bader, E. et al. (2016). Identification of proliferative and mature β-cells in the islet of Langerhans, Nature, DOI: 10.1038/nature18624

Corresponding reviews of the research group:
Migliorini, A. et al. (2016). Impact of islet architecture on beta cell heterogeneity, plasticity and function, Diabetologia, doi: 10.1007/s00125-016-3949-9

Roscioni, S. et al. (2016). Impact of islet architecture on beta cell heterogeneity, plasticity and function, Nature Reviews Endocrinology, in press

The Helmholtz Zentrum München, the German Research Center for Environmental Health, pursues the goal of developing personalized medical approaches for the prevention and therapy of major common diseases such as diabetes and lung diseases. To achieve this, it investigates the interaction of genetics, environmental factors and lifestyle. The Helmholtz Zentrum München is headquartered in Neuherberg in the north of Munich and has about 2,300 staff members. It is a member of the Helmholtz Association, a community of 18 scientific-technical and medical-biological research centers with a total of about 37,000 staff members.

The research activities of the Institute of Diabetes and Regeneration Research (IDR) focus on the biological and physiological study of the pancreas and/or the insulin producing beta cells. Thus, the IDR contributes to the elucidation of the development of diabetes and the discovery of new risk genes of the disease. Experts from the fields of stem cell research and metabolic diseases work together on solutions for regenerative therapy approaches of diabetes. The IDR is part of the Helmholtz Diabetes Center (HDC).

Technical University of Munich (TUM) is one of Europe’s leading research universities, with more than 500 professors, around 10,000 academic and non-academic staff, and 39,000 students. Its focus areas are the engineering sciences, natural sciences, life sciences and medicine, reinforced by schools of management and education. TUM acts as an entrepreneurial university that promotes talents and creates value for society. In that it profits from having strong partners in science and industry. It is represented worldwide with a campus in Singapore as well as offices in Beijing, Brussels, Cairo, Mumbai, San Francisco, and São Paulo. Nobel Prize winners and inventors such as Rudolf Diesel, Carl von Linde, and Rudolf Mößbauer have done research at TUM. In 2006 and 2012 it won recognition as a German “Excellence University.” In international rankings, TUM regularly places among the best universities in Germany.

The German Center for Diabetes Research (DZD) is a national association that brings together experts in the field of diabetes research and combines basic research, translational research, epidemiology and clinical applications. The aim is to develop novel strategies for personalized prevention and treatment of diabetes. Members are Helmholtz Zentrum München – German Research Center for Environmental Health, the German Diabetes Center in Düsseldorf, the German Institute of Human Nutrition in Potsdam-Rehbrücke, the Paul Langerhans Institute Dresden of the Helmholtz Zentrum München at the University Medical Center Carl Gustav Carus of the TU Dresden and the Institute for Diabetes Research and Metabolic Diseases of the Helmholtz Zentrum München at the Eberhard-Karls-University of Tuebingen together with associated partners at the Universities in Heidelberg, Cologne, Leipzig, Lübeck and Munich.

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type 1 diabetes type 2 diabetes differences

Differences Between Type 1 and Type 2 Diabetes

Understanding the Two Major Types of Diabetes: Type 1 vs Type 2

We often hear about diabetes, but do we understand this complex health condition? How do we tell the differences between type 1 vs type 2? Sure, they might share a name. And yet they each have distinct characteristics, causes, symptoms, and management methods.

If we have a clearer understanding of these two types of diabetes. We can help those living with the disease, promote awareness, and understand the role that research plays.

In this post, we’ll shed light on type 1 vs type 2 diabetes. We will walk you through their symptoms, risk factors, diagnosis methods, and more. Furthermore, we will delve into current research developments and their implications for the future of diabetes treatment.

For T1D-friendly recipes and tips, make sure to subscribe to our newsletter.

Type 1 Diabetes

Type 1, used to be known as juvenile diabetes. It is a form of diabetes where the body’s immune system attacks and destroys cells.

These insulin-producing beta cells are in the pancreas. This results in a deficiency of insulin. Insulin is a hormone critical for allowing glucose to enter cells, providing them with the energy they need.

But what are the telltale signs that someone might have developed type 1 diabetes? The symptoms often occur suddenly and may include excessive thirst and urination, unexplained weight loss, constant hunger, vision changes, and fatigue.

You need to seek medical advice if you or a loved one experiences these symptoms. It might not be diabetes, but an early diagnosis can prevent severe complications.

So, who is at risk? Some risk factors for developing type 1 diabetes include having a family history of diabetes and certain genetic factors. Nevertheless, anyone can be diagnosed with type 1 diabetes, regardless of lifestyle, fitness level, or body weight.

After being diagnosed patients are advised to monitor their blood sugar levels regularly. They also have to manage their condition with insulin injections or the use of an insulin pump. The insulin pump is a device that delivers insulin constantly throughout the day, helping to keep blood glucose levels stable.

If left unchecked or improperly managed, type 1 diabetes can lead to a life-threatening condition known as diabetic ketoacidosis (DKA). DKA occurs when your body begins to run out of insulin, causing harmful acids to build up in your body. Symptoms include frequent urination, excessive thirst, nausea or vomiting, abdominal pain, weakness or fatigue, and shortness of breath.

Type 2 Diabetes

Type 2, on the other hand, presents a different scenario. This type of diabetes typically develops in adulthood. It has been increasingly seen in younger individuals in recent years, partially due to rising obesity rates.

Unlike type 1, where the body doesn’t produce enough insulin. In type 2 diabetes, the body still produces insulin, but it’s unable to use it effectively. This is known as insulin resistance. Over time, the demand for insulin overpowers the pancreas’ ability to produce it, leading to an insulin deficiency.

The symptoms of type 2 diabetes can be subtle and may develop slowly over several years. They can be similar to those of type 1, such as increased thirst and urination, constant hunger, fatigue, and blurred vision. However, some people with type 2 may also experience slow healing of wounds and frequent infections.

The risk factors for developing type 2 diabetes are more diverse than for type 1. A family history of diabetes, obesity, a sedentary lifestyle, poor diet, and certain ethnicities are all associated with a higher risk of developing type 2. Aging also increases the risk.

After being diagnosed with type 2, the management methods vary depending on the severity of the condition. Lifestyle changes, including a healthier diet, increased physical activity, and weight loss, are usually the first steps. Some people may also need medication to control their blood sugar levels or to deal with insulin resistance.

When we talk about type 2 vs type 1. It’s important to remember the differences not only in the causes and symptoms but also in the management methods.

Understanding these differences allows us to adapt our strategies for prevention, treatment, and support for those living with diabetes. In the following section, we will lay out these differences side by side for a more direct comparison.

Type 1 vs Type 2 Diabetes

In the realm of diabetes, it’s crucial to understand the differences between type 1 and type 2.

They share some similarities – being chronic conditions that affect how the body regulates blood glucose, or blood sugar. However, they differ in causes, symptoms, management strategies, and risk factors.


Type 1 is an autoimmune disease, and it is still unclear why the immune system attacks its own insulin-producing cells. Meanwhile, type 2 is primarily a lifestyle disease. However, genetics and family history also play a significant role in both types.


Type 1 diabetes can manifest at any age but is commonly diagnosed in children and young adults. In contrast, type 2 diabetes is more common in adults. Although type 2 diabetes is increasingly diagnosed in younger individuals due to lifestyle changes.


Both types share several symptoms like frequent urination, excessive thirst, fatigue, and blurred vision. The symptoms of type 1 come quickly and are more intense. Type 2 symptoms are more subtle and come slowly over years.


Type 1 diabetes requires regular insulin administration because the body doesn’t produce it. This insulin can be administered through injections or an insulin pump. On the flip side, type 2 diabetes is initially managed through lifestyle changes such as dietary, exercise, and weight loss. However, as the disease progresses, medication or insulin may become necessary.

Risk Factors

Both types share a risk factor in the form of a family history of diabetes. But with type 1, certain genetic markers can indicate a higher risk. As for type 2, lifestyle choices significantly impact the risk.

With type 2 vs type 1, it’s clear that while they share a common name, they have different journeys. By understanding these differences, we can help with either condition and to contribute to research towards improved treatments and a cure. But what does the future look like for diabetes research?

The Future is Bright: Current Research and Advances in Diabetes

While there are significant differences between type 1 and type 2 diabetes. The shared goal among scientists, healthcare professionals, and community advocates is clear. To improve quality of life for individuals with diabetes and, ultimately, to find a cure.

Thanks to advancements in technology and research, progress is being made in our understanding and treatment of both types of diabetes.


Research in type 1 diabetes is steadily progressing. A key focus is on developing an artificial pancreas, a device that can monitor and regulate blood glucose levels automatically, reducing the need for constant vigilance. Stem cell research is another exciting field, with the potential to create insulin-producing cells that could replace those destroyed by the immune system.

Meanwhile, research in type 2 diabetes has a significant emphasis on preventing the disease, given its strong ties to lifestyle factors. Understanding how diet, exercise, and other factors influence insulin resistance and the body’s ability to regulate blood glucose levels is a major research focus. There’s also promising work being done in the field of gene therapy to understand how genetic factors contribute to the development of type 2 diabetes.

But what ties both types of diabetes together is the hope for a future where diabetes can be cured or prevented. Ongoing research is not just about managing the condition but also about learning how we can stop the disease from developing in the first place.

Every discovery, every breakthrough, brings us one step closer to a world where diabetes no longer poses a threat to our health and well-being. To get there, we need continued support and resources for research and development. As a society, we can make a difference by supporting these research initiatives, raising awareness about diabetes, and promoting healthy lifestyle choices.

The path may be long, but with every stride, we’re getting closer to the finish line. Remember, understanding is the first step. From there, we take the journey together, supporting each other until we achieve our goal: a world without diabetes.

Moving Forward

Diabetes is a complex health condition with multiple facets. The differences between type 1 and type 2 are significant, and understanding these differences is crucial for anyone diagnosed with diabetes, their loved ones, healthcare professionals, and the public at large. Awareness and understanding foster empathy and encourage proactive action, leading to better management, improved treatments, and the promise of a future cure.

While there are challenges associated with both type 1 and type 2 diabetes, advancements in medical research and technology provide hope. We are continually progressing towards a world where diabetes is a thing of the past.

By understanding these conditions better, we can support those who are managing them daily, contribute to essential research, and potentially prevent the onset in future generations.


And this is where we all come in. By supporting ongoing research, spreading awareness, and advocating for healthier lifestyles, we contribute to a future where diabetes is fully understood, effectively managed, and potentially curable. At the Diabetic Research Connection, we believe in this future and invite you to join us in our mission.

Thank you for taking the time to read about type 1 and type 2 diabetes. Let’s continue to learn, share, and take action, for ourselves and for those around us. Together, we can make a significant difference. Donate now!

Embracing the Future of Diabetes Research and Advocacy

As we forge ahead, it’s crucial to stay hopeful and engaged in the quest to improve lives impacted by diabetes, whether type 1 or type 2. In this era of scientific discovery and technological advancement, we can contribute to a collective effort to not only manage but conquer diabetes.

Understanding the differences between diabetes type 1 and type 2 is a start, but it’s vital to convert this knowledge into action – through research, community participation, improved healthcare policies, and increased advocacy.

Embracing technology’s role in managing diabetes, like the insulin pump, artificial pancreas, and digital health applications, is also critical. Simultaneously, we must uphold the importance of lifestyle changes in preventing and managing type 2 diabetes. Spreading awareness about these practices is key.

At the heart of it all is support. Every healthcare professional, patient, friend, family member, or just someone who wants to make a difference has a role. Each understanding gesture, fundraiser, research grant, and shared knowledge piece brings us closer to a diabetes-free world. Let’s face this future together, equipped with knowledge, understanding, and a shared vision for a healthier tomorrow. Together, we are stronger, and together, we can make a real difference in the battle against diabetes.

Above all, it’s important to keep in mind just how different these two diseases are, and how much we still have to learn about them. To stay up-to- date on type 1 diabetes research and learn more about managing and living with diabetes, sign up for our newsletter.

If you are looking for information regarding Type 2 Diabetes, we highly recommend looking at Type 2 Digest.

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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
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?
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)?
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