Articles tagged with Beta Cells
Scientists at Eastern Virginia Medical School have identified a vital step in the development of Type 1 diabetes and hope to develop a novel therapeutic approach by blocking an enzyme called 12-LO. Preliminary results are promising, and further research is underway.
Researchers have identified pathways that control partial pancreatic regeneration induced by sodium tungstate treatment, revealing its anti-diabetic effects.
Scientists discover a single transcription factor that can convert alpha cells into functional beta cells, increasing their number eight-fold in mice. The study shows promise for a potential new treatment for type I diabetes, where the body autodestructs beta cells leading to insulin deficiency and complications.
Scientists have discovered a way to regenerate insulin-producing beta cells from non-insulin-producing alpha cells, offering new hope for treating type 1 diabetes. The research found that modifying the expression of a specific gene in alpha cells can drive their conversion into functional beta cells.
A protein called Pdx1 plays a previously unknown regulatory role in the development of immature endocrine system cells, ultimately giving rise to pancreatic islet cells. This discovery may facilitate beta-cell growth in labs and lead to new therapies for diabetes.
A Phase II trial shows that a low dose of oral interferon alpha preserves beta cell function in patients with newly diagnosed type 1 diabetes, delaying the need for insulin. The study found significant improvement in preserving insulin-producing beta cell function compared to placebo, offering hope for managing the disease.
Researchers at the University of Pittsburgh School of Medicine have identified a key molecular pathway that regulates replication of pancreatic beta cells. Knocking out two cell cycle proteins leads to robust beta cell replication in mouse experiments.
Researchers from USC's Keck School of Medicine presented new findings on the role of exercise in preventing post-exercise hypoglycemia and ways to modulate pancreatic beta cell mass to prevent type 2 diabetes. The studies aim to improve diabetes treatment guidelines, including medication timing and exercise recommendations.
A LSUHSC student has developed a groundbreaking treatment for diabetes using ACE2 gene therapy, which improves pancreatic beta cell function and restores glucose stability in diabetic mice. The award recognizes the student's outstanding research contributions to the field of endocrinology and metabolism.
Pancreatic islet transplantation has been shown to improve glucose control and lead to insulin independence in some individuals with type 1 diabetes. However, obstacles remain, including limited engraftment and chronic immunosuppression.
Scientists have developed a device that protects transplanted pancreatic precursor cells from the immune system, allowing them to mature into functional beta cells. This breakthrough approach could alleviate the need for long-term immunosuppression in cell transplantation therapy.
Researchers found that HIV-1 protease inhibitors like nelfinavir induce oxidative stress in pancreatic beta-cells, leading to decreased insulin secretion. Thymoquinone, an antioxidant from black seed oil, protects these cells by decreasing reactive oxygen species and increasing antioxidant levels.
A new study found that over 60% of pancreases from children with type 1 diabetes showed evidence of enteroviral infection, suggesting a potential link between viruses and the disease. The research suggests that enteroviral infection may trigger an immune response that destroys beta cells in the pancreas.
Scientists have created synthetic microtissues that can perform functions like secreting hormones and responding to stimuli, surpassing individual cell capabilities. The technique uses DNA hybridization as a programmable glue to link cells together in 3D arrangements.
Researchers have identified two causes of critical illness hypeglycemia in children: peripheral insulin resistance and primary beta-cell dysfunction. The study found that those with respiratory failure only had CIH caused by elevated insulin resistance, while those with both respiratory and cardiovascular failure had CIH caused by prim...
JDRF-funded researchers have identified compounds that can stimulate insulin-producing cells in the pancreas, paving the way for potential regenerative medicines for type 1 diabetes. The study found two compounds that promote beta cell replication via different biological pathways.
Researchers at LSU Health Sciences Center have discovered a protein that can interrupt normal cellular proliferation in pancreatic cancer cells. This breakthrough may lead to new treatments for type 1 and 2 diabetes by controlling the growth of islet cells.
A recent study found that CXCL10 is a key factor behind the destruction of insulin-producing β cells in diabetes. The inflammatory marker was found to decrease β cell viability and impair insulin production in isolated human pancreatic cells. This discovery may lead to new treatments for preventing β cell death or restoring lost function.
JDRF-funded researchers at the University of Pittsburgh School of Medicine discovered a protein called cdk6 that regulates human beta cell replication. This finding provides proof-of-principle for stimulating human beta cell production and function.
Researchers at the University of Pittsburgh School of Medicine have successfully induced human insulin-producing beta cells to replicate in a living animal and in the lab. The discovery could improve models and methods for studying diabetes and lead to techniques for generating new beta cells in patients with diabetes.
Researchers at Albert Einstein College of Medicine developed a technique to make foreign pancreatic cells invisible to the immune system, dramatically protecting them from rejection. The new method could pave the way for routine use of cell transplants as a therapy for type 1 diabetes in humans.
Researchers have developed a mouse model of neonatal diabetes that replicates human disease, providing new insight into the condition. Additionally, studies have identified a link between endothelial dysfunction and altered metabolic responses, particularly in relation to high-fat diets and glucose regulation.
Scientists at Oxford University created a mouse model of neonatal diabetes that mimics the human condition, showing the V59M mutant Kir6.2 protein disrupts insulin production and leads to increased blood glucose levels.
Researchers at Joslin Diabetes Center have identified pancreatic progenitors that can form into insulin-producing cells after birth or injury, contradicting earlier studies. This finding offers new hope for treating and potentially curing diabetes through replacement therapy.
In an animal model, sulfonylureas' effects were found to be reversible after cessation, suggesting beta cells can recover and produce insulin again. This finding may lead to rethink treatment strategies, such as using older drugs or alternating periods of drug treatment with insulin injections.
Researchers found that sulfonylurea treatment failure is not due to cell death, but rather permanent depolarization of potassium channels. Reversible effects on insulin release were observed in mice treated with slow-release sulfonylureas.
Researchers at Beth Israel Deaconess Medical Center discovered that the AAT protein can restore normal blood glucose levels in a mouse model of Type 1 diabetes. The study suggests that inflammation plays a key role in the disease and provides evidence for using the protein as an alternative treatment option.
Researchers found that SREBP-2 induces expression of type 2 taste receptors in cultured mouse intestinal cells and enhances T2R-induced secretion of cholecystokinin. This mechanism may inform the gut about food-borne toxins and initiate a response to limit their absorption.
Researchers at Tel Aviv University develop a way to cultivate cells derived from insulin-producing beta cells, potentially implanting them into patients with type 1 diabetes. This innovative method could reduce the need for life-saving organ transplants and one day be as simple as a blood transfusion.
Researchers found that interferon-alpha plays a key role in the onset of type 1 diabetes by triggering an immune response that destroys pancreatic beta cells. This discovery could provide new insights into the disease and potentially lead to new treatments.
A new USC study found that overweight Hispanic children are at significant risk for pre-diabetes, with persistent pre-diabetes during growth associated with progression towards type 2 diabetes. The study highlights the importance of regular monitoring of these children to detect potential risks early.
Researchers at Broad Institute will explore ways to regenerate human cells lost in type 1 diabetes, using chemical biology and genomic tools. The goal is to find ways to replenish missing cells, potentially reducing or eliminating lifelong insulin therapy.
Researchers at Uppsala University develop new image analysis methods to study the release of insulin and cAMP in beta cells. The findings show that ATP causes an increase in cAMP concentration, which varies rhythmically and coincides with variations in calcium signals, resulting in pulsatile insulin secretion.
A USC study found that progressive weight gain in Hispanic women is a key factor in the decline of beta cell function, leading to rising glucose levels and an increased risk of developing diabetes. The study's findings highlight the importance of reducing excess fat to prevent or delay diabetes.
Researchers found a previously unknown cooperation between pancreatic beta cells and alpha cells, crucial for glucose balance. The discovery may lead to better blood sugar regulation in diabetes patients by targeting the glucagon/glutamate pathway.
Researchers at UT Southwestern have developed a mouse model that mimics hyperglycemia and allows pancreatic beta-cell regeneration. The PANIC-ATTAC mouse model provides insights into improved treatments for type 1 and gestational diabetes, as well as temporary hyperglycemia.
A new vaccine approach using microspheres has prevented and reversed new-onset cases of type 1 diabetes in animal models. The microspheres, developed by the Children's Hospital of Pittsburgh, reprogram dendritic cells to block the immune system's attack on insulin-producing beta cells.
Researchers at Washington University School of Medicine have identified dendritic cells carrying insulin fragments as a key player in the development of type 1 diabetes. The discovery sheds light on how an immune system attack can destroy the islets of Langerhans, leading to insulin deficiency and the disease.
Scientists have discovered a way to genetically manipulate embryonic stem cells into insulin-producing pancreatic tissue, potentially treating type-1 and type-2 diabetes. The team found that the transcription factor PAX4 encouraged high numbers of stem cells to become beta cells with insulin-producing capabilities.
Scientists at JDRF have identified a new pancreatic progenitor cell capable of generating insulin-producing beta cells. These cells, similar to embryonic progenitors, show promise for regenerating lost beta cells in people with type 1 diabetes.
A team of researchers has identified pancreatic stem cells with the capacity to generate new insulin-producing beta cells in adult mice. These findings represent a significant breakthrough in understanding the pancreas's ability to regenerate beta cells, a crucial step towards developing effective treatments for diabetes.
Professor Jens Høiriis Nielsen from the University of Copenhagen receives a JDRF research grant to investigate beta cell expansion during pregnancy. The goal is to discover new approaches for treating type 1 diabetes, potentially leading to regenerative drugs and therapies.
Researchers at WashU Medicine found that fat cells release an enzyme called Nampt, which enhances glucose-stimulated insulin secretion from pancreatic beta cells. This discovery could lead to new methods for improving glucose metabolism in type 2 diabetic or insulin-resistant individuals.
New findings suggest that misfolded proinsulin can cause beta cell dysfunction and death, leading to an insulin shortage. This can result in the hallmark symptoms of diabetes, including high blood glucose levels.
A new study led by Joslin Diabetes Center researchers shows that leptin plays a major role in islet cell growth and insulin secretion, potentially leading to new treatments for type 2 diabetes. The study found that mice lacking leptin receptors in the pancreas showed improved glucose tolerance and greater insulin secretion.
Researchers discover ghrelin promotes thymopoiesis during aging, boosting T cell output, while also finding PPAR-gamma agonists exacerbate cardiac dysfunction due to glucolipotoxicity. Additionally, a study finds osteopontin deficiency in mice leads to improved insulin sensitivity despite obesity.
Researchers found that immunosuppressive drugs suppress beta-cell regeneration in diabetic mice, casting doubt on long-term islet transplantation success. This could lead to breakthroughs in regenerative islet transplantation and improved treatment for type 1 diabetics.
Researchers at UT Southwestern Medical Center found that dietary fats can kill transplanted pancreas cells, leading to a decline in insulin production. Limiting fat formation might make pancreatic cell transplants more effective.
Researchers at Johns Hopkins have developed a new technique to track and protect transplanted insulin-producing cells in a diabetic animal model. The method uses magnetic capsules to encapsulate the cells, avoiding immune rejection and allowing for successful long-term function.
Researchers found that pumpkin extract promotes regeneration of damaged pancreatic cells in diabetic rats, boosting insulin levels and reducing the need for daily insulin injections. The extract's protective effect is attributed to antioxidants and D-chiro-inositol, which may provide a new source of medication for diabetics.
A new study published in Journal of Biological Chemistry reveals that glucose enables the development of healthy beta cells, which secrete insulin. Understanding how to switch on genes crucial for beta cell development may enable the creation of insulin-producing cells from stem cells.
Adult stem cells are not responsible for producing insulin, contrary to previous research. Instead, beta cells slowly divide to replenish their own population. This discovery advances basic knowledge of insulin biology and could lead to eventual therapies.
Researchers at the University of Pennsylvania School of Medicine have demonstrated that injured pancreatic cells readily regenerate back into healthy acinar cells. This finding holds promise for treating cancer and inflammation of the pancreas, while shifting focus from regenerating insulin-producing beta cells.
A Joslin-led study identified insulin receptors as crucial for promoting beta cell growth, a potential target for treating type 2 diabetes. The research found that mice lacking insulin receptors failed to grow more islet cells, highlighting the importance of insulin receptors in overcoming insulin resistance.
Researchers found that hypoglycemic neuronal death is triggered by glucose reperfusion and activation of NADPH oxidase. Treatment with CD40Ig allows rats to accept heart grafts from non-genetically identical donors by enhancing regulatory immune cells.
A recent Joslin Diabetes Center-led study has discovered that the appetite hormone melanin concentrating hormone (MCH) plays a crucial role in the growth of insulin-producing beta cells and insulin secretion. This finding may lead to the development of new treatments that stimulate beta cell growth to treat type 1 and type 2 diabetes.
Scientists discovered that cells passed from mother to child during pregnancy can differentiate into functioning islet beta cells producing insulin. Higher levels of maternal DNA were found in the blood of children and young adults with Type 1 diabetes, suggesting a beneficial role for microchimerism.
Researchers found maternal cells in children with type 1 diabetes that produce insulin and may aid in pancreas repair. The study indicates that microchimerism, the transfer of mother's cells to child during pregnancy, might have therapeutic benefits.
A genetic mutation in the beta1-adrenergic receptor alters the response to certain heart failure drugs, highlighting the potential for personalized medicine. The study found that a single amino acid change in the receptor can affect how well patients respond to beta blockers, with some variants showing increased sensitivity to carvedilol.
A high-fat diet induces insulin resistance in mice, leading to increased beta-cell mass as the body attempts to compensate. Glucose levels are found to be a crucial trigger for this process, with GCK and IRS-2 playing key roles in the mechanism.