In islets from individuals with type 2 diabetes and in islets exposed to chronic elevated glucose, mitochondrial energy metabolism is impaired. Here, we studied early metabolic changes and mitochondrial adaptations in human beta cells during chronic glucose stress.Respiration and cytosolic ATP changes were measured in human islet cell clusters after culture for 4 days in 11.1 mmol/l glucose. Metabolomics was applied to analyse intracellular metabolite changes as a result of glucose stress conditions. Alterations in beta cell function were followed using insulin secretion assays or cytosolic calcium signalling after expression of the calcium probe YC3.6 specifically in beta cells of islet clusters.At early stages of glucose stress, mitochondrial energy metabolism was augmented in contrast to the previously described mitochondrial dysfunction in beta cells from islets of diabetic donors. Following chronic glucose stress, mitochondrial respiration increased (by 52.4%, p ...
Type 2 diabetes can be viewed as a failure of the pancreatic beta-cell to compensate for peripheral insulin resistance with enhanced insulin secretion. This failure is explained by both a relative loss of beta-cell mass as well as secretory defects that include enhanced basal secretion and a selective loss of sensitivity to glucose. These features are reproduced by chronic exposure of beta-cells to fatty acids (FAs), suggesting that hyperlipidemia might contribute to decompensation. Using MIN6 cells pretreated for 48 h with oleate or palmitate, we have previously defined alterations in global gene expression by transcript profiling and described additional secretory changes to those already established (Busch A-K, Cordery D, Denyer G, Biden TJ: Diabetes 51:977-987, 2002). In contrast to a modest decoupling of glucose-stimulated insulin secretion, FA pretreatment markedly enhanced the secretory response to an acute subsequent challenge with FAs. We propose that this apparent switch in sensitivity from
Developmental insults during gestation, such as under-nutrition, are known to restrict the number of beta cells that form in the fetal pancreas and are maintained in adulthood, leading to increased risk of type 2 diabetes. There are now substantial data indicating that glucocorticoids mediate this effect of under-nutrition on beta cell mass and that even at physiological levels they restrain fetal beta cell development in utero. There are emerging clues that this occurs downstream of endocrine commitment by neurogenin 3 but prior to terminal beta cell differentiation. Deciphering the precise mechanism will be important as it might unveil new pathways by which to manipulate beta cell mass that could be exploited as novel therapies for patients with diabetes.. ...
Analysis of Beta-Cell Gene Expression Reveals Inflammatory Signaling and Evidence of Dedifferentiation following Human Islet Isolation and Culture. . Biblioteca virtual para leer y descargar libros, documentos, trabajos y tesis universitarias en PDF. Material universiario, documentación y tareas realizadas por universitarios en nuestra biblioteca. Para descargar gratis y para leer online.
Researchers at the Icahn School of Medicine at Mount Sinai have discovered a novel combination of two classes of drugs that, together, cause the highest rate of proliferation ever observed in adult human beta cells-the cells in the pancreas that produce insulin-without harming most other cells in the body. The result is an important step toward a diabetes treatment that restores the bodys ability to produce insulin.. The finding involved one type of drug that is known to cause beta cells to proliferate and another that is already in widespread use in people with diabetes. Together, they caused the cells to proliferate at a rate of 5 to 6 percent per day. The study was published today in Science Translational Medicine online.. "We are very excited about this new drug combination because for the first time ever, we are able to see rates of human beta-cell replication that are sufficient to replenish beta-cell mass in humans with diabetes," said Andrew Stewart, MD, Director of the Mount Sinai ...
Shop Pancreatic beta cell growth factor ELISA Kit, Recombinant Protein and Pancreatic beta cell growth factor Antibody at MyBioSource. Custom ELISA Kit, Recombinant Protein and Antibody are available.
The prevalence of Diabetes Mellitus has reached epidemic proportions world-wide, and is predicted to increase rapidly in the years to come, putting a tremendous strain on health care budgets in both developed and developing countries. There are two major forms of diabetes and both are associated with decreased beta-cell mass. No treatments have been devised that increase beta-cell mass in vivo in humans, and transplantation of beta-cells is extremely limited due to lack of appropriate donors. For these reasons, increasing functional beta-cell mass in vitro, or in vivo prior to or after transplantation, has become a "Holy Grail" of diabetes research. Our previous studies clearly show that adult human beta-cells can be induced to replicate, and - importantly - that cells can maintain normal glucose responsiveness after cell division. However, the replication rate achieved was still low, likely due in part to the known age-related decline in the ability of the beta-cell to replicate. We propose to ...
phdthesis{ef479246-001e-4db0-bb31-b145ccaa5214, abstract = {Beta cell function is an important factor in the development of both Type 1 (T1D) and Type 2 (T2D) diabetes mellitus. T1D is characterized by a primary defect in insulin secretion due to the immune-mediated beta cell destruction, however, the more common T2D beside insulin resistance also include impaired beta cell function as a consequence to abnormal glucose homeostasis. Genetic susceptibility is involved in both types of diabetes. We have studied several genetic and immunological factors affecting beta cell function. ,br/,,br, ,br/,,br, First, we tested whether single nucleotide polymorphisms (SNPs) of the human Free Fatty Acid Receptor 1 (FFAR1) are associated with T2D and insulin secretion. Another genetic study focused on FOXP3 association with T1D and the disease-related clinical parameters. The role of microRNAs (miRNAs) on beta cell function was studied in the third project using a novel genetically engineered mouse model. ...
Foodborne Cereulide Causes Beta-Cell Dysfunction and Apoptosis. . Biblioteca virtual para leer y descargar libros, documentos, trabajos y tesis universitarias en PDF. Material universiario, documentación y tareas realizadas por universitarios en nuestra biblioteca. Para descargar gratis y para leer online.
all beta cells and people with the disease would have to take insulin for life But we know that some beta cells do survive and secrete insulin even when the patients have had type 1 diabetes for 50 years says senior author Rohit N Kulkarni M D Ph D Associate Professor of Medicine at Harvard Medical School and the principle investigator of the project at Joslin In this study Joslin researchers were interested in learning exactly how immune cells could promote beta cell growth and identifying the type of cell and the mechanisms underlying this effect In a series of experiments the researchers injected NOD mice with immune cells from the pancreatic islets of donor NOD mice and assessed their effects on beta cells The immune cells tested included subtypes of B or T immune cells Dirice the lead author of the study found that it is T cells not B cells that are associated with beta cell proliferation Mice that received B cells showed no difference in beta cell growth Mice that received the T cell ...
PubMed comprises more than 30 million citations for biomedical literature from MEDLINE, life science journals, and online books. Citations may include links to full-text content from PubMed Central and publisher web sites.
Increased glycemic variability has been proposed as an independent predictor of hypoglycemia in diabetic patients. Likewise, episodes of dysglycemia have been found to be predictive of diabetes in antibodypositive nondiabetic individuals. We hypothesise that an in-depth observational study comparing state-of-the-art measures of functional beta cell mass and glycemic variability will specify the relationship between both variables over a broad range of residual function and will identify treatment goals for functional beta cell mass to be reached in future beta cell therapy trials in order to avoid frequent hypoglycemia in patients and dysglycemia in risk groups. The available expertise and infrastructure (see background and (inter)national context) place the promoters of the present project in a unique position to carry out the planned experiments and support their feasibility ...
Juan-Mateu, Jonàs et al "SRp55 Regulates a Splicing Network that Controls Human Pancreatic Beta Cell Function and Survival." Diabetes (2017): db170736. Web. 22 Jan. 2018. ...
A significant reduction of beta cell mass has been described during the post partum period in the endocrine rat pancreas. We examined the mechanisms of this involution in Sprague Dawley rats by analyzing beta cell mass, beta cell replication, and beta cell size at end of pregnancy and 4 and 10 days …
While the mechanisms by which glucose regulates insulin secretion from pancreatic beta cells are now well described, the way glucose modulates gene expression in such cells needs more understanding. Here, we demonstrate that MondoA, but not its paralogue ChREBP, is the predominant glucose-responsive transcription factor in human pancreatic beta EndoC-βH1 cells and in human islets. In high glucose conditions, MondoA shuttles to the nucleus where it is required for the induction of the glucose-responsive genes ARRDC4 and TXNIP, the latter being a protein strongly linked to beta-cell dysfunction and diabetes. Importantly, increasing cAMP signaling in human beta cells, using forskolin or the GLP-1 mimetic Exendin-4, inhibits the shuttling of MondoA and potently inhibits TXNIP and ARRDC4 expression. Furthermore, we demonstrate that silencing MondoA expression improves glucose uptake in EndoC-βH1 cells. These results highlight MondoA as a novel target in beta cells that coordinates transcriptional ...
Our What?. One of the family of signals that the Huising lab studies, is named for the stress peptide Corticotropin Releasing Factor, or CRF in short. CRF was originally discovered as the principal hypothalamic factor to initiate the stress response by acting on the pituitary gland. It turns out that the insulin-producing beta cells of the pancreas can respond directly to CRF with increased insulin secretion, increased beta cell proliferation and reduced beta cell death in the face of pro-inflammatory insults, which is a promising set of beneficial characteristics united in a single molecule. Urocortin3 (Ucn3), a peptide related to CRF, is abundantly expressed by mature beta cells. We discovered that Ucn3 is co-released with insulin to trigger somatostatin release from neighboring delta cells, which in turn inhibits insulin secretion. In essence, Ucn3 triggers a negative feedback loop that attenuates insulin secretion, provided that glucose levels are successfully reduced. Ucn3 expression also ...
BACKGROUND: The expression of interleukin-1-receptor antagonist is reduced in pancreatic islets of patients with type 2 diabetes mellitus, and high glucose concentrations induce the production of interleukin-1beta in human pancreatic beta cells, leading to impaired insulin secretion, decreased cell proliferation, and apoptosis. METHODS: In this double-blind, parallel-group trial involving 70 patients with type 2 diabetes, we randomly assigned 34 patients to receive 100 mg of anakinra (a recombinant human interleukin-1-receptor antagonist) subcutaneously once daily for 13 weeks and 36 patients to receive placebo. At baseline and at 13 weeks, all patients underwent an oral glucose-tolerance test, followed by an intravenous bolus of 0.3 g of glucose per kilogram of body weight, 0.5 mg of glucagon, and 5 g of arginine. In addition, 35 patients underwent a hyperinsulinemic-euglycemic clamp study. The primary end point was a change in the level of glycated hemoglobin, and secondary end points were ...
D-glucose regulates maintenance and function of pancreatic beta-cells. Several studies have shown that IRS-2, but not IRS-1, is necessary to maintain and sufficient to expand functional beta-cell mass. We therefore analyzed the expression of IRS-2 and IRS-1 in beta-cells after culture in the presence of various concentrations of D-glucose and other metabolisable or non-metabolisable hexoses. D-glucose increased Irs-2 transcription and IRS-2 accumulation in a dose-dependent manner (1.6 to 25 mmol/l), with a 3-fold increased plateau after 10 h. In contrast, the expression of IRS-1 remained unaffected. D-glucose also induced phosphorylation of IRS-2 while non-metabolisable hexoses did neither affect expression nor phosphorylation. D-glucose-mediated elevation and phosphorylation of IRS-2 were independent of autocrine insulin action although insulin itself could transiently and slightly enhance IRS-2 expression. ...
Prof. Melton stated his optimism about the future of diabetes treatment: "Semmas scientists have very effectively dedicated themselves to systems that reliably generate cells indistinguishable from human pancreatic beta cells and to the invention of novel devices that are immunologically protective and surgically practical. Were very encouraged and excited about the potential this program has for diabetic patients and their families.". ...
Several groups have overexpressed Pdx1 protein in the liver of STZ-induced diabetic mice but have not succeeded in producing selective pancreatic endocrine differentiation (4,6,7,21). Instead, severe hepatitis, presumably caused by the production of exocrine enzymes such as amylase, elastase, and chymotrypsin (7), and dysmorphogenesis, such as abnormal lobe structures and multiple cystic lesions (21), were recently reported. The conclusion drawn from these in vivo animal studies is that ectopic expression of Pdx1 alone in the liver initiates both endocrine and exocrine pancreas differentiation and is insufficient to induce selective endocrine pancreas differentiation. Recent work by Zalzman et al. (22) has shown that introduction of Pdx1 into human fetal liver progenitor cells by lentivirus resulted in the expression of Ngn3, Beta2, and Nkx6.1 genes, but not Nkx2.2, Isl-1, Pax4, and Pax6 genes and was able to rescue diabetic mice, although a complete analysis was not performed. This observation ...
With an RD Lawrence Fellowship from Diabetes UK, Dr Cantley will use state-of-the-art techniques in molecular and cell biology to study the mechanisms by which ACC1 works in human and mouse beta cells in the laboratory. Specifically, he will look at the influence of ACC1 on beta cell size and number in response to metabolic challenges such as obesity and pregnancy. Dr Cantley will focus on ACC1 activity in mice, isolated mouse islets, mouse and human beta cells in the lab, and human islets. He will then monitor its impact on different aspects of beta cell function (such as insulin release, cell structure within the pancreas and the expression of genes and proteins).. ...
With a single stimulatory molecule, human insulin-producing beta cell replication can be sustained for at least four weeks in a mouse model of diabetes...
Oxidative Medicine and Cellular Longevity is a unique peer-reviewed, Open Access journal that publishes original research and review articles dealing with the cellular and molecular mechanisms of oxidative stress in the nervous system and related organ systems in relation to aging, immune function, vascular biology, metabolism, cellular survival and cellular longevity. Oxidative stress impacts almost all acute and chronic progressive disorders and on a cellular basis is intimately linked to aging, cardiovascular disease, cancer, immune function, metabolism and neurodegeneration. The journal fills a significant void in todays scientific literature and serves as an international forum for the scientific community worldwide to translate pioneering
A hot topic in the type 2 diabetes world is whether we have in hand the tools to stop the decline in beta cell function that typifies this disease and, consequently, a therapy or therapies that successfully control blood glucose for many years - so-called treatment durability. Actually this is three topics. What are the specific mechanisms for the beta cell failure? Do any of our existing therapies, or those on the drawing board, reverse these mechanisms to slow or stop the beta cell failure? ...
Insufficient pancreatic beta-cell mass is fundamental to the pathogenesis of both types 1 and 2 diabetes and constitutes the basis for the goal of beta-cell replacement therapy. Current methods for isolating islets from organ donor pancreases do not come close to supplying all in need, thus providing a compelling need to find new sources of insulin-producing cells. Possible sources include generation of cells from embryonic stem cells (ESC), adult stem/precursor cells, transdifferentiation of other cell types and xenodonors. Bioengineering can be used to improve secretory performance and strengthen cells to better withstand the challenges of transplantation. Strategies include protection against hypoxia, inflammation, and immune attack.
Compromised function of insulin-secreting pancreatic β cells is central to the development and progression of Type 2 Diabetes (T2D). However, the mechanisms underlying β cell failure remain incompletely understood. Here, we report that metabolic stress markedly enhances macroautophagy-independent lysosomal degradation of nascent insulin granules. In different model systems of diabetes including of human origin, stress-induced nascent granule degradation (SINGD) contributes to loss of insulin along with mammalian/mechanistic Target of Rapamycin (mTOR)-dependent suppression of macroautophagy. Expression of Protein Kinase D (PKD), a negative regulator of SINGD, is reduced in diabetic β cells. Pharmacological activation of PKD counters SINGD and delays the onset of T2D. Conversely, inhibition of PKD exacerbates SINGD, mitigates insulin secretion and accelerates diabetes. Finally, reduced levels of lysosomal tetraspanin CD63 prevent SINGD, leading to increased insulin secretion. Overall, our findings
In vitro expansion of beta-cells from adult human islets could solve the tissue shortage for cell replacement therapy of diabetes. Culture of human islet cells typically results in |16 cell doublings and loss of insulin expression. Using cell lineage
Viral infections and local production of IFNgamma might contribute to beta-cell dysfunction/death in Type 1 diabetes. Double stranded RNA accumulates in the cytosol of viral-infected cells, and exposure of purified rat beta cells to dsRNA (polyinosinic-polycytidylic acid, PIC) in combination with IFNgamma results in beta-cell dysfunction and apoptosis. To elucidate the molecular mechanisms involved in PIC + IFNgamma-effects, we determined the global profile of genes modified by these agents in primary rat beta cells. FACS-purified rat beta cells were cultured for 6 or 24 h in control condition or with IFNgamma, PIC or a combination of both agents. The gene expression profile was analyzed in duplicate with the Affymetrix RG U34A microarray.
PubMed comprises more than 30 million citations for biomedical literature from MEDLINE, life science journals, and online books. Citations may include links to full-text content from PubMed Central and publisher web sites.
As reported by JDRF, funded scientists at the University of Pittsburgh in America have uncovered a new way to grow human beta cells in the lab.. The team led by Professor Andrew Stewart, were able to get human beta cells to divide and make more cells. Not only that, but they then managed to stop the cells dividing again. The research was published in this months issue of the journal Diabetes.. The researchers added genes called cdk and cyclin d into the beta cells. These genes make the cells divide and are usually switched off in beta cells. To deliver these genes into the cells they used a virus that can get into cells easily. Once they had enough beta cells, they added a drug to the cells which switched off the virus and stopped the cells dividing.. In the body, beta cells divide very slowly or not at all so when the immune system attacks them, the cells are not replaced. Usually in type 1 diabetes there are a few beta cells remaining and if scientists could make these cells divide they could ...
Type 2 diabetes mellitus (T2DM) is a complex metabolic disease characterized by the loss of beta-cell secretory function and mass. The pathophysiology of beta-cell failure in T2DM involves a complex...
Human beta cell proliferation was once unthinkable, but now it is absolutely possible, says the senior author of a new study in cell cultures and in mice. The field is moving rapidly.
Its important to remember that individual cells do not last as long as people live. Cells naturally die and new cells grow within your body all the time. Research (mostly in animals) has suggested that Vildagliptin might have two separate effects on beta cells. On the one hand, it seems to cause beta cells to naturally divide and grow, and on the other hand, it seems to delay beta cells "natural death", so they live longer. Both of these effects may be important to curing type-1 diabetes, but it is not clear. This is why research is important. For example, even if Vildagliptin triggers a divide-and-grow reaction, it will only be effective if there are some beta cells to start with, and we just dont know if there are enough to get things started. On the cell death side, if the autoimmune attack directly kills beta cells, then stopping natural cell death may have little impact. Those cells will be killed by autoimmunity before they can die of "old age". However, if the autoimmune attack works ...
Their non-profit company, Tenth Muse Films, hopes to raise the curtain in 2017 on The Human Trial, a film that will showcase the need for sustained philanthropic investment to bring about breakthrough technologies, in this case the implantation of pancreatic cells. Their first project is focused on ViaCyte, a San Diego biotech which is trying to use a novel approach to implant pancreatic progenitor cells into people with diabetes that will mature into functional beta cells. (The filmmakers have no affiliation nor financial connection with any of the companies or entities appearing in the film.). ViaCyte is testing a product identified as a VC-01 combination device. Its a mesh pouch encapsulated in a pliable membrane which allows hormones, metabolic fluids, and oxygen to migrate, but resists immune system T-cell invasion. T-cells in people with Type 1 often target implanted beta cells, making beta cell transplant a very frustrating treatment option.. The VC-01, dubbed the "teabag", is designed ...
Researchers in the lab of Gordon Weir, M.D., looked at a cellular stress mechanism called the unfolded protein response or endoplasmic reticulum (ER) stress response in beta cells. This response is triggered when the ER, part of the cells protein assembly line, struggles to fold newly formed proteins into their exactly right shapes.. Earlier studies suggested this process contributes to the high mortality and low insulin production often displayed in beta cell transplants, which aim to replace cells that the bodys own immune system kills off in type 1 diabetes.. In work reported in the journal PLoS One in June, the scientists compared healthy human beta cells from surgical donors with beta cells that had been transplanted into mice with suppressed immune systems. They found that the transplanted cells strongly activate genes that help to guard against damage from ER stress, and suppress other genes that may trigger cellular attempts to self-destruct.. "Not only is this response likely to be ...
J:194010 Iglesias J, Barg S, Vallois D, Lahiri S, Roger C, Yessoufou A, Pradevand S, McDonald A, Bonal C, Reimann F, Gribble F, Debril MB, Metzger D, Chambon P, Herrera P, Rutter GA, Prentki M, Thorens B, Wahli W, PPARbeta/delta affects pancreatic beta cell mass and insulin secretion in mice. J Clin Invest. 2012 Nov 1;122(11):4105-17 ...
Search PubMed for more publications by Feyza Engin. 1. Engin, F. "ER Stress and Development of Type 1 Diabetes" J Investig Med. 2015.. 2. Brozzi, F., Nardelli, TR., Lopes, M., Millard, I., Barthson, J., Igoillo-Esteve, M., Grieco, FA., Villate, O., Oliveira, JM., Casimir, M., Bugliani, M., Engin, F., Hotamisligil, GS., Marchetti, PM., Eizirik, DL. "Cytokines induce endoplasmic reticulum stress in human, rat and mouse beta cells via different mechanisms". Diabetologia. 2015.. 3. Engin, F., Ngyuen T., Yermalovich A., Hotamisligil, GS. "Aberrant unfolded protein response in type 2 diabetes". Sci Rep. 2014.. 4. Engin, F., Yermalovich, A., Fu, W., Ngyuen, T., Hummasti, S., Decio, L., Eizirik., Mathis, D., Hotamisligil, GS. "Restoration of the unfolded protein response in pancreatic beta cells protects mice against type 1 diabetes". Sci. Transl. Med. 2013.. 5. Engin, F., Hotamisligil, GS. "Chemical modulation of ER function in metabolic diseases". Diabetes Obes. Metab. 2010. 12 Suppl 2:108-15.. 6. ...
Over the past several years, JDRF-funded researchers have found evidence that beta cell stress may play a role in the onset of T1D, and are exploring possible ways to stop it from occurring, thus potentially protecting beta cell health and maintaining normal beta cell function. In April, JDRF-funded researchers in Finland released new findings in the journal CellPress that add another piece to the puzzle of beta cell stress and T1D.
But what if other cells in the body could be coaxed into ever pancreatic beta cells? Could we possibly cure diabetes?Researchers at UCLA Larry L www.erectalis
MODY is believed to be caused by at least 13 different genes. Five rare mutations at the BLK locus, including only one non-synonymous p.A71T variant, were reported to segregate with diabetes in three MODY families. The p.A71T mutation was shown to abolish the enhancing effect of BLK on insulin content and secretion from pancreatic beta cell lines. Here, we reassessed the contribution of BLK to MODY and tested the effect of BLK-p.A71T on type 2 diabetes risk and variations in related traits ...
DI-fusion, le Dépôt institutionnel numérique de lULB, est loutil de référencementde la production scientifique de lULB.Linterface de recherche DI-fusion permet de consulter les publications des chercheurs de lULB et les thèses qui y ont été défendues.
Type 2 diabetes (T2D) is a major health problem worldwide. Identifying modifiable risk factors is key in decreasing the incidence and associated economic burden...
Rulifson IC, Karnik SK, Heiser PW, et al. "Wnt signaling regulates pancreatic beta cell proliferation." Proc Natl Acad Sci U S A. 2007;104:6247-6252. Abstract ...
Rulifson IC, Karnik SK, Heiser PW, et al. "Wnt signaling regulates pancreatic beta cell proliferation." Proc Natl Acad Sci U S A. 2007;104:6247-6252. Abstract ...
The Lens serves almost all the patents and scholarly work in the world as a free, open and secure digital public good, with user privacy a paramount focus.
Interleukin-1beta (IL-1beta) is a potent inflammatory cytokine involved in type 1 diabetes and acts through defined IL-1beta signaling pathways. In the present work we describe induction of DNA binding activity to signal transducer and activator of transcription (STAT) in response to IL-1beta in clo …
Diabetes is a chronic health condition wherein either the pancreatic beta cells are not able to produce or manage insulin. Insulin is nothing but a special...
the pancreas is like an air-conditioner, insulin is like cold air, beta cells are like light bulbs, glucose is like fire, and carbohydrates are the fuel... what else do you need to understand how and why you get diabetes?
Pretreatment of pancreatic beta cells with pertussis toxin resulted in a 30% increase in peak whole-cell Ca2+ currents recorded in the absence of exogenous intracellular guanine nucleotides. Intracellular application of 90 microM GTP[gamma S], by liberation from a caged precursor, resulted in 40% reduction of the peak Ca2+ current irrespective of whether the current was carried by Ca2+ or Ba2+. Effects on the delayed outward K+ current were small and restricted to a transient Ca(2+)-dependent K+ current component. Inhibition by GTP[gamma S] of the Ca2+ current was not mimicked by standard GTP and could not be prevented either by pretreatment with pertussis toxin or by inclusion of GDP[beta S] or cyclic AMP in the intracellular medium. The inhibitory effect of GTP[gamma S] could be counteracted by a prepulse to a large depolarizing voltage. A similar effect of a depolarizing prepulse was observed in control cells with no exogenous guanine nucleotides. These observations indicate that inhibition of beta
Author: Gylfe, E. et al.; Genre: Journal Article; Published in Print: 1993-08; Title: Triphasic changes of cytoplasmic CA2+ associated with early glucose effects on beta-cell membrane potential.