Articles tagged with Beta Cells
Researchers at UNIGE have found that the S100A9 protein can significantly improve insulin metabolism in diabetic patients, reducing the risk of severe side effects associated with insulin therapy. The protein's anti-inflammatory effect may also help to normalize ketone production and prevent life-threatening conditions.
Researchers at the University of Chicago have made a breakthrough in understanding the development of type 1 diabetes by targeting the role of pancreatic beta cells. Deleting a gene called Alox15 in mice preserved their beta cells, reduced immune T cell infiltration, and prevented diabetes from developing.
A recent study at Tokyo Institute of Technology reveals that dopamine regulates insulin secretion through a complex of receptors, specifically D1 and D2. The discovery offers new insights into the mechanism behind this regulation and has potential therapeutic targets for preventing, treating, and managing diabetes.
A new study reveals that IL18 signaling is essential for β-cell development and insulin secretion, using specific receptors on acinar and β cells. This finding may provide insights into the role of IL18 in regulating islet β cell proliferation and guide future efforts to expand β cells and increase islet mass in diabetes.
A high-fat diet can lead to increased fructose metabolism in the small intestine, resulting in the release of glycerate into circulation. This can cause damage to insulin-producing pancreatic beta cells, increasing the risk of glucose tolerance disorders and Type 2 diabetes mellitus.
A team from UNIGE demonstrates that stem cells giving rise to beta cells cease to exist after birth, and defines the 'identity card' of other hormone-producing cells. This discovery has significant implications for developing cell-based therapies to treat diabetes.
Researchers at NTU Singapore's Lee Kong Chian School of Medicine found that saturated fatty acids degrade protein FIT2, leading to insulin-producing cells' loss of function and death. This impairs the body's ability to secrete enough insulin, resulting in diabetes.
Researchers at Karolinska Institutet have identified a new antidiabetic substance that preserves beta cell activity and prevents high blood glucose in mice. This approach may prevent the exhaustion of beta cells and improve long-term diabetes treatment.
Researchers found that verapamil treatment delayed disease progression, lowered insulin requirements, and preserved some beta cell function in patients with Type 1 diabetes. The study used proteomics analysis and RNA sequencing to examine changes in circulating proteins in response to verapamil treatment.
Scientists have successfully produced fully functional pancreatic beta cells from stem cells for the first time, offering a breakthrough in treating type 1 diabetes. The study's findings demonstrate that these stem cell-derived beta cells can regulate insulin secretion and manage glucose metabolism in both cell cultures and mice studies.
Researchers developed genetic modifications to increase stress resistance and immune evasion in stem cell-derived beta cells, leading to improved survival rates. The study suggests a potential breakthrough for treating type 1 diabetes through transplantation of these cells.
Researchers have revealed that during Type 1 Diabetes development, pancreatic duct cells reprogram to suppress autoimmune T cell responses. This discovery advances understanding of the disease by creating a map of pancreatic islet cells over time.
A new study published in Nature Communications identifies a harmful cellular pathway that causes pancreatic beta cell death, leading to type 1 diabetes. Blocking this pathway preserved beta cells, increased insulin production, and prevented or delayed diabetes in mice models.
Researchers at UNIGE found that fat can aid pancreatic beta cells in adapting to excess sugar levels. The study reveals a dynamic cycle of fat storage and mobilization allows cells to maintain near-normal insulin secretion. Regular physical activity may help give this beneficial cycle a chance to be active.
Microtubule structures play a crucial role in regulating insulin release from pancreatic beta cells, with dynamic turnover leading to increased insulin secretion. The findings have important implications for understanding diabetes and could lead to new treatments.
The study analyzed data from 8,502 genetically high-risk children and found that half developed type 1 diabetes before age 6, while the other half developed it between ages 6 and 12. The findings suggest a different form of type 1 diabetes emerges in children as they grow older.
A transgenic pig model has been developed allowing for the first time the in vivo fluorescent labeling of age-distinct insulin secretory granule pools. This model enables researchers to study insulin turnover in normoglycemic conditions, closing the translational gap between humans and rodents.
Researchers used human pluripotent stem cells and organoids to study SARS-CoV-2 infection, finding that it can infect multiple cell types, including lung, colon, heart, liver, and pancreatic cells. The virus alters cellular function, including reducing insulin production in pancreatic beta cells.
Researchers developed an experimental device to improve blood sugar control in HI patients. The bihormonal bionic pancreas (BHBP) helps maintain stable glucose levels without human error in calculating doses.
Researchers at UC San Diego will use $6.4 million in NIH funding to study the influence of external signals on insulin production in beta cells. They aim to create a roadmap of genetic variations that can predict changes in insulin output, which may help prevent and treat diabetes.
Researchers found that certain peptides associated with migraine pain can regulate insulin production in mice, potentially preventing type 2 diabetes. The study suggests that these peptides could be developed into therapeutic strategies to control blood sugar levels, while minimizing the risk of migraines.
Using human stem cells and small molecules, researchers successfully differentiated them into insulin-producing pancreatic beta cells. This breakthrough could lead to a personalized treatment option for type 1 diabetes, reducing costs and increasing accessibility for those affected.
Researchers found that a gene called REST is crucial for boosting insulin-producing cells during early pancreas development. Inactivating this gene increased the number of insulin-producing cells, which were maintained into adulthood in mice.
Researchers at Salk Institute develop efficient method to produce insulin-producing cells from stem cells, bringing hope for type 1 diabetes treatment. The new approach resulted in beta cell yields of up to 80 percent and biologically functional transplanted cells in mouse model.
Researchers developed a nanofiber-integrated cell encapsulation device that protects insulin-secreting cells from the immune system, allowing them to secrete insulin and control blood sugar levels. The implant was successful in mice with diabetes for up to 200 days without suppressing the immune system.
Researchers at UCSF have found a way to stimulate the natural surveillance system of immune cells to eliminate senescent cells, which contribute to aging and chronic diseases. This discovery offers an alternative to existing senolytic therapies and may lead to new treatments for age-related chronic diseases.
Researchers at The University of Tokyo have developed a novel cell therapy using a lotus-root-shaped device to transplant human pancreatic beta-cells in the long term. The device, called LENCON, was shown to successfully control blood glucose levels for over 180 days in diabetic mice.
Scientists use monoclonal antibodies against the glucagon receptor to convert alpha cells into beta cells, significantly increasing the number of cells in the pancreas. This could potentially treat both Type 1 and Type 2 diabetes by restoring natural insulin production.
The JDRF Center of Excellence in New England will focus on accelerating gene editing approaches for beta cell replacement therapy, aiming to solve the problem of immune rejection of beta cells. The center will collaborate with leading Massachusetts-based experts to develop new technologies and strategies to prevent beta cell destructio...
Researchers found that an experimental treatment converted cells to generate insulin, reducing diabetic symptoms and increasing insulin cell mass. The treatment showed promise for regenerating insulin-producing capacity and restoring normal blood glucose balance.
Dopamine plays a key role in regulating blood glucose levels, and its blockade by antipsychotic medications can lead to uncontrolled glucose production and obesity. The study reveals that pancreatic alpha cells produce dopamine, which acts on both insulin-producing beta cells and other receptors.
Researchers at Monash University have discovered a biological process that prevents the human body from regenerating new cells or tissue after birth. By demethylating specific genes, they can reawaken progenitor cells to become insulin-producing beta cells, offering a potential breakthrough for treating Type 1 and Type 2 diabetes.
Researchers have discovered a novel and druggable insulin inhibitory receptor named inceptor. Blocking its function leads to increased sensitisation of the insulin signalling pathway in pancreatic beta cells, allowing for potential protection and regeneration of beta cells for diabetes remission.
A new drug combination combining a widely used diabetes treatment with an experimental cancer drug has shown significant improvements in blood glucose control and weight loss in mice. The combination treatment enhanced insulin secretion and reduced body weight, paving the way for clinical studies.
Scientists have developed advanced imaging techniques to observe pancreatic beta cells packaging insulin and responding to drug treatments. The new methods provide a more complete picture of the cell's functions and components, shedding light on the mechanisms responsible for preventing diabetes.
A study published in PNAS reports a breakthrough treatment for type 1 diabetes in mice, utilizing a combination of haploidentical mixed chimersim and administration of gastrin and epidermal growth factor. This approach successfully reversed autoimmunity, augmented beta cell regeneration, and normalized blood glucose levels by reactivat...
Scientists from UNIGE and HUG identified the essential role of circadian clocks in beta cell regeneration. The study found that regeneration is significantly greater at night, when mice are active, and that the BMAL1 gene plays a crucial role in this process.
A study using genome sequencing and CRISPR gene editing tools has uncovered a new biological pathway essential for insulin production in the YIPF5 gene. The research shows that genetic changes in this gene result in high stress levels, leading to cell death in insulin-producing cells.
Researchers developed a novel photodynamic therapy to target insulin-producing lesions, showing promise in slowing tumor growth and inducing cell death. The treatment could provide a minimally invasive option for hyperinsulinemic hypoglycemia, improving patient management.
A recent study suggests that the evolution of insulin has encountered a roadblock, rendering most people vulnerable to Type 2 diabetes. The researchers discovered that even slight variations in the insulin-sequencing process can impair insulin folding and induce cellular stress.
Researchers at UAB have developed a biocompatible coating that delays allograft and autoimmune-mediated rejection in mouse models of T1D. The coating, consisting of multiple layers of tannic acid, protects transplanted islets from immune cells and oxidative stress.
A team of researchers from CNIO describes how the enterovirus coxsackievirus type B4 can induce diabetes by deregulating the URI protein and silencing the Pdx1 gene. This finding has potential implications for understanding the relationship between SARS-CoV-2 infection and diabetes.
Researchers at Pennington Biomedical Research Center will investigate how the SGK1 enzyme regulates beta-cell mass when more insulin is needed. The study aims to understand how beta-cell growth mechanisms influence insulin release, potentially leading to new medications for diagnosing and treating metabolic diseases.
A new study confirms the existence of residual, non-functioning beta cells in living individuals with longstanding type 1 diabetes. Researchers used a non-invasive imaging technique to detect these cells, which may be restored if adequate treatments are available.
A study found that a ferry protein in the pancreas plays a crucial role in regulating insulin levels and protecting against the negative effects of a high-fat diet. The researchers discovered that this protein, VMAT2, helps to shield beta cells from oxidative stress, which can lead to diabetes.
Researchers found that CNOT3 protein silences genes that cause insulin-producing cells to malfunction, leading to diabetes. Knocking out CNOT3 in mice results in the development of diabetes due to the activation of normally silenced genes.
A new study from La Jolla Institute for Immunology found that blocking nerve signals to the pancreas could stop patients from ever developing type 1 diabetes. The researchers used a mouse model and discovered that blocking sympathetic nerve signals protected mice from beta cell death.
Researchers develop a new mouse model of permanent neonatal diabetes using the Kuma mutation, which exhibits severe insulin-deficiency and beta-cell dysfunction in an immune deficient background. The study successfully reverses hyperglycemia with insulin implants, making it suitable for islet transplantation research.
Joslin Diabetes Center researchers discover targeting renalase protein strengthens beta cells against stress and autoimmune attack. An FDA-approved drug, pargyline, is shown to protect human cells, potentially slowing disease progression in a clinical trial.
Scientists have developed a method to culture human pancreatic slices for nearly two weeks, allowing them to study the regeneration of insulin-producing beta cells. The discovery has important therapeutic implications for treating diabetes.
Researchers identified two classes of compounds that prevent most of the effects of interferon-α on human beta cells, paving the way for potential clinical trials. IFN-α promotes rapid changes in chromatin accessibility, which may contribute to triggering autoimmunity and type 1 diabetes.
Researchers developed a novel approach to decontaminate single-cell RNA seq data, allowing for accurate quantification of cell-specific drug effects in pancreatic islets. The method revealed species-specific and cell-type-specific responses to drugs, including the induction of insulin production in alpha cells.
A study by Korean researchers found that breastfeeding lowers maternal postpartum diabetes incidence and improves metabolic health through serotonin production. The research showed sustained improvements in pancreatic beta cells lasting years after lactation cessation, reducing the risk of developing diabetes.
Researchers developed an improved pluripotent stem cell differentiation protocol to generate beta cells in vitro, leading to more mature and functional beta cells. The use of CD177 as a quality control marker increases the efficiency and homogeneity of beta cell generation.
Researchers successfully reversed diabetes in mice by using genetically edited stem cells derived from patients with a rare genetic form of insulin-dependent diabetes. The CRISPR-Cas9 gene-editing tool corrected a genetic defect that caused the disease, allowing the human stem cells to normalize blood sugar levels.
Researchers found that even small increases in blood glucose levels can cause significant changes in the behavior of insulin-producing beta cells, making them more vulnerable to autoimmunity and inflammation. This discovery may improve understanding of type 1 and type 2 diabetes and shed light on potential treatments.
Researchers at UW-Madison discovered that removing a specific gene from insulin-producing cells can prevent Type 1 diabetes in mice by allowing the cells to disguise themselves from immune cells. This genetic manipulation enabled the cells to evade an autoimmune response, leading to normal glucose levels and insulin production.
Research suggests that beta cells produce signals that aid their own demise in Type 1 diabetes, leading to increased inflammation and damage. The study found that the absence of a specific enzyme enhances anti-inflammatory responses, while its overexpression promotes inflammatory ones.
Researchers have discovered a new drug combination that can restore beta cell function in an animal model, showing promise for diabetes remission. The treatment, which combines GLP-1/estrogen with insulin, was found to be more effective than single-treatments and increase pancreatic insulin content and beta cell numbers.
Researchers at Mount Sinai discovered a novel combination of two classes of drugs that cause the highest rate of human beta cell proliferation without harming most other cells in the body. This finding is an important step toward a diabetes treatment that restores insulin production. The study, published in Science Translational Medici...