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What Structure Of The Beta Cells Of The Pancreas Are Most Likely Affected By The Immune System

How Does Friendly Fire Happen In The Pancreas?

How Does Friendly Fire Happen In The Pancreas?

Follow all of ScienceDaily's latest research news and top science headlines ! How does friendly fire happen in the pancreas? Helmholtz Zentrum Muenchen - German Research Centre for Environmental Health In type 1 diabetes, the body attacks its own insulin-producing cells. Scientists have now reported on a mechanism used by the immune system to prepare for this attack. They were able to inhibit this process through targeted intervention and are now hoping this will lead to new possibilities for treatment. Treatment with an antagomir directed against miR92a results in reduced attacks of immune cells (green) on the insulin (white) producing beta cells directly in the pancreas. Moreover, the treatment leads to more regulatory T cells (red) able to protect the beta cells. Treatment with an antagomir directed against miR92a results in reduced attacks of immune cells (green) on the insulin (white) producing beta cells directly in the pancreas. Moreover, the treatment leads to more regulatory T cells (red) able to protect the beta cells. In type 1 diabetes, the body attacks its own insulin-producing cells. Scientists at Helmholtz Zentrum Mnchen, partner in the German Center for Diabetes Research, and their colleagues at Technical University of Munich have now reported in the journal PNAS about a mechanism used by the immune system to prepare for this attack. They were able to inhibit this process through targeted intervention and are now hoping this will lead to new possibilities for treatment. Type 1 diabetes is an autoimmune disease in which the body destroys its own beta cells in the pancreas.* Researchers are still seeking to find out what causes this malfunction of the immune system in order to intervene therapeutically in the processes. A team led by Dr. Carolin Daniel, g Continue reading >>

The Connection Between Diabetes And Your Pancreas

The Connection Between Diabetes And Your Pancreas

A direct connection exists between the pancreas and diabetes. The pancreas is an organ deep in your abdomen behind your stomach. It’s an important part of your digestive system. The pancreas produces enzymes and hormones that help you digest food. One of those hormones, insulin, is necessary to regulate glucose. Glucose refers to sugars in your body. Every cell in your body needs glucose for energy. Think of insulin as a lock to the cell. Insulin must open the cell to allow it to use glucose for energy. If your pancreas doesn’t make enough insulin or doesn’t make good use of it, glucose builds up in your bloodstream, leaving your cells starved for energy. When glucose builds up in your bloodstream, this is known as hyperglycemia. The symptoms of hyperglycemia include thirst, nausea, and shortness of breath. Low glucose, known as hypoglycemia, also causes many symptoms, including shakiness, dizziness, and loss of consciousness. Hyperglycemia and hypoglycemia can quickly become life-threatening. Each type of diabetes involves the pancreas not functioning properly. The way in which the pancreas doesn’t function properly differs depending on the type. No matter what type of diabetes you have, it requires ongoing monitoring of blood glucose levels so you can take the appropriate action. Type 1 diabetes In type 1 diabetes the immune system erroneously attacks the beta cells that produce insulin in your pancreas. It causes permanent damage, leaving your pancreas unable to produce insulin. Exactly what triggers the immune system to do that isn’t clear. Genetic and environmental factors may play a role. You’re more likely to develop type 1 diabetes if you have a family history of the disease. About 5 percent of people with diabetes have type 1 diabetes. People who ha Continue reading >>

Diabetes

Diabetes

What is diabetes? Diabetes is disease that causes the body to either not produce insulin or not react properly to the insulin. There are two types of diabetes: Type 1 diabetes is when the body simply does not produce insulin. This type develops in teens and is less common than Type 2. When you have Type 1 diabetes, your immune system turns on the pancreas, causing it not to produce insulin. This causes blood sugar levels to get too high. People with Type 1 take insulin injections to help regulate their blood glucose levels. Type 2 diabetes is when the cells in the body do not react properly with the insulin being produced. The signal to the GLUT4 is never sent from the receptors, so the cells don't allow glucose to enter. Insulin injections can sometimes help people with Type 2, however they usually can only watch what they eat and be careful to exercise a certain amount. How is glucose tolerance testing used to diagnose diabetes? The GTT is usually administered after an abnormal urine test. Doctors use glucose tolerance testing to monitor the amount of glucose in the patient's blood at a given moment in time and to see if their body reacts properly in response to the glucose. If the glucose levels rise drastically and don't fall back down this indicates that there is a high chance that the patient has diabetes. The insulin test can determine the difference between Type 1 and Type 2 diabetes; if the levels of insulin in the blood are high, the patient has Type 2 diabetes, and if there is no insulin in the blood the patient has Type 1. How does the development of Type 1 and Type 2 diabetes relate to how the body produces and uses insulin? In type one diabetes the persons immune system attacks the pancreas causing it to shut down insulin production, leaving the person wit Continue reading >>

Beta Cell Dysfunction And Insulin Resistance

Beta Cell Dysfunction And Insulin Resistance

Go to: Abstract Beta cell dysfunction and insulin resistance are inherently complex with their interrelation for triggering the pathogenesis of diabetes also somewhat undefined. Both pathogenic states induce hyperglycemia and therefore increase insulin demand. Beta cell dysfunction results from inadequate glucose sensing to stimulate insulin secretion therefore elevated glucose concentrations prevail. Persistently elevated glucose concentrations above the physiological range result in the manifestation of hyperglycemia. With systemic insulin resistance, insulin signaling within glucose recipient tissues is defective therefore hyperglycemia perseveres. Beta cell dysfunction supersedes insulin resistance in inducing diabetes. Both pathological states influence each other and presumably synergistically exacerbate diabetes. Preserving beta cell function and insulin signaling in beta cells and insulin signaling in the glucose recipient tissues will maintain glucose homeostasis. Keywords: beta cell compensation, diabetes, obesity, oxidative stress, proliferation Go to: Introduction Both beta cell dysfunction and insulin resistance lead to persistent hyperglycemia which characterizes type 2 diabetes. Many of the susceptibility genes associated with type 2 diabetes by genome-wide investigations (GWAS) were identified as regulators of cell turnover or regeneration (McCarthy and Hattersley, 2008). Most risk variants for type 2 diabetes in healthy populations act through impairing insulin secretion (resulting in beta cell dysfunction) rather than insulin action (resulting in insulin resistance) which establishes that inherited abnormalities of beta cell function or mass (or both) are critical precursors in type 2 diabetes (Florez, 2008; McCarthy, 2010; Voight et al., 2010; Petrie Continue reading >>

Human Beta Cell Mass And Function In Diabetes: Recent Advances In Knowledge And Technologies To Understand Disease Pathogenesis - Sciencedirect

Human Beta Cell Mass And Function In Diabetes: Recent Advances In Knowledge And Technologies To Understand Disease Pathogenesis - Sciencedirect

Volume 6, Issue 9 , September 2017, Pages 943-957 Human beta cell mass and function in diabetes: Recent advances in knowledge and technologies to understand disease pathogenesis Author links open overlay panel ChunguangChen123 Christian M.Cohrs123 JuliaStertmann12 RobertBozsak12 StephanSpeier12 Plasma insulin levels are predominantly the product of the morphological mass of insulin producing beta cells in the pancreatic islets of Langerhans and the functional status of each of these beta cells. Thus, deficiency in either beta cell mass or function, or both, can lead to insufficient levels of insulin, resulting in hyperglycemia and diabetes. Nonetheless, the precise contribution of beta cell mass and function to the pathogenesis of diabetes as well as the underlying mechanisms are still unclear. In the past, this was largely due to the restricted number of technologies suitable for studying the scarcely accessible human beta cells. However, in recent years, a number of new platforms have been established to expand the available techniques and to facilitate deeper insight into the role of human beta cell mass and function as cause for diabetes and as potential treatment targets. This review discusses the current knowledge about contribution of human beta cell mass and function to different stages of type 1 and type 2 diabetes pathogenesis. Furthermore, it highlights standard and newly developed technological platforms for the study of human beta cell biology, which can be used to increase our understanding of beta cell mass and function in human glucose homeostasis. In contrast to early disease models, recent studies suggest that in type 1 and type 2 diabetes impairment of beta cell function is an early feature of disease pathogenesis while a substantial decrease in beta Continue reading >>

You And Your Hormones

You And Your Hormones

Where is the pancreas? The pancreas is a large gland that lies alongside the stomach and the small bowel. It is about six inches (approximately 15 cm) long and is divided into the head, body and tail. What does the pancreas do? The pancreas carries out two important roles: It makes digestive juices, which consist of powerful enzymes. These are released into the small bowel after meals to break down and digest food. It makes hormones that control blood glucose levels. The pancreas produces hormones in its 'endocrine' cells. These cells are gathered in clusters known as islets of langerhans and monitor what is happening in the blood. They then can release hormones directly into the blood when necessary. In particular, they sense when sugar (glucose) levels in the blood rise, and as soon as this happens the cells produce hormones, particularly insulin. Insulin then helps the body to lower blood glucose levels and 'store' the sugar away in fat, muscle, liver and other body tissues where it can be used for energy when required. The pancreas is very close to the stomach. As soon as food is eaten, the pancreas releases digestive enzymes into the bowel to break food down. As the food is digested, and nutrient levels in the blood rise, the pancreas produces insulin to help the body store the glucose (energy) away. Between meals, the pancreas does not produce insulin and this allows the body to gradually release stores of energy back into the blood as they are needed. Glucose levels remain very stable in the blood at all times to ensure that the body has a steady supply of energy. This energy is needed for metabolism, exercise and, in particular, to fuel the parts of the brain that 'run' on glucose. This makes sure that the body doesn't starve between meals. What hormones does th Continue reading >>

G-protein-coupled Receptors, Pancreatic Islets, And Diabetes

G-protein-coupled Receptors, Pancreatic Islets, And Diabetes

© 2010 Nature Education All rights reserved. Figure Detail Following a meal, glucose levels in the blood circulation increase. Multiple factors regulate the level of glucose in the blood, and central among these are insulin and glucagon. Glucose is taken up into pancreatic beta cells through a glucose transporter called GLUT2 (Figure 1). As glucose is taken up into beta cells, it is metabolized, which leads to an increased production of ATP. This, in turn, increases the ATP/ADP ratio, which results in closing of potassium channels in the cell membrane and subsequent depolarization of the cell. As potassium channels close and cell depolarization increases, this causes calcium channels in the cell membrane to open and allow the flow of calcium into the cell. This accumulation of calcium causes the secretion of insulin into the blood by particular cells in the islet called beta cells. Subsequently, insulin circulates and acts on cells in a variety of tissues. Important among these are fat, muscle, and liver. Insulin binds to a receptor for insulin in the plasma membrane of the cells in these tissues, and stimulates intracellular signaling pathways that ultimately cause the translocation of glucose transporters (GLUT4 in the case of fat and muscle cells) to the cell membrane. These transporters increase glucose uptake into the cell. In fat and muscle cells, glucose normally serves as an important source of energy which can be converted into fat or glycogen (as a form of stored energy) if necessary. In liver cells, an important function is to produce glucose (either by the breakdown of glycogen or de novo synthesis of glucose). The binding of insulin to its receptor on liver cells leads to increased synthesis of glycogen and inhibition of glucose production by liver cells. Continue reading >>

Dri Biohub: Supply

Dri Biohub: Supply

Islet transplantation has clearlyshown the ability to restore natural insulin production and normalize blood sugar levels in people with type 1 diabetes. But, some hurdles remain before this cell replacement therapy can be offered more broadly to those who can benefit. Two notable ones are the complex challengesof the immune system and the shortage of insulin-producing cells available for transplant. Currently, islets used for transplantation come from the pancreases of deceased donors. With organ donation in the United States at critically low levels, there are clearly not enough cellsfor everyone. The DRI is developing several pioneeering strategies to create areliable supplyof insulin-producing cells. Scientists have discovered that different types ofcells within the non-insulin producing portion of the pancreas, which makes up 98 percent of the organ, have the ability to become insulin-producing cells. In particular, they have focused on a unique population of stem cells that remain intact after the autoimmune attack in a large percentage of patients. The DRI's Cell Supply team has been developing methods to stimulate these pancreatic stem cells to turn into insulin-producing cells with very promising results. Using a natrually occurring protein called bone morphogenetic protein 7 (BMP-7), DRI reseachers demonstrated that these stem cells within the non-endocrine tissue can become new islets when cultured in the lab. Their pioneering findings using this FDA-approved molecule were published in the journal Diabetes . In itself, the discovery could potentially open the door to transplanting multiple patients from a single donor pancreas, but the results have other promising implications. After observing that these stem cells remained in the pancreas after the onset of Continue reading >>

Facts About Diabetes And Insulin

Facts About Diabetes And Insulin

Diabetes is a very common disease, which, if not treated, can be very dangerous. There are two types of diabetes. They were once called juvenile-onset diabetes and adult diabetes. However, today we know that all ages can get both types so they are simply called type 1 and type 2 diabetes. Type 1, which occurs in approximately 10 percent of all cases, is an autoimmune disease in which the immune system, by mistake, attacks its own insulin-producing cells so that insufficient amounts of insulin are produced - or no insulin at all. Type 1 affects predominantly young people and usually makes its debut before the age of 30, and most frequently between the ages of 10 and 14. Type 2, which makes up the remaining 90 percent of diabetes cases, commonly affects patients during the second half of their lives. The cells of the body no longer react to insulin as they should. This is called insulin resistance. In the early 1920s, Frederick Banting, John Macleod, George Best and Bertram Collip isolated the hormone insulin and purified it so that it could be administered to humans. This was a major breakthrough in the treatment of diabetes type 1. Insulin Insulin is a hormone. Hormones are chemical substances that regulate the cells of the body and are produced by special glands. The hormone insulin is a main regulator of the glucose (sugar) levels in the blood. Insulin is produced in the pancreas. To be more specific, it's produced by the beta cells in the islets of Langerhans in the pancreas. When we eat, glucose levels rise, and insulin is released into the bloodstream. The insulin acts like a key, opening up cells so they can take in the sugar and use it as an energy source. Sugar is one of the top energy sources for the body. The body gets it in many forms, but mainly as carbohydr Continue reading >>

Beta Cell

Beta Cell

Beta cells (β cells) are a type of cell found in the pancreatic islets of the pancreas. They make up 65-80% of the cells in the islets. Function[edit] The primary function of a beta cell is to store and release insulin. Insulin is a hormone that brings about effects which reduce blood glucose concentration. Beta cells can respond quickly to spikes in blood glucose concentrations by secreting some of their stored insulin while simultaneously producing more. Control of insulin secretion[edit] Voltage-gated calcium channels and ATP-sensitive potassium ion channels are embedded in the cell surface membrane of beta cells. These ATP-sensitive potassium ion channels are normally open and the calcium ion channels are normally closed. Potassium ions diffuse out of the cell, down their concentration gradient, making the inside of the cell more negative with respect to the outside (as potassium ions carry a positive charge). At rest, this creates a potential difference across the cell surface membrane of -70mV. When the glucose concentration outside the cell is high, glucose molecules move into the cell by facilitated diffusion, down its concentration gradient through the GLUT2 transporter.[1] Since beta cells use glucokinase to catalyze the first step of glycolysis, metabolism only occurs around physiological blood glucose levels and above. Metabolism of the glucose produces ATP, which increases the ATP to ADP ratio.[2] The ATP-sensitive potassium ion channels close when this ratio rises. This means that potassium ions can no longer diffuse out of the cell.[3] As a result, the potential difference across the membrane becomes more positive (as potassium ions accumulate inside the cell). This change in potential difference opens the voltage-gated calcium channels, which allows cal Continue reading >>

Autoimmune Destruction Of Pancreatic Beta Cells.

Autoimmune Destruction Of Pancreatic Beta Cells.

Abstract Type 1 diabetes results from the destruction of insulin-producing pancreatic beta cells by a beta cell-specific autoimmune process. Beta cell autoantigens, macrophages, dendritic cells, B lymphocytes, and T lymphocytes have been shown to be involved in the pathogenesis of autoimmune diabetes. Beta cell autoantigens are thought to be released from beta cells by cellular turnover or damage and are processed and presented to T helper cells by antigen-presenting cells. Macrophages and dendritic cells are the first cell types to infiltrate the pancreatic islets. Naive CD4+ T cells that circulate in the blood and lymphoid organs, including the pancreatic lymph nodes, may recognize major histocompatibility complex and beta cell peptides presented by dendritic cells and macrophages in the islets. These CD4+ T cells can be activated by interleukin (IL)-12 released from macrophages and dendritic cells. While this process takes place, beta cell antigen-specific CD8+ T cells are activated by IL-2 produced by the activated TH1 CD4+ T cells, differentiate into cytotoxic T cells and are recruited into the pancreatic islets. These activated TH1 CD4+ T cells and CD8+ cytotoxic T cells are involved in the destruction of beta cells. In addition, beta cells can also be damaged by granzymes and perforin released from CD8+ cytotoxic T cells and by soluble mediators such as cytokines and reactive oxygen molecules released from activated macrophages in the islets. Thus, activated macrophages, TH1 CD4+ T cells, and beta cell-cytotoxic CD8+ T cells act synergistically to destroy beta cells, resulting in autoimmune type 1 diabetes. Continue reading >>

Differential Cell Autonomous Responses Determine The Outcome Of Coxsackievirus Infections In Murine Pancreatic And Cells

Differential Cell Autonomous Responses Determine The Outcome Of Coxsackievirus Infections In Murine Pancreatic And Cells

Differential cell autonomous responses determine the outcome of coxsackievirus infections in murine pancreatic and cells National Institute for Health and Welfare, Finland University of Exeter Medical School, United Kingdom 0 Open annotations (there are currently 0 annotations on this page). Cite as: eLife 2015;4:e06990 doi: 10.7554/eLife.06990 Type 1 diabetes (T1D) is an autoimmune disease caused by loss of pancreatic cells via apoptosis while neighboring cells are preserved. Viral infections by coxsackieviruses (CVB) may contribute to trigger autoimmunity in T1D. Cellular permissiveness to viral infection is modulated by innate antiviral responses, which vary among different cell types. We presently describe that global gene expression is similar in cytokine-treated and virus-infected human islet cells, with up-regulation of gene networks involved in cell autonomous immune responses. Comparison between the responses of rat pancreatic and cells to infection by CVB5 and 4 indicate that cells trigger a more efficient antiviral response than cells, including higher basal and induced expression of STAT1-regulated genes, and are thus better able to clear viral infections than cells. These differences may explain why pancreatic cells, but not cells, are targeted by an autoimmune response during T1D. Type 1 diabetes is caused by a person's immune system attacking the cells in their pancreas that produce insulin. This eventually kills off so many of these cellsknown as beta cellsthat the pancreas is unable to make enough insulin. As a result, individuals with type 1 diabetes must inject insulin to help their bodies process sugars. One of the mysteries of type 1 diabetes is why the beta cells in the pancreas are killed by the immune system while neighboring alpha cells, which Continue reading >>

The Role Of Endoplasmic Reticulum Stress In Autoimmune-mediated Beta-cell Destruction In Type 1 Diabetes

The Role Of Endoplasmic Reticulum Stress In Autoimmune-mediated Beta-cell Destruction In Type 1 Diabetes

Experimental Diabetes Research Volume 2012 (2012), Article ID 238980, 12 pages 1The Center for Biomedical Research, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, 1095 Jiefang Avenue, Wuhan 430030, China 2The Center for Biotechnology and Genomic Medicine, Medical College of Georgia, 1120 15th Street, CA4098, Augusta, GA 30912, USA 3Affiliated Hospital of Guangdong Medical College, 57 Ren-Ming Road, Zhanjiang 524001, China 4The Department of Clinical Immunology, Guangdong Medical College, 1 Xincheng Avenue, Dongguan 523808, China Academic Editor: Muthuswamy Balasubramanyam Copyright © 2012 Jixin Zhong et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. Abstract Unlike type 2 diabetes which is caused by the loss of insulin sensitivity, type 1 diabetes (T1D) is manifested by the absolute deficiency of insulin secretion due to the loss of β mass by autoimmune response against β-cell self-antigens. Although significant advancement has been made in understanding the pathoetiology for type 1 diabetes, the exact mechanisms underlying autoimmune-mediated β-cell destruction, however, are yet to be fully addressed. Accumulated evidence demonstrates that endoplasmic reticulum (ER) stress plays an essential role in autoimmune-mediated β-cell destruction. There is also evidence supporting that ER stress regulates the functionality of immune cells relevant to autoimmune progression during T1D development. In this paper, we intend to address the role of ER stress in autoimmune-mediated β-cell destruction during the course of type 1 diabetes. The potential implication of Continue reading >>

Beta Cells

Beta Cells

Tweet Beta cells are unique cells in the pancreas that produce, store and release the hormone insulin. Located in the area of the pancreas know as the islets of Langerhans (the organ’s endocrine structures), they are one of at least five different types of islet cells that produce and secrete hormones directly into the bloodstream. What is the role of beta cells? The main function of a beta cell is to produce and secrete insulin - the hormone responsible for regulating levels of glucose in the blood. When blood glucose levels start to rise (e.g. during digestion), beta cells quickly respond by secreting some of their stored insulin while at the same time increasing production of the hormone. This quick response to a spike in blood glucose usually takes about ten minutes. In people with diabetes, however, these cells are either attacked and destroyed by the immune system (type 1 diabetes), or are unable to produce a sufficient amount of insulin needed for blood sugar control (type 2 diabetes). Amylin and C-peptide In addition to insulin, beta cells also secrete the hormone Amylin and called C-peptide, a byproduct of insulin production. Amylin slows the rate of glucose entering the bloodstream, making it a more short-term regulator of blood glucose levels. C-peptide is a molecule that helps to prevent neuropathy and other vascular complications by assisting in the repair of the muscular layers of the arteries. It is secreted into the bloodstream in equal quantities (or moles) to insulin. Beta cells in type 1 diabetes In type 1 diabetes, beta cells die from a misguided attack by the body’s immune system. How and why that happens is not clear, but the results of a study published in early 2011 suggest that these pancreatic cells become stressed at the earliest stages of Continue reading >>

Beta Cell Dysfunction

Beta Cell Dysfunction

Beta cells reside in the pancreas, where they do the important job of producing insulin for the body. Beta cells produce insulin, and also secrete insulin when they are signaled to do so by an increase in glucose levels in the blood. Without adequate insulin, blood glucose levels rise too high, a defining characteristic of any type of diabetes. In type 2 diabetes, beta cells churn out a lot of insulin early in the disease process; type 2 is characterized by both high glucose levels, and high insulin levels in the blood. The main problem is that the body's tissues are resistant to insulin, and can't use it properly. As type 2 diabetes progresses over time, however, the beta cells seem to wear out, and eventually produce less insulin. Some people with type 2 diabetes end up having to take insulin because their beta cells are not producing enough of it. In type 1 diabetes, the beta cells do not produce enough insulin. This is generally due to the death of the beta cells. By the time someone is diagnosed with type 1 diabetes, they may have lost 70-80% of their beta cells (it is thought, although more recent studies are testing this number). Beta cell loss occurs gradually over time, beginning before diagnosis, and continuing afterwards, until most beta cells are lost (Cnop et al. 2005). However, new research is also finding that some people with type 1 continue to produce insulin for many years (Davis et al. 2014; Oram et al. 2014), as well as proinsulin (a precursor to insulin) (Steenkamp et al. 2017), and that beta cell dysfunction (not just death) may also be a significant cause of high blood sugar, at least around the time of diagnosis (Pugliese et al. 2014). Further new research suggests that beta cell mass and function is actually maintained until just before diagnosi Continue reading >>

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