Articles tagged with Beta Cells
The Juvenile Diabetes Research Foundation (JDRF) honored five researchers for their outstanding contributions to type 1 diabetes research, including breakthroughs in beta cell autoimmunity and immune therapies. The awards recognize significant progress toward curing T1D, with funded research totaling over $2.2 billion.
Researchers identified growth differentiation factor 15 (GDF15) as a key player in delaying type 1 diabetes onset in diabetic mice. Treatment with GDF15 reduced development of diabetes by 53% in non-obese diabetic mice, providing a potential target for prevention and treatment.
Researchers at Karolinska Institutet found that CaV3.1 channels lead to excessive calcium influx, impairing beta cell function and glucose homeostasis. This hyperactivation is a critical pathogenic mechanism in diabetes development.
Researchers have discovered a link between prolonged enterovirus infection and the development of autoimmunity against insulin-producing pancreatic beta-cells, which precedes type 1 diabetes. Early adenovirus C infection was found to confer protection from autoimmunity.
Researchers at Weill Cornell Medicine discovered that higher levels of protein adipsin in the blood protect against type 2 diabetes. Adipsin helps shield pancreatic beta cells, improving insulin production and preventing cell death.
A study has identified a new mechanism by which pancreatic beta-cells respond to inflammatory environments, leading to the onset of Type 1 Diabetes. Researchers mapped approximately 3,600 non-coding DNA regions that activate in response to inflammation.
Scientists develop optogenetic approach to control glucose levels in diabetic mice, achieving improved tolerance and regulation of glucose without pharmacological intervention. The light-switchable cells can produce more than two- to three-fold the typical level of insulin in response to glucose levels.
A new study by Lund University researchers has identified a key mechanism in insulin release by a cholesterol metabolite. The receptor GPR183 plays a major role in stimulating insulin secretion in human cells and rats.
Researchers at the Hubrecht Institute have created a new method called GateID that allows for the purification of cell types to high purity without using antibodies or genetic reporters. This enables the detailed study of individual cell types, such as stem cells and tumor cells, which are crucial for understanding their properties and...
Researchers at Joslin Diabetes Center have made a breakthrough in identifying diseased beta cells in type 2 diabetes by uncovering the role of m6A mRNA methylation. The discovery has significant research and therapeutic implications, offering new insights into how the disease progresses.
Researchers have identified microRNA-204 as a biomarker for early beta cell death in Type 1 diabetes, which can identify disease onset in children and adults with recent-onset Type 1 diabetes. Serum miR-204 levels were found to be elevated in individuals with Type 1 diabetes and inversely correlated with remaining beta-cell function.
Researchers have discovered new members of a protein complex that maintains functional beta cells in the pancreas, crucial for regulating blood glucose levels. The study reveals the complex's association with enzymes RNF20 and RNF40, which play a key role in gene expression and insulin release.
Researchers at Scripps Research Institute have discovered a potential biological marker for early detection of type 1 diabetes using single-cell analysis of immune cells. The discovery could lead to earlier intervention and prevention of the disease, which affects over 1.25 million Americans.
Researchers have developed an 'Islet-on-a-Chip' device that integrates organ-on-a-chip and stem-cell technologies to screen insulin-producing cells, test insulin-stimulating compounds, and study the fundamental biology of diabetes. The device makes it easier to monitor islet function and study cell therapies for diabetes.
Researchers will use human pluripotent stem cells, CRISPR and human organoids to dissect beta cell defects and create a human cell model of type 1 diabetes. The goal is to identify the cellular actions leading to disease onset and potentially rescue surviving beta cells.
Researchers at Ohio University are investigating the pulsatility of pancreatic islets in an effort to prevent or reverse type 2 diabetes. By forcing exhausted beta cells to pulse, they aim to restore their healthy functioning and improve health prospects for patients with pre-diabetes and diabetes.
A study from Joslin Diabetes Center found that a minority of patients treated for decades with type 1 diabetes may have monogenic diabetes, which can be treated with oral drugs. The research suggests screening for genetic mutations in young people diagnosed with type 1 diabetes to identify potential treatment options.
A team of researchers has identified highly-connected cluster of 'leader' cells in the pancreas that coordinate insulin response and help understand how diabetes develops. By selectively deleting these leader cells, they disrupted the level of coordination in subsequent responses to glucose.
Researchers found substantial T cell infiltration and few surviving beta cells in a patient's pancreas after IC therapy, contradicting previous reports of elevated PD-L1 expression
A study of adults and youth with type 2 diabetes found that improvements in insulin release wane after treatment stops, highlighting the need for continued treatment. In contrast, youth experience more aggressive disease progression during and after treatment.
Researchers found that mouse brain, liver, and pancreas contain populations of young and old cells, with some as old as neurons. This discovery, known as age mosaicism, suggests complex aging processes in organs beyond the brain.
A study from Joslin Diabetes Center found that removing senescent beta-cells can recover their function and improve glucose metabolism in mice with insulin resistance. The researchers hope to develop a potential treatment using senolytics, which target aging cells contributing to disease dysfunction.
A newly discovered immune cell, the 'X cell', has been found to be a major driver of the autoimmune response believed to cause type 1 diabetes. The X cell can act as both a B cell and a T cell, amplifying the autoimmune response.
Researchers discovered that removing a pair of negative immune signals can stimulate beta cell proliferation, allowing the pancreas to produce more insulin. The findings, made in mice, could lead to new treatments for Type 1 and Type 2 diabetes and obesity.
Research reveals that insulin-producing beta cells can change their function in diabetes, producing somatostatin instead of insulin. This change may be reversible with the restoration of normal environment or chemical treatment. The study provides new insights into the effects of high blood sugar on hormone-producing cells.
Transplanting islets of Langerhans into mice reveals early autoimmune markers of type 1 diabetes, allowing for intervention before beta cell destruction. The study's findings offer hope for developing new drugs and clinical transplantation strategies to prevent damage.
Researchers at Harvard University have improved the laboratory process of converting stem cells into insulin-producing beta cells, increasing purity to 80 percent. This breakthrough may improve beta cell transplants for patients with type 1 diabetes.
Researchers at Joslin Diabetes Center found that increasing beta cell growth before signs of type 1 diabetes can halt the disease. In animal models, continuous generation of new insulin-producing beta-cells protected against autoimmune reactions.
Researchers developed a new machine learning model to describe the dynamics of cell development, estimating selection pressure and formation of new cells. The tool simplifies the interpretation of single-cell time series observations, shedding light on vital questions in biology.
A team from Massachusetts General Hospital has developed a new method to encapsulate human stem-cell-derived beta cells, which restored glucose metabolism in diabetic mice and protected the cells from immune system attack. The use of an immune-repellent protein, CXCL12, significantly prolonged the survival and function of the cells.
Lian's team developed a new method to differentiate stem cells into pancreatic beta cells, using small molecules that stimulate cell signaling pathways. The approach aims to create functional beta cells from stem cells for Type 1 diabetes treatment and has the potential for broad commercial impact.
A plant-based meal has been shown to increase the postprandial secretion of insulin and incretin hormones, particularly GLP-1, in individuals with type 2 diabetes. This improvement in beta-cell function parameters suggests a potential solution for managing and treating the condition.
Researchers discovered that pancreatic beta cells themselves may play a role in T1 diabetes, and found that eliminating senescent cells prevents the disease in mice. The study suggests a paradigm shift for T1 diabetes therapy and opens up new avenues for treatment.
Researchers have engineered a human pluripotent stem cell line containing two 'suicide genes' that induce cell death in all but the desired insulin-producing cells. This approach addresses the limitations of PSC-derived beta cells and opens the door to creating safe cell-replacement therapies for people living with type 1 diabetes.
Researchers have shown that human cells can differentiate into different cell types, changing their original function. This breakthrough may lead to new treatments for diabetes by influencing glucagon-producing cells in the pancreas to produce insulin instead.
Researchers found that low-calorie diets can protect the brain from neuronal cell death associated with diseases such as Alzheimer's, Parkinson's, and cerebral vascular accident. Caloric restriction also improved insulin secretion and increased mitochondria efficiency in cells.
The discovery of glucose-regulated protein GRP94 as a chaperone assisting proinsulin folding has significant implications for understanding insulin production. Removing GRP94 from beta cells impaired insulin secretion, suggesting its specialized function in maintaining cellular response to misfolded proinsulin.
Researchers at Washington University School of Medicine have developed a new method for producing insulin-producing beta cells from human stem cells, which are more responsive to fluctuating glucose levels. The resulting cells were transplanted into diabetic mice and effectively controlled blood sugar for several months.
Scientists at the University of Bergen found that glucagon-producing cells in the pancreas can change identity and adapt to produce insulin for damaged or missing cells. This discovery may lead to new treatments where the body produces its own insulin with minimal assistance.
Researchers at Mount Sinai have discovered a novel combination of drugs that induces the highest rate of proliferation in adult human beta cells, increasing insulin production and potentially treating diabetes. The study found a 5-8% daily growth rate, which is significant progress toward a cure for the disease.
Researchers at Stanford University have developed a zinc-based regenerative drug that selectively targets insulin-producing cells in the pancreas, potentially paving the way for more appealing alternatives to insulin injections. The method uses chelation to deliver a drug to beta cells, which have a strong affinity for zinc.
Scientists have mapped the signal determining pancreatic progenitor cell fate, enabling the manufacturing of insulin-producing beta cells from stem cells. The research facilitates combating type 1 diabetes by understanding how extracellular matrix interactions influence cell destiny.
A new $3.3 million grant will fund a high-resolution reference map of pancreatic cells to identify molecular changes leading to type 1 diabetes.
Scientists have discovered a way to restore normal insulin cell function in type 2 diabetes by blocking a protein called VDAC1. The study showed that the substance can prevent the development of the disease and improve glucose control. Further studies are needed, but the findings offer new hope for treatment options.
C3 regulates autophagy in beta cells, enabling protection from stress and potentially treating diseases like type 2 diabetes. Disruption of this mechanism can contribute to disease development.
A new study suggests that weight loss can put type 2 diabetes into remission by improving pancreatic beta cell function. Nearly half of participants who lost fat from around the liver and pancreas achieved diabetes remission, compared to six in the control group.
Researchers have developed a novel PET imaging method that can measure beta-cell mass, enhancing the ability to monitor and guide diabetes therapies. The new imaging method uses a radioligand to identify beta cells and has shown promising results in differentiating between healthy individuals and those with type 1 diabetes.
A recent study found that nearly half of individuals with type 2 diabetes achieved remission after a weight-loss intervention. The research suggests that substantial weight loss at diagnosis can rescue beta cells and reverse the condition. However, only those who experienced early and sustained improvement in beta-cell function were ab...
A study published in Diabetes Care found that the rapid decline in insulin production associated with Type 1 diabetes follows a two-phase pattern: an initial exponential fall and a subsequent stable phase. This discovery suggests that people with Type 1 diabetes may retain some working beta-cells for seven years after diagnosis.
Researchers at Salk Institute report a potential new approach for treating diabetes by protecting beta cells with vitamin D. The study identified a compound that enhances the activation of the vitamin D receptor, leading to improved survival of beta cells and normal glucose levels in mice.
Bariatric surgery induces changes in alpha cells to produce beneficial GLP-1, combating insulin resistance and islet dysfunction associated with type 2 diabetes. Researchers aim to develop a drug mimicking this effect, making surgery's benefits more accessible.
A study in mice suggests that protective immune cells forming outside the thymus may defend against autoimmune diabetes. Gut microbes affecting this cell population may also protect against disease.
GABA is crucial for maintaining and potentially generating new beta cells, as well as regulating insulin secretion in type 2 diabetes. The anti-inflammatory effect of GABA also shields pancreatic islets from toxic white blood cells, protecting beta cells.
A global project aims to create a detailed, virtual 3D model of the pancreatic beta cell and its components within five years. The project involves experts from various fields and is expected to provide new insights into understanding diabetes.
A new study reveals that non-specific bystander T cells can counteract type 1 diabetes by limiting access to beta cells and interfering with inflammatory signals. This challenge to the traditional notion of regulatory T cells' anti-inflammatory effects opens up new avenues for treatment.
Researchers created a biomaterial that can be seeded with insulin-producing beta cells, reversing diabetes in a mouse model. The study found normalized glucose levels and increased survival in treated mice, without triggering an immune response.
A five-year grant will help researchers study arsenic's impact on pancreatic beta cells and the protective effects of selenoproteins. The study aims to identify factors that counteract arsenic's effects and potentially develop interventions for diabetes prevention.
Scientists have identified progenitor cells within the human pancreas that can be stimulated to develop into glucose-responsive beta cells. These findings open the door to developing regenerative cell therapies for those living with type 1 diabetes.
A new study shows that a plant-based diet improves beta-cell function and insulin sensitivity in overweight adults without a history of diabetes. Participants who followed a low-fat vegan diet experienced increased meal-stimulated insulin secretion and decreased blood sugar levels.
A study at Queen Mary University of London reveals a new gene, MAFA, that affects insulin-producing cells, leading to rare genetic forms of diabetes and insulinomas. The research found that the same gene defect can cause both high and low blood sugar levels in the same family.