Articles tagged with Beta Cells
A rare genetic disorder has provided insight into pancreatic development, suggesting that GATA6 plays a crucial role in programming stem cells to become pancreatic cells. The study sheds light on the underlying causes of most cases of pancreatic agenesis and may help develop new treatments for type 1 diabetes.
Researchers discovered a mutation in the GATA6 gene linked to pancreatic agenesis, a rare condition where the pancreas fails to develop. This finding provides insight into how stem cells can be programmed to become pancreatic cells, potentially leading to new treatments for type 1 diabetes.
Researchers at La Jolla Institute create cellular movies showing the destruction underlying type 1 diabetes in real-time, providing new insights into disease process and potential therapeutic directions. The studies use two-photon microscope to illuminate cell processes previously extrapolated from photos or lab experiments.
A study from Lund University has discovered a molecular link between type 2 diabetes and cancer, highlighting the role of the TCF7L2-p53-p53INP1 pathway in protecting pancreatic beta cells. The risk variant of TCF gene is common and linked to both diabetes and certain types of cancer.
Researchers found that connexin 36 protects mouse pancreatic beta-cells against apoptosis triggered by immune molecules prevalent at the onset of Type 1 diabetes. Promoting connexin 36 expression and function could provide a therapeutic strategy to protect beta-cells from immune system attack.
Scientists have determined that master transcription factors control gene expression in response to signaling pathways, tailoring cell state and function. This discovery sheds light on disease mechanisms and potential therapeutic targets.
Researchers at Stanford University School of Medicine have identified a key molecular pathway responsible for the decrease in insulin-producing cells with age. Activating this pathway may lead to a new treatment for diabetes, and recent studies have shown promising results in mice.
Scientists at Stanford University have identified a molecular pathway responsible for the decline of beta cell division with age. By manipulating this pathway, they can restore the ability of older beta cells to divide and generate new cells, potentially leading to breakthroughs in treating both type 1 and type 2 diabetes.
Researchers have discovered a method to harness patient-derived neural stem cells as an alternative source of insulin-producing beta cells for regenerative treatments. This breakthrough could potentially overcome the shortage of donor pancreatic beta cells and provide a safer, more accessible way to treat diabetes.
Researchers at Yale University have successfully converted uterine stem cells into insulin-producing cells, which could lead to the development of a new treatment for Type 1 diabetes. The study found that these stem cells can adopt the characteristics of beta cells in the pancreas and produce insulin in response to glucose.
Hebrew University researchers have identified a key signal that prompts production of insulin-producing beta cells, which may help restore or increase beta cell function in people with type 1 diabetes. The study found that glucose levels trigger the regeneration of beta cells through a specific enzyme, glucokinase.
JDRF-funded researchers identify a protein and chemical compound that stimulate beta cell growth, providing a new drug target for diabetes treatment. The discovery may lead to the development of tests to measure beta cell number using Tmem27 fragments as a biomarker.
Scientists at UCSF discover that fetal tissue, called mesenchyme, secretes chemicals essential for mature beta cell formation. This breakthrough may lead to new ways of addressing Type 1 and Type 2 diabetes, including generating fully functional beta cells from stem cells or increasing beta cell numbers in people with Type 2 diabetes.
Scientists identify uroguanylin as a potential target for controlling appetite and obesity. They also found a link between Parkinson disease and fat levels in the blood, with implications for treating this neurodegenerative disorder.
A new study found that high levels of fat interfere with key transcription factors, leading to diminished glucose sensing in pancreatic beta cells. This pathway is activated in type 2 diabetes and contributes to metabolic defects, including insulin resistance.
Researchers at Tel Aviv University have discovered that adult-derived stem cells can retain 'memories' of their pancreatic beta cell origins, making them more efficient at producing insulin. This breakthrough may pave the way for new treatment options for juvenile or type 1 diabetes.
Researchers used gene therapy to increase a protein in mouse pancreas that prevents immune attack, potentially leading to new drugs for type 1 diabetes and organ rejection prevention. The discovery may also apply to other autoimmune disorders.
Researchers used bifurcation diagrams to analyze bursting electrical activity in pancreatic beta cells, finding distinct behavioral patterns under critical parameter regions. Dynamical systems approaches are gaining importance in biology due to their ability to dissect complex systems and understand cell-signaling mechanisms.
Barbara E. Corkey, PhD, is being honored by the American Diabetes Association for her 35-year contributions to understanding diabetes and its treatment. Her work has shown that oscillations in beta cell Ca2+ fluxes influence insulin secretion and that elevated glucose and lipids cause tissue malfunction in diabetes.
The DIAPREV-IT study, a three-year project funded by the Juvenile Diabetes Research Foundation, aims to vaccinate healthy children at high risk of developing type 1 diabetes. The researchers believe that vaccinating earlier in the disease process can save more beta cells and increase the vaccine's effectiveness.
An experimental gene therapy has reversed type 1 diabetes in mice with a nearly 80 percent success rate, reversing autoimmune destruction of insulin-producing beta cells. The treatment uses neurogenin3 and betacellulin to stimulate new islet growth and inhibits immune system activity.
Researchers created a new mouse model that can be used to study degenerative diseases, such as type I diabetes and Parkinson's disease. The Mos-iCsp3 mouse allows for targeted destruction of specific cell types, providing a valuable tool for developing therapies.
Scientists at Johns Hopkins University developed an approach to sensitize prostate cancer cells to radiation therapy by knocking down the expression of a gene responsible for DNA repair. Meanwhile, researchers at Weill Cornell Medical College found that a multiple sclerosis drug causes adverse effects in the lungs by degrading S1P rece...
UCLA researchers may have discovered a way to convert non-insulin-producing cells into functional beta cells, which could lead to a permanent solution for diabetes. The study found that chemical tags called methyl groups play a crucial role in maintaining cell identity and converting cells into insulin-secreting beta cells.
Georgia Health Sciences University researchers are exploring whether low levels of interleukin-1 receptor antagonist (IL-1ra) can identify children at risk for developing type 1 diabetes. They also plan to investigate using IL-1 inhibitors to prevent the disease.
Researchers found that mice with short telomeres developed higher blood sugar levels and secreted less insulin, mimicking early stages of human diabetes. The study suggests that shorter telomeres may predispose people to age-related diabetes, paving the way for potential biomarkers.
Scientists have identified a protein called Snapin as the molecular switch that controls insulin secretion in pancreatic beta cells. This discovery provides an explanation for the failure of these cells in type 2 diabetes and may lead to new therapies.
Researchers found alpha cells can harm beta cells through glutamate toxicity, leading to diabetes. A protective protein called GLT1 helps regulate glutamate levels and may offer a new diagnostic test or therapeutic target.
A research team led by Makoto Tominaga found that TRPM2, a body temperature sensor, plays a crucial role in regulating insulin secretion. In TRPM2-deficient mice, impaired insulin secretion and elevated blood glucose levels were observed.
Researchers at UT Southwestern Medical Center have discovered a key mechanism by which the 'starvation hormone' adiponectin functions, promoting cell survival and inhibiting cell death in both pancreatic beta cells and cardiomyocytes. This finding has implications for treating conditions like diabetes, heart disease, and cancer.
A study published in Nature Chemical Biology reveals how pancreatic beta cells interpret incoming signals and find that three proteins relay signals similar to an electrical circuit. The discovery may lead to repairing deficient cells in treating diabetes.
Researchers have found that beta cells in humans do not replicate after age 30, which could lead to breakthroughs in treating type 1 and 2 diabetes. The discovery uses radioactive carbon-14 dating to determine the number of beta cells remains static after this age.
Researchers have discovered haptoglobin as a reliable serum biomarker for predicting the onset of virus-induced type 1 diabetes in rats. The findings suggest that sustained elevations of serum haptoglobin are predictive of ensuing diabetes, with early detection potentially allowing for timely intervention.
Two researchers, Dr. Matthew Poy and Dr. James Poulet, have been awarded $1.5 million starting grants from the European Research Council to improve diabetes treatment and understand brain function.
Researchers have identified a potential target for diabetes drugs by discovering how certain insulin gene mutations cause proinsulin proteins to misfold in pancreatic beta cells. The study found that misfolding of normal proinsulin proteins occurs when mutant protein is present, leading to insulin deficiency and diabetes.
A new consensus statement recommends regular glycemia screening and early identification of patients at metabolic risk to slow or reverse beta-cell decline. The Endocrine Society has launched a website to promote pathophysiology-based clinical practices and aid primary care physicians in interpreting concepts of disease pathogenesis.
UC San Diego researcher Maike Sander leads a team in developing replacement insulin-producing beta cells from patient-derived induced pluripotent stem cells. The goal is to create a cell-based approach for treating type 1 diabetes, providing patients with insulin independence and reduced risk of hypoglycemia.
A multi-center team of scientists from OHSU is part of the prestigious Beta Cell Biology Consortium, aiming to develop a cell-based therapy for insulin delivery in type 1 diabetes patients. The researchers hope to produce abundant quantities of functional human insulin-producing beta cells that can be used for transplantation.
A single stimulatory molecule has been found to sustain human insulin-producing cell replication in a mouse model of diabetes, indicating potential treatment options for the condition.
A study by researchers funded by JDRF found that the serotonin hormone increases insulin-producing beta cells during pregnancy. This discovery could lead to the development of new drugs to promote beta cell regeneration in people with type 1 diabetes, offering a potential cure for the disease.
Researchers at UCSF have found a link between serotonin, a neurotransmitter, and gestational diabetes, suggesting that high protein diets may trigger the condition. The study's findings offer new insights into possible ways to reverse non-gestational diabetes and provide potential therapeutic solutions.
Researchers developed an experimental cure for Type 1 diabetes using gene therapy, which successfully reversed the disease in about half of nonobese diabetic mice. The treatment protected new beta cells from autoimmune attack by adding a protective gene, allowing them to function normally.
Researchers have discovered that type 1 diabetes patients experience a 10-fold increase in islet cell replication after diagnosis. This finding suggests that immune cells are involved in triggering the replication process. The study offers promising results for developing a therapy to encourage beta cells to reproduce and produce insulin.
Researchers have identified eIF5A as a crucial player in pancreatic beta cell dysfunction in diabetes. Blocking hypusine modification of eIF5A protected mice in a model of diabetes, suggesting potential therapeutics for preserving beta cell function.
A study found that the protein tPA protects nerve cells in the brain from death caused by reduced blood flow, leading to two proposed models for its protective effect. Another study identified IL-15 as a potential new target for treating type II refractory celiac disease.
Scientists found that alpha cells can spontaneously reprogram into beta cells, restoring insulin production and potentially treating type 1 diabetes. The study demonstrated that removing nearly all beta cells allowed the pancreas to regenerate new ones, offering a new strategy for regenerating insulin-producing cells.
Researchers at EVMS Strelitz Diabetes Center have received a $1.076 million grant from the Department of Defense to develop new treatments for Type 1 diabetes, focusing on regeneration of insulin-producing beta cells and neutralizing the immune system's attack. The goal is to create a functional cure using a combination therapy regimen.
Researchers at the University of Chicago have developed a new method to study cellular dynamics by applying chemical pulses, allowing them to quantify cell behavior and function in detail. This technique, called chemical perturbation spectroscopy, may lead to breakthroughs in understanding insulin secretion and other biological processes.
A team of LMU researchers has created a genetically modified strain of pigs that consistently develop the essential symptoms of type 2 diabetes. The pigs' physiology is similar to humans', making them an ideal model system for studying the disease, testing new treatments and diagnostic methods.
In this study, researchers discovered autoantibodies that target the natural protein Trib2 in narcolepsy patients with cataplexy, indicating that narcolepsy may be an autoimmune disorder. Additionally, a team of researchers identified a potential therapeutic target for neuroblastoma by studying human neuroblastoma cells and mice.
A new study published by researchers at Eastern Virginia Medical School has identified a protein-based enzyme called 12-Lipoxygenase (12-LO) as a key player in the development of Type 1 diabetes. The enzyme produces specific lipids that cause inflammation and lead to beta cell death, highlighting a potential target for new therapies.
Researchers at the Salk Institute for Biological Studies have made a breakthrough in understanding how stress hormones affect insulin-producing cells. The study found that the hormone CRF can increase the rate of cell growth and proliferation, which could potentially lead to new approaches for treating type 1 diabetes.
Researchers at the Salk Institute have discovered that corticotropin-releasing factor (CRF) plays a part in the pancreas, increasing insulin secretion and promoting beta cell division. This finding may provide new insights into diabetes, particularly type 1, and suggest novel targets for drug intervention.
Researchers found that increasing G6PD levels can prevent negative effects of high sugar on beta cells, which produce insulin. This discovery may lead to targeted treatments for diabetes.
Researchers found that injections of rituximab slowed beta cell destruction in patients with newly diagnosed type 1 diabetes, suggesting a potential treatment option. The study suggests targeting B cells may improve beta-cell function in early type 1 diabetes.
Two UCSF teams, one for diabetes and one for brain tumors, have received grants from the California Institute for Regenerative Medicine to advance stem cell-based therapies. The goal is to file new drug applications with the FDA within four years, driving potential therapies toward clinical trials.
Researchers discovered that T cells recognize a specific marker on insulin-producing cells to gain access to the islets, triggering inflammation and destruction. The findings suggest new approaches to halt or prevent type I diabetes by blocking T cell entry into the islets.
A team from CHEO Research Institute used genetic engineering to remove the Lkb1 gene from beta cells of laboratory mice, resulting in increased insulin production and storage. The improved function lasted at least five months, even on a high-fat diet.
Dr. Francesca M. Spagnoli is investigating the possibility of repurposing hepatic cells to produce insulin in diabetic patients. Her research aims to identify molecular signals that determine why one progenitor cell develops into a hepatic cell and another into a beta cell.
University of Iowa researchers discovered a new molecular mechanism regulating pancreatic cells and insulin secretion in children with permanent neonatal diabetes mellitus. The mechanism involves the protein ankyrin, which regulates the KATP channel complex.