Articles tagged with Beta Cells
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.
Researchers found that a cell aging program increases insulin secretion in human and mouse pancreatic beta cells, improving their function. This discovery suggests that cellular aging can bring unexpected benefits to the production of insulin, potentially leading to new insights and treatments for diabetes.
Researchers have discovered that tissue from the lower stomach has the greatest potential to be reprogrammed into beta-cell state. Engineered mini-organs produced insulin and refreshed themselves with stem cells, giving the tissue a sustainable regenerative boost.
Long-term use of liraglutide can lead to a gradual exhaustion of insulin-producing beta cells, reducing their secretion of insulin. This study using humanized mice suggests the need for caution when prescribing long-term GLP-1 analogues.
Researchers found liraglutide, a promising diabetes drug, can lead to pancreatic beta cell burnout in mice after six months of high-dose treatment. The study highlights the need for further investigation into the potential risks of this medication.
Children diagnosed with type 1 diabetes before age seven develop a more aggressive form of the disease compared to teenagers. Researchers found that those diagnosed in childhood retain fewer insulin-producing beta cells than previously thought.
Researchers have discovered a molecular link between psychiatric disorders and type 2 diabetes, with the DISC1 gene playing a critical role in pancreatic beta cell function. The study found that disrupting the DISC1 gene led to increased beta cell death, impaired glucose regulation, and reduced insulin secretion.
Scientists at the University of Montreal Hospital Research Centre have discovered an enzyme that can stop the toxic effects of sugar in various organs. The enzyme, glycerol 3-phosphate phosphatase (G3PP), plays a central role in controlling glucose and fat utilization and has been shown to detoxify excess sugar from cells.
Researchers at the Gladstone Institutes have successfully converted human skin cells into fully-functional insulin-producing pancreatic cells. These new cells protected mice from developing diabetes in a mouse model of the disease, offering a promising approach to personalized cell therapy for patients with diabetes.
Researchers at Joslin Diabetes Center have identified a key liver protein that accelerates the growth of insulin-producing beta cells, a critical step in treating all forms of diabetes. The protein, serpinB1, was found to be highly expressed in liver cells and boosted beta cell proliferation in human and mouse islets.
Researchers found that microtubules limit glucose-stimulated insulin secretion, but also allow for increased release when destabilized. Targeting microtubule regulation may offer new ways to treat type 2 diabetes.
A new form of immunotherapy aims to protect insulin-producing cells using patients' own immune cells. The therapy, called regulatory T cells, was well-tolerated and durable in a Phase 1 clinical trial, supporting the development of a Phase 2 efficacy trial.
Research at Boston Children's Hospital identifies IGFBP3 as the hormone destroying intestinal stem cells in type 1 diabetes, leading to a potential treatment strategy with TMEM219. The study also suggests a new approach to cell therapy by exploiting hormones controlling stem cell production.
Researchers create insulin-producing cells using adult tissue and transcription factors, offering a potential cure for type 1 diabetes. The cells can be transplanted into diabetic mice and may lead to clinical trials for human patients.
Researchers at Duke University Medical Center and the University of Alberta have discovered a new biochemical pathway that controls insulin secretion from islet beta cells in the pancreas. The study found that impairing this pathway, known as S-AMP production, disrupts normal glucose-stimulated insulin secretion.
A study published in PLOS ONE suggests that neurogenin 3-expressing cells in the exocrine pancreas have the capacity to become insulin-producing beta cells. This discovery may lead to novel drug therapies to replenish cells destroyed or damaged by diabetes.
Researchers at UMMS have discovered a new pathway that triggers regeneration of beta cells in the pancreas. This innovative approach may aid in the development of diabetes treatments by increasing the number of insulin-producing cells in response to increased demand.
Researchers at Karolinska Institutet have discovered a mechanism that explains how insulin-producing cells can be both insulin-resistant and insulin-sensitive at the same time. The study identifies a key factor, PI3K-C2α, that causes a switch in signaling pathways, leading to beta cell proliferation.
Researchers developed a drug that blocks hyaluronan buildup in pancreatic islets, preventing immune cell infiltration and destruction of insulin-producing cells. The study suggests a potential preventive treatment for type 1 diabetes in humans if initiated before the onset of the disease.
Researchers from Penn and Baylor have precisely quantified the loss of insulin-producing beta cells in dogs with diabetes, revealing a key similarity with human type I diabetes. The study also identifies features unique to canine diabetes, highlighting potential insights into treating human patients.
Researchers at Johns Hopkins Medicine have developed a high-throughput screening technique using zebrafish embryos to identify 24 potential new diabetes drugs. The novel method may also be applied to other diseases, including heart disease and neurodegenerative conditions.
Researchers have discovered that cathelicidins, antimicrobial peptides produced by gut bacteria, play a crucial role in preventing the development of type 1 diabetes. By re-establishing a normal level of cathelicidin in diabetic mice, scientists were able to suppress autoimmune disease.
Research demonstrates impaired activation of mitochondrial energy metabolism in patients with type 2 diabetes, leading to decreased insulin secretion. A novel fluorescence microscopic assay reveals a subtle disharmony between bioenergetic supply and demand pathways, suggesting a shift towards systems-level approaches to fight the disease.
The T1DAL study found that alefacept treatment preserved beta cell function in 30% of participants with new-onset type 1 diabetes. Alefacept also reduced insulin dose requirements and major hypoglycemic events compared to the placebo group.
Researchers have discovered a potential target for the treatment of type 2 diabetes by inhibiting the S6K1 protein, which increases insulin sensitivity in mice. In animal models, S6K1 deficient mice displayed improved insulin response and reduced risk of developing diabetes.
A drug already FDA-approved for osteoporosis has been found to stimulate the production of cells controlling insulin balance in diabetic mice. This could lead to a potential new treatment for type 2 diabetes.
The study identified urocortin 3 as a key player in regulating insulin production and blood sugar levels. By understanding how this hormone interacts with other cells and systems, researchers hope to develop new treatments for diabetes.
Researchers have developed a novel approach using liposomes to prevent the onset of Type 1 Diabetes in mice, offering a promising candidate for human vaccination. The technique avoids damaging insulin-producing pancreatic cells and induces immunological tolerance, providing a potential solution for this incurable disease.
Researchers have identified a gene that may help reactivate insulin-producing beta cells in diabetics. The team, led by Professor Tessem and including four students with Type 1 diabetes, has made significant breakthroughs in understanding the molecular pathways involved.
In a study published in ETH Zurich, researchers discovered that the microRNA-200 family triggers the death of beta cells, leading to type 2 diabetes. By blocking miR-200 production, scientists can guarantee the survival of these vital cells. This finding has significant implications for the development of new treatments for diabetes.
Researchers at UC Davis may have discovered a new way to regenerate beta cells in the pancreas, which could potentially lead to a cure for juvenile diabetes. The study's findings suggest that immature beta cells can arise from alpha cells, offering a new paradigm shift in the treatment of the disease.
Researchers at Columbia University Irving Medical Center have found a defect in pancreatic cells that can lead to high blood sugar levels and impaired glucose balance. An experimental drug called Rycal has been shown to stop the leaky channels and normalize glucose levels in mouse models.
Exposure to BPA during pregnancy may raise a mother's susceptibility to weight gain and diabetes later in life. The study found that BPA can harm glucose metabolism in offspring exposed in utero, leading to an increased predisposition to developing metabolic syndrome or diabetes.
Researchers found that young mice don't possess cellular machinery for regeneration after weaning, leading to reduced insulin secretion and replication of beta cells. A new developmental step in beta cell maturation is triggered by dietary change from high-fat milk to chow.
A study published in Nature Medicine found that a novel drug candidate, harmine, can drive human insulin-producing beta cells to multiply and triple the number of beta cells in mice. This breakthrough could potentially lead to more effective treatment for diabetes.
The Endocrine Society has selected 22 winners of the Helmsley Charitable Trust Abstract Awards in Type 1 Diabetes, recognizing outstanding work in clinical care and underlying mechanisms. The award winners will present their research at ENDO 2015 and received travel grants to attend.
Researchers at Stanford University School of Medicine identified limostatin, a hormone that decreases insulin levels during recovery from fasting or starvation, in fruit flies and found a similar protein in humans. This discovery has critical ramifications for understanding metabolism and may inform new efforts to combat diabetes.
Researchers at Saint Louis University have found a way to prevent type I diabetes in an animal model by blocking the autoimmune process that destroys beta cells. The study uses a selective ROR alpha and gamma t inverse agonist to reduce autoimmunity, suggesting a new treatment option for the illness.
Researchers aim to convert human liver cells into pancreatic beta cells using a novel factor identified in mouse studies. This strategy could provide a patient-specific, autologous cell-based therapy for type 1 and potentially type 2 diabetes.
A new study published in the journal Diabetes shows that a chemical produced in the pancreas, gamma-aminobutryic acid (GABA), can prevent and reverse Type 1 diabetes in mice with human beta cells transplanted into their bodies. GABA also improved the survival rate of pancreatic cells during transplantation.
Researchers at Harvard University have successfully reprogrammed adult cells into insulin-producing beta cells in mice, showing promise for treating both Type 1 and Type 2 diabetes. The study's long-term findings suggest that the newly created cells remain functional over a period of approximately half the animal's normal lifespan.
A recent study published in PNAS shows that young capillary vessels can rejuvenate aged pancreatic islets, suggesting a new way to treat age-dependent dysregulation of blood glucose levels. By replacing the islet vasculature with young capillaries, glucose homeostasis was fully restored.
Scientists found that cilia play a crucial role in the release and signal transduction of insulin, a hormone that reduces sugar levels. Ciliary dysfunction leads to impaired insulin secretion and increased blood sugar levels, linking it to type 2 diabetes.
A new study published in Nature Communications reveals that cilia on pancreatic beta cells are covered with insulin receptors, and altered ciliary function is associated with type 2 diabetes. The research found that ciliary defects impaired insulin release, leading to elevated blood glucose levels in mice.
Research suggests that physical exercise preserves beta cell function, reducing complications and improving blood sugar control. However, large-scale trials are necessary to confirm the benefits of exercise in slowing the onset of type 1 diabetes in children and adults.
Researchers at Harvard University have made a breakthrough in producing human insulin-producing beta cells equivalent to normally functioning cells, offering hope for new diabetes treatment. The development involves massive quantities of human embryonic stem cells and could lead to drug discovery and transplantation therapy.
Researchers at UC San Diego aim to bioengineer the irregularly shaped patches of the pancreas called Islets of Langerhans in a dish. This could lead to studying the events that trigger beta cell destruction and developing new drug therapies, as well as understanding the genetic component of the disease.
Researchers at Karolinska Institutet found that age-dependent reduction of mitochondrial function in beta cells leads to reduced insulin release. Impaired calcium ion dynamics is the molecular mechanism underlying this process.
New research finds children exposed to gestational diabetes are at increased risk of developing impaired glucose tolerance and type 2 diabetes. The study suggests a growing number of women with gestational diabetes will lead to an alarming rise in early childhood diabetes, emphasizing the need for preventive measures.
Researchers discover that 12-lipoxygenase (12-LO) enzyme promotes pre-diabetes and diabetes by causing oxidative stress in pancreatic cells. The study shows that a high-fat diet leads to the production of harmful molecules, ultimately damaging the cell's ability to produce insulin.
Researchers at Sanford Burnham Prebys Institute have discovered a promising technique to restore insulin production in people with Type 1 diabetes. A peptide called caerulein was found to convert existing alpha cells into insulin-producing beta cells, potentially freeing patients from daily insulin doses.
A team of researchers from UCLA discovered that autophagy, a process that clears damaged proteins, is impaired in people with Type 2 diabetes, leading to the destruction of insulin-producing beta cells. This impairment contributes to the accumulation of toxic IAPP protein.
Researchers at Columbia University Irving Medical Center have successfully retrained human gastrointestinal cells to produce insulin in response to glucose. This breakthrough could potentially replace damaged cells lost in type 1 diabetes, offering a new avenue for treating the condition.
A genetic risk component of type 1 diabetes has been shed light on by a study identifying the role of gene Clec16a in faulty cell recycling. Healthy mitochondria are crucial to insulin production and blood sugar control, making this finding a significant step towards treating or preventing both type 1 and type 2 diabetes.
A susceptibility gene for type 1 diabetes has been found to regulate self-destruction of the cell's energy factory. Researchers discovered that this pathway could be targeted for prevention and control of type-1 diabetes and may extend to treatment of other metabolic-associated diseases.
Researchers developed a non-invasive imaging technique to track beta cell status in type 1 diabetes patients. The PET scan detects the amount of radiotracer in the pancreas, indicating the overall amount or volume of active beta cells present.
Researchers have discovered a potential therapeutic target for preserving beta cell health in people with type 1 diabetes, according to a new JDRF-funded study. The MANF protein has been shown to reduce beta cell stress and promote regeneration.
Researchers found that blocking the effects of CMPF may help prevent and treat diabetes. A fat metabolite called CMPF was dramatically increased in both gestational and type 2 diabetic individuals, impairing insulin secretion from beta cells.