Articles tagged with Beta Cells
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.
A gene therapy approach using AAV vectors reprograms alpha cells into functional insulin-producing beta cells, restoring normal blood glucose levels for an extended period. The strategy shows promise for treating autoimmune diabetes without immunosuppression.
The study found that increased cell death is linked to elevated levels of three death receptor family members, TNFR-1, TRAILR-2, and Fas. High blood sugar and fats subject blood vessels and insulin-producing cells to stress, triggering a cell suicide program.
A collaborative study has identified a novel cluster of dysregulated genes in the pancreatic islets of patients with type 2 diabetes. The findings suggest that these altered genes are responsible for beta cell failure in diabetes and may hold new insights into how to prevent and treat the disease.
Researchers found that inhibiting microRNA-204 could lead to better treatment of diabetes by regulating the cell surface receptor GLP1R. This could result in lower-drug doses and reduced dose-dependent side effects. The study suggests a novel approach to targeting beta-cell function and improving glucose control.
A new study published in Nature Cell Biology shows that human stem cells can be used to produce insulin-producing cells that can be transplanted into diabetes patients. The development of these cells depends on their sense of direction and polarity, which can be controlled using a specific signal pathway.
A recent study from UC Davis researchers refutes the use of an anti-malaria drug to create new insulin-producing cells for Type 1 diabetes treatment. The findings highlight the crucial need for reproducibility in scientific research, contradicting a previous report that sparked excitement in the field.
Artificial beta cells mimic the body's natural glucose-controllers and can be subcutaneously inserted into patients or delivered via a painless skin patch. In lab experiments and animal models, they demonstrated rapid responsiveness to excess glucose levels and normalized blood glucose levels in diabetic mice.
Altered MAIT cell concentration and function are linked to T1D pathogenesis, compromising gut mucosa homeostasis and favoring autoimmune responses.
Researchers at Mount Sinai Hospital discovered a genomic recipe in rare benign tumors that can regenerate insulin-producing human beta cells, potentially treating diabetes. The study's findings have the potential to develop new drugs that increase healthy beta cell mass.
Researchers have developed a better understanding of how to improve the production of beta cells, the cells responsible for insulin regulation in diabetics. The study shows that genes NXK6.1 and MNX1 play a crucial role in the development of beta cells.
Researchers discovered that epicatechin monomers in cocoa enhance beta cells' ability to secrete insulin, improving blood glucose control. The study suggests these compounds could potentially delay or prevent type 2 diabetes onset in patients.
Researchers at the University of Wisconsin-Madison have developed a new measurement for the volume and activity of beta cells, which are responsible for producing insulin. The new test uses PET scanning to detect minute levels of a radioactive chemical in the mouse pancreas, providing a more accurate assessment of insulin production.
Scientists have identified a molecular handle to purify cells destined to become insulin-producing cells, enabling a streamlined and cost-efficient process for generating glucose-responsive beta cells. The discovery aims to address safety and end product consistency challenges in cell therapy for type 1 diabetes.
Researchers found Epac2A controls insulin release amount and timing at cell membrane sites. Patients with type 2 diabetes have lower Epac2A levels, suggesting a link to reduced insulin secretion.
Researchers have discovered significant differences in G protein-coupled receptor expression between humans and mice, highlighting the need for new approaches to develop effective diabetes drugs.
A study suggests that vitamin A plays an important role in the development and function of beta-cells, leading to improved insulin secretion. Researchers found that partially blocking the vitamin A receptor impaired cell survival and insulin secretion, highlighting its potential as a new target for diabetes treatment.
A recent study has made a breakthrough in understanding the autoimmune process that leads to type 1 diabetes, finding a way to protect beta cells from destruction. By targeting the activation of B cells, researchers were able to prevent diabetes in non-obese diabetic mice.
Researchers at UT Health San Antonio have developed a gene-transfer technique that increases insulin-producing cells, potentially curing Type 1 and improving Type 2 diabetes. The therapy has cured diabetes in mice without side effects, offering a major advance over traditional insulin therapy.
Researchers at UC San Diego School of Medicine have mapped out beta cell growth pathways that could be exploited to regenerate cells. This new information opens the door for finding drugs that stimulate these pathways to improve blood sugar levels in people with diabetes.
Researchers identified markers of aging in insulin-producing beta cells, revealing diverse populations with different lifespans. Insulin resistance accelerates beta cell aging, contributing to type 2 diabetes development.
Researchers at the University of California, Davis have discovered a possible new route to regenerating beta cells, giving insight into healthy metabolism and diabetes. This discovery could lead to better treatment or cures for diabetes by understanding how these cells mature into functioning beta cells.
Researchers at Joslin Diabetes Center have discovered a biological mechanism that prevents insulin-producing cells from dividing successfully. The study found that the proteins centromere protein A and polo-like kinase-1 are essential for beta-cell growth, and their loss leads to cell death.
A fasting-mimicking diet has been shown to reverse diabetes in mice by promoting the growth of new insulin-producing pancreatic cells. In humans, the diet also increased expression of a protein that accelerates insulin production in type 1 diabetes patients, suggesting potential for alleviating symptoms.
A new study suggests that a fasting-mimicking diet can reprogram pancreas cells in diabetic mice, enabling them to produce insulin and repair themselves. The researchers found that the diet triggered developmental reprogramming in the pancreas, rebuilding damaged areas and restoring function.
Scientists have successfully converted mouse alpha cells into insulin-producing beta cells by blocking the expression of two specific genes. The research suggests that this natural flexibility in cell fate may be exploited to develop a new therapeutic approach for Type 1 diabetes.
Researchers discovered a subpopulation of beta cells that resists immune attack and acquires stemness to persist despite immune attack. This finding may lead to therapies targeting these cells to restore insulin production in type 1 diabetic patients.
The Helmholtz Zentrum München will receive 1.5 million euros to develop stem cell culture models on a chip for investigating pancreatic diseases and testing therapy options. The goal is to explore biology, identify points of attack, and potentially develop beta cell replacement therapy.
A new study found that high levels of air pollution can make insulin-creating cells less efficient, increasing the risk for type 2 diabetes in obese Latino children. Exposure to poor air quality during childhood increases the risk for obesity and Type 2 diabetes.
A new study found that low thyroid hormone levels before birth impair the growth and development of the fetal pancreas, affecting insulin-secreting cells. This could lead to increased risk of pancreatic disorders and type 2 diabetes in later life.
Researchers at the University of Oregon have identified a novel bacterial protein, BefA, that stimulates the growth of insulin-producing cells in zebrafish. This discovery highlights the crucial role of resident microbes in pancreas development and may lead to new diagnostic, preventative, and therapeutic approaches for Type 1 diabetes.
Researchers at ETH Zurich have created artificial beta cells that can effectively regulate blood sugar levels. These cells work by measuring glucose concentrations in the blood and producing insulin when necessary, making them a promising solution for diabetes treatment.
Researchers found that artemisinins transform glucagon-producing alpha cells into insulin-producing cells by activating GABA receptors, producing insulin. The study uses FDA-approved malaria drugs and has been shown to increase beta cell mass and improve blood sugar homeostasis in animal models.
Researchers have successfully reactivated oscillations in insulin-producing pancreatic beta cells using mathematical models and microfluidic devices. By delivering controlled glucose levels to dormant cells, scientists can test how insulin-producing cells get turned off and whether they can be reactivated.
Researchers found that pancreatic beta cells release proteins and their packaging, exosomes, which target the immune system. The study suggests a new direction for treatments focused on inhibiting immune cell activation.
Scientists at the University of Michigan are studying protein degradation in pancreatic beta cells to better understand diabetes at the molecular level. They found that proinsulin misfolding can lead to diabetic disease and identified a way to stimulate the degradative pathway to restore normal insulin secretion.
A new study found that pulses of glucose can reactivate the insulin clock in beta cells, which regulate blood sugar. The research suggests that controlled glucose solutions may be used to treat Type 2 diabetes.
Teresa Mastracci, a researcher at the Indiana Biosciences Research Institute, has received a $750,000 JDRF grant to study polyamine and hypusine biosynthesis for reversing the progression of type 1 diabetes. The goal is to identify new drugs that preserve or regenerate healthy beta cells.
Teresa Mastracci, a Senior Scientist at IBRI, has received a $750,000 JDRF Career Development Award to investigate polyamine and hypusine biosynthesis in reversing type 1 diabetes. Her research aims to identify new drugs that preserve or regenerate healthy beta cells, slowing or halting disease progression.
A study by CRCHUM researchers reveals that chronic kidney disease can cause secondary diabetes through the buildup of urea in the blood. The disease impairs insulin secretion from pancreatic beta cells, leading to increased blood glucose levels and potentially progressing to diabetes.
Researchers found that just 1-10% of beta cells control islet responses to glucose, serving as pacemakers for insulin secretion. This discovery could pave the way for therapies targeting these 'hubs' to treat type 2 diabetes.
Researchers at Helmholtz Munich discovered a new marker, Flattop, that subdivides insulin-producing beta cells into mature and immature subgroups. The study suggests that the Flattop-negative cells are a reserve pool for replenishing mature beta cells.
Researchers have discovered at least four separate subtypes of human insulin-producing beta cells, which could lead to a better understanding of the disease process and the development of new treatments for type 2 diabetes. The study found that these cell subtypes produce different amounts of insulin and may regenerate at varying rates.
Researchers found CART hormone increases insulin secretion and decreases glucagon production, a potential target for new type 2 diabetes drugs. CART is overexpressed in human type 2 diabetic islets, suggesting a link between glucose levels and hormone production.
A study by University of Illinois researchers suggests that protein S supplementation can inhibit beta-cell death and improve blood glucose levels, insulin sensitivity, and kidney damage in mice with type 1 and type 2 diabetes. The findings offer a potential new approach to treating the disease.
A novel cellular membrane protein called TSPAN2 has been identified as a key player in beta-cell apoptosis. The study suggests that targeting TSPAN2 could become a new treatment strategy for type 2 diabetes.
A recent study published in PLOS Genetics has identified a single gene, RCAN1, that may contribute to insulin secretion problems in both conditions. Overexpression of this gene leads to mitochondrial dysfunction and reduced insulin production in beta cells.
A recent study published in The Journal of Clinical Investigation found that certain bacteria can activate killer T-cells, which destroy insulin-producing cells and lead to type 1 diabetes. This discovery sheds light on the potential external factors contributing to the disease's development.
Scientists at Washington University School of Medicine and Harvard University have produced insulin-secreting cells from stem cells derived from patients with type 1 diabetes. The new cells can produce insulin in response to glucose and may offer a potential cure for the disease.
A study published in Cell Metabolism reveals significant differences in gene expression patterns and DNA modifications between pancreatic cells of donors under 9 and those over 28. The findings highlight the importance of genes SIX3 and SIX2, which mature with age and may contribute to diabetes risk.
The adAPT trial is a clinical study evaluating the effectiveness of metformin in preventing type 1 diabetes. Researchers aim to identify children at high risk and examine the impact of administering metformin on beta cell stress.
Scientists have discovered a nuclear receptor protein, estrogen-related receptor γ (ERRγ), that enables the maturation of human beta cells in vitro. This breakthrough overcomes a major challenge in diabetes research and holds promise for creating functional insulin-producing cells at will.
Salk researchers have found a hidden energy switch that powers up pancreatic cells to respond to glucose, enabling the production of functional human beta cells. The breakthrough could lead to a viable treatment for type 1 and 2 diabetes.
Scientists have successfully extracted stem cells from a 50-year-old test subject's fatty tissue, applied genetic reprogramming, and produced mature, insulin-producing beta cells. The researchers' technique has the potential to treat diabetes by implanting new functional beta cells made from the patient's own adipose tissue.
A recent study by University of Montreal researchers has discovered a common genetic defect in beta cells that may lead to the loss of insulin production in both type 1 and type 2 diabetics. The findings suggest that genetics play a critical role in beta cell survival, with fragile cells being more prone to damage and disease.
A new study discovered that a common genetic defect in beta cells may underlie both form of diabetes. The research found that genetics is critical for the survival of beta cells, and a genetic predisposition for fragile beta cells may lead to diabetes development.
Patients with maturity-onset diabetes of the young (MODY1) benefit from therapies targeting a specific pathway regulating insulin secretion, not oral medications linked to beta-cell destruction. Research suggests MODY1 patients may become dependent on insulin injections sooner due to cellular stress levels.
Researchers at UNC and NC State create a synthetic patch filled with natural beta cells that can secrete insulin on demand, avoiding rejection risks and hypoglycemia. The 'smart cell patch' demonstrated successful blood sugar regulation in small animal models of type-1 diabetes.
Researchers at Lund University discovered a link between nicotine and type 2 diabetes, finding that nicotinic acetylcholine receptors influence insulin release. A genetic alteration affecting these receptors increases the risk of developing type 2 diabetes.