Articles tagged with Beta 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.
A new hypothesis proposes that a deficiency in the enzyme Pancreatic Endoplasmic Reticulum Kinase (PERK) during fetal development can lead to permanent neonatal diabetes. The research found that PERK-deficient mice have impaired beta cell proliferation, differentiation, and clustering, resulting in reduced insulin production.
Researchers at Stanford University School of Medicine have made a significant breakthrough in understanding the connection between calcineurin and diabetes. By inhibiting calcineurin, they were able to prevent beta cells from increasing their numbers and producing insulin, offering new hope for treating type-2 diabetes. The findings al...
Researchers at the University at Buffalo are part of a global effort to prevent type 1 diabetes through a $172 million grant from the National Institutes of Health. The project aims to identify 100,000 individuals at risk and test interventions to halt the onset of the disease.
Researchers found that mice lacking pancreatic beta cell M3 receptors developed impaired glucose tolerance and reduced insulin release. In contrast, mice with increased M3 receptors showed improved glucose tolerance and insulin release, becoming resistant to developing symptoms of diabetes.
Researchers found that Gardenia extract contains the chemical genipin, which blocks UCP2 enzyme and improves insulin secretion. In both animals and humans, high concentrations of UCP2 appear to inhibit insulin secretion from the pancreas and increase the risk of type 2 diabetes.
Researchers used adeno-associated virus to insert genes for interleukin-4 (IL-4) or interleukin-10 (IL-10) into insulin-producing beta cells, preventing hyperglycemia in non-obese diabetic mice. Gene therapy shows promise as a viable method for preventing type 1 diabetes in genetically at-risk individuals.
A nationwide survey shows a significant gap in understanding of type 2 diabetes management, with patients feeling knowledgeable about their condition but not following treatment regimens as prescribed. The Diabetes Roundtable advocates for a team-centered approach involving patients, physicians, and educators to improve care outcomes.
Researchers have developed a non-invasive method to measure beta cell mass in individuals with diabetes using PET-based quantitation of VMAT2 receptors. This approach allows for the estimation of beta cell mass in rats with type 1 diabetes, providing insights into the pathogenesis of diabetes and potential therapeutic interventions.
A new study has demonstrated the use of PET imaging to track diabetes progression by measuring beta cell mass. The method uses a molecule expressed in both beta cells and the central nervous system, allowing for non-invasive imaging of beta cells in rats and potentially human subjects.
Researchers at Columbia University have developed a non-invasive method to measure beta cell mass in diabetic rats using positron emission tomography (PET)-based quantitation of pancreatic radiolabeled VMAT2 receptors. This method has the potential to study the pathogenesis of diabetes and monitor therapeutic interventions.
A new study discovered that BMP4 signaling is necessary and sufficient for the proliferation of pancreas progenitor cells, leading to an increase in Id expression. The researchers also found that inhibition of BMP4 results in a decrease in proliferating duct cells and an increase in the expression of a bHLH protein-dependent factor PAX6.
A recent study found that blocking ghrelin may improve insulin sensitivity and glucose control in mice, potentially providing a new approach for treating type 2 diabetes. However, the study also raised concerns about potential long-term risks of increasing ATP production by pancreatic cells.
Researchers found a gene in obese mice that increases the risk of type 2 diabetes, which could lead to new drug targets and better diagnosis methods for humans. The study provides insight into how insulin-producing cells function and may help clinicians identify individuals at high risk of developing the disease.
Researchers at Joslin Diabetes Center found that beta cells can develop and grow normally even when both insulin and IGF-I receptors are missing. This discovery suggests the presence of independent growth factors and pathways necessary for beta cell development, which may lead to new treatments for people with diabetes.
Researchers at La Jolla Institute for Immunology have made a major finding on a potential cure for type 1 diabetes by combining two therapies, producing better efficacy and longer-lasting results in preclinical trials. The combination therapy is being planned to begin human clinical trials later this year.
Researchers found a synergistic combination of a low-dose CD3 antibody and proinsulin peptide to reverse recent-onset type 1 diabetes in mice, promoting pancreatic beta cell regeneration. This approach may hold great potential for the treatment of individuals with recent-onset type 1 diabetes.
Researchers develop a combination therapy that reverses recent-onset type 1 diabetes in mice by inducing regulatory T cells to shield insulin-producing cells from autoimmune destruction. The therapy, which combines an oral and intranasal treatment, shows greater efficacy than individual treatments alone.
Researchers found that new islet cells are host-derived, not from donor spleen cells, and that beta-cell growth was permitted when autoimmunity was suppressed. The study suggests that CFA alone may be effective in treating type 1 diabetes without the need for donor spleen cells.
Researchers found that injections of spleen cells and transplants of islets from healthy mice temporarily cured diabetes in 4 out of 22 mice, but failed to restore insulin-producing beta cells. The procedure's success was confirmed by three independent labs, challenging the previous hypothesis on how it works.
Three research teams successfully replicated a controversial diabetes therapy, curing 32% of treated mice by manipulating the immune system. However, they were unable to regenerate beta cells from spleen-derived stem cells, leaving the source of these cells unknown.
A study published in the Journal of Clinical Investigation reveals that expression of CXCR2 on blood vessel wall cells mediates neutrophil influx into the lung during acute bacterial infection. Additionally, researchers found that FoxO1 plays a critical role in regulating beta cell numbers during insulin resistance and inhibiting acety...
A single gene encoding the enzyme GnT-4a is key to enabling pancreatic beta cells to sense blood glucose levels and produce insulin. In mice fed a high-fat diet, this enzyme's suppression led to type 2 diabetes.
A high-fat diet suppresses the activity of GnT-4a glycosyltransferase, leading to impaired insulin secretion and type 2 diabetes. The study suggests that people with an inherited predisposition to type 2 diabetes may have variations in the gene for GnT-4a.
A USC study reveals that high sugar intake during childhood may play a key role in the development of diabetes in Latino children. The research found that children who consumed more sugary drinks had signs of decreased beta cell function, implying they were heading toward type 2 diabetes.
A new method to create a reversibly immortalized beta-cell line offers significant progress in developing an effective treatment for type 1 diabetes. The breakthrough, achieved by manipulating human beta-cells, has successfully controlled blood sugar levels in diabetic mice for over 30 weeks.
Researchers found that increasing Sirt1 in pancreatic Beta cells improves insulin secretion and glucose metabolism in mice. This study suggests that therapies targeting Sirt1 could provide new treatments for type 2 diabetes.
Researchers at Joslin Diabetes Center have identified a new gene, ARNT, that plays a crucial role in the development of type 2 diabetes. The study, which used DNA chips to analyze islet cells from patients with the disease, found a marked down-regulation of ARNT, suggesting a possible new target for treatment.
Researchers found that taking pioglitazone for three years significantly reduced the risk of developing type 2 diabetes in women who had previously had gestational diabetes. This is promising news for preventing and treating type 2 diabetes, as it may help stabilize beta-cell function.
A new study found that adults performed better remembering pictures of imaginary animals than real cats. The researchers suggest that some types of memory may be enhanced when people approach a subject with a child-like sense of naïveté. The ability to categorize can lead to problems such as stereotypes and ignoring individual details.
Excess body fat accelerates diabetes onset by activating the GPR40 receptor, which causes insulin production to increase. The receptor's excessive activation can lead to beta cell exhaustion and the onset of full-blown diabetes.
Researchers at Joslin Diabetes Center have identified genetic regions involved in autoimmune diseases, including type 1 diabetes. The study found a chromosomal region where T-cells were given the green light to attack beta cells, leading to insulitis and later type 1 diabetes.
Researchers at Northwell Health's Institute for Medical Research have identified a crucial gene in type 1 diabetes development, which triggers the immune system to attack and kill beta cells. Blocking this protein may halt the harmful process and allow remaining beta cells to produce insulin.
Researchers discovered human islet-derived precursor cells that reproduce easily and can differentiate into hormone-producing cells. The findings may eventually have implications for islet transplantation, an experimental treatment for type 1 diabetes.
Researchers identified a mechanism for beta-cell growth during insulin resistance, which occurs as a normal protective response to delay type 2 diabetes onset. PDX-1 plays a crucial role in regulating this growth, and modulating key proteins involved may enhance beta cell replication or transplantation
Researchers have developed a fruitfly model that can mimic human diabetes, offering new insights into the regulation of blood sugar levels. The study provides potential benefits for pancreatic cell transplantation and may guide the development of stem cells to produce insulin.
A University of Toronto study discovered precursor cells within the adult pancreas that can make new pancreatic cells, potentially providing a plentiful supply of beta cells for transplant treatments. The research also found that these cells can generate both beta cells and neurons, challenging existing dogma on development.
New studies suggest that embryonic stem cells or mature beta cells are the primary source of new beta cells for diabetes treatment. The findings highlight a significant proliferative capacity of beta cells, offering a potential clinical direction for boosting insulin production in patients with residual beta cells.
Researchers identified four genetic variants strongly associated with type 2 diabetes in Finnish and Ashkenazi Jewish populations. The variants cluster in the regulatory region of the HNF4A gene, influencing insulin secretion in response to glucose.
Researchers develop gene therapy to enhance islet cell function and survival after transplantation. The technique uses a growth factor DNA to induce cell division, improving insulin production and glucose control in rat models. However, standard immunosuppression drug therapy may be harmful, inducing insulin resistance and diabetes.
Researchers developed a novel assay to examine T cell responses to autoantigens in islet cells, revealing distinct pathways of T cell differentiation and maturation in normal individuals versus patients with T1DM. These findings suggest proinflammatory polarization in diabetes but regulatory phenotypes in health.
Researchers at the University of Virginia Health System have discovered that Lisofylline can protect insulin-producing beta cells from autoimmune destruction, allowing transplanted islet cells to function for over 65 days without immunosuppression. This breakthrough could lead to a new treatment approach for type 1 diabetes patients.
Human bone marrow-derived single stem cell lines can proliferate and differentiate into islet-like cells capable of glucose-related insulin production. Researchers implanted these cells into mice with type 1 diabetes, observing an apparent reduction in glucose levels after two weeks.
Researchers found that blood vessel formation in the pancreas is crucial for normal insulin production in fetuses. Exendin-4, a pancreatic hormone analog, can rescue insulin-producing cells and prevent diabetes by regulating PDX protein.
Researchers found that pioglitazone reduced the risk of developing type 2 diabetes by 55 percent, with only one woman out of 76 participants developing diabetes after a year. The study suggests that pioglitazone can protect women from developing insulin resistance and related health issues.
Researchers discovered that PERK enzyme is a key regulator of protein synthesis in humans, leading to growth retardation, skeletal abnormalities and diabetes. Treatments targeting IGF-1 may offer therapeutic interventions for diseases like Wolcott-Rallison Syndrome.
Researchers at Baylor College of Medicine have made a breakthrough in developing a gene therapy that can cure diabetes in mice. The treatment uses the NeuroD gene to induce liver cells to produce insulin and other hormones associated with the pancreas' endocrine system.
Researchers successfully transplanted bone marrow cells from a male donor mouse to a female recipient, where they developed into functional insulin-expressing cells. The findings suggest that bone marrow may be a viable source for ex vivo expansion and autologous transplantation of pancreatic beta-cell precursors.
Researchers have identified bone marrow stem cells with the ability to produce functional insulin-producing cells, offering a new potential avenue for treating diabetes. The study used a molecular biology technique called CRE-loxP to isolate and study these cells, which were found to exhibit characteristics of pancreatic beta cells.
Sick Kids researchers discovered that nervous system autoimmunity attacks insulin-producing cells in the earliest stages of Type 1 diabetes. By modifying the attack on nervous tissue, they prevented subsequent diabetes in animal models, suggesting a critical role for early neuronal autoimmunity.
Scientists at British Columbia's Children's Hospital reveal a method for directly measuring the level of self-destructive white blood cells in mouse blood, distinguishing those that go on to develop diabetes from those that do not. The technique may also be used to detect other autoimmune disorders.
Researchers at MGH Laboratory of Molecular Endocrinology found that GLP-1 causes adult islet stem cells to differentiate into functional beta cells. This discovery may help devise strategies for using islet stem cells to treat diabetes.
Researchers are studying abnormal beta cell function to better understand canine and feline diabetes. They found that certain proteins play a crucial role in insulin secretion, which may contribute to the development of diabetes.
Researchers found that an antioxidant, AEOL 10113, can prevent type 1 diabetes by modifying the immune system's recognition of antigens. The treatment lasted for up to four weeks, suggesting a promising new line of research for autoimmune diseases.
A recent study has identified a protein called Akt1 that promotes the growth and increase in size of pancreatic β cells, which can help prevent or treat type 2 diabetes. The researchers found that mice bred to produce excess Akt1 protein were more tolerant of glucose and resistant to diabetes.
A USC study found that administering a drug to lower insulin resistance in women at high risk for type 2 diabetes successfully prevents or stalls its onset. The study tested whether reducing the demands on beta cells could prevent diabetes in Latinas with recent gestational diabetes.