Cause Of Inflammation In Diabetes Identified
Follow all of ScienceDaily's latest research news and top science headlines ! Cause of inflammation in diabetes identified Inflammation is one of the main reasons why people with diabetes experience heart attacks, strokes, kidney problems and other, related complications. Now, in a surprise finding, researchers have discovered, in mice, that when certain immune cells cant manufacture fat, the mice dont develop diabetes and inflammation, even when consuming a high-fat diet. Too much fat in the diet promotes insulin resistance by spurring chronic inflammation. In the image above, immune cells (shown in green) produce fatty acids that contribute to diabetes-related inflammation. Researchers at Washington University School of Medicine have developed a way to block production of fatty acids in these immune cells in mice and protect them from diet-induced diabetes. Credit: Semenkovich lab/ Washington University Too much fat in the diet promotes insulin resistance by spurring chronic inflammation. In the image above, immune cells (shown in green) produce fatty acids that contribute to diabetes-related inflammation. Researchers at Washington University School of Medicine have developed a way to block production of fatty acids in these immune cells in mice and protect them from diet-induced diabetes. Credit: Semenkovich lab/ Washington University Inflammation is one of the main reasons why people with diabetes experience heart attacks, strokes, kidney problems and other, related complications. Now, in a surprise finding, researchers at Washington University School of Medicine in St. Louis have identified a possible trigger of chronic inflammation. Too much fat in the diet promotes insulin resistance by spurring chronic inflammation. But the researchers discovered, in mice, that Continue reading >>
Diabetes And Inflammation
Inactivity and obesity increase the risk for diabetes, but exactly how is unclear. Recent research suggests that inflammation inside the body plays a role in the development of type 2 diabetes. The good news: An "anti-inflammatory" diet and exercise plan can help prevent and treat type 2 diabetes. The effects of inflammation are familiar to anyone who has experienced a bug bite, rash, skin infection, or ankle sprain. In those situations, you will see swelling in the affected area. With type 2 diabetes, inflammation is internal. People with type 2 diabetes don't produce enough insulin or their bodies can't use the insulin adequately. Insulin is a hormone that is made by cells in the pancreas. It controls the amount of sugar in the blood. Insulin may also have an impact on tissue in the body. Its effects on tissue are influenced by many factors, including obesity and the accumulation of fat around the belly and on major organs in the abdomen. The fat cells can produce chemicals that lead to inflammation. Scientists are only beginning to understand the role this form of internal inflammation may play in the development of chronic diseases like diabetes. Decades ago, researchers identified higher levels of inflammation in the bodies of people with type 2 diabetes. The levels of certain inflammatory chemicals called cytokines are often higher in people with type 2 diabetes compared to people without diabetes. Obesity and inactivity have long been known to be the most important risk factors that drive the development of type 2 diabetes. How could carrying extra weight and sofa-sitting be connected to higher levels of inflammatory chemicals in the body and the development of diabetes? Researchers discovered that in people with type 2 diabetes, cytokine levels are elevated insi Continue reading >>
Inflammation And Diabetes
Inflammation is a general term for the immune system's response to something, such as an infection or injury, and chronic means the response persists over time. At the cellular level, inflammation involves the release and increased activity of various immune system cells. The inflammatory reaction in type 1 diabetes where the beta cells are attacked is called "insulitis." The immune system cells involved in the attack include various types of white blood cells (T-cells and macrophages), and/or the substances they secrete, including cytokines, nitric oxide, and free radicals (Cnop et al. 2005). (See the oxidative stress page for more on free radicals). Certain cytokines and other markers of inflammation may be associated with development of both type 1 and type 2 diabetes (Goldberg 2009). People with type 1 diabetes have higher levels of inflammatory markers than those without diabetes; even patients with good blood sugar control (Snell-Bergeon et al. 2010). A lot of researchers are trying to identify how exactly this inflammatory process works in the development of type 1 and type 2 diabetes: what cells are involved, and what their roles are (e.g., Cnop et al. 2005). As for why it happens in the first place, we don't know. Cytokines are essentially messenger proteins that affect the behavior of other cells. There are various types of cytokines. Some cytokines can reduce inflammation, while other contribute to it: it is the pattern of cytokines that is critical in perpetrating autoimmune disease. Cytokines are secreted by immune system cells, and control the duration and strength of the immune response (Duramad et al. 2007). In type 1 diabetes, various cytokines act together in complex ways to induce beta cell death (apoptosis) (Gysemans et al. 2008). Cytokines can affec Continue reading >>
Inflammatory Biomarkers: Impact For Diabetes And Diabetic Vascular Disease
Inflammatory biomarkers: impact for diabetes and diabetic vascular disease University Cardiology Clinic, Medical School Correspondence address. Tel: +61-3-99192737; Fax: + Centre for Chronic Disease, College of Health and Biomedicine Centre for Chronic Disease, College of Health and Biomedicine Acta Biochimica et Biophysica Sinica, Volume 47, Issue 12, 1 December 2015, Pages 10291031, Marijan Bosevski, Lily Stojanovska, Vasso Apostolopoulos; Inflammatory biomarkers: impact for diabetes and diabetic vascular disease, Acta Biochimica et Biophysica Sinica, Volume 47, Issue 12, 1 December 2015, Pages 10291031, Physical inactivity and sedentary lifestyles are believed to be independent risk factors for the occurrence of obesity, type-2 diabetes, and metabolic syndrome [ 13 ]. The incidence of type-2 diabetes characterized by chronic hyperglycemia and glucose intolerance, has increased in parallel with obesity, and as of 2010, 285 million people were diagnosed with type-2 diabetes compared with 30 million 25 years ago [ 4 ]. Even with statin therapy, type-2 diabetes has been shown to lead to accelerated atherosclerosis and excessive risk of vascular disease [ 5 ]. Risk factors such as hyperglycemia and glucose intolerance, hyperlipidemia, obesity, and hypertension lead to diabetic vascular disease [ 6 ]. It is not well understood why some patients with the same duration of diabetes and metabolic control have different extents of atherosclerosis spread through multiple vascular regions or limited to only one vascular territory. Use of statins and fibrates in people with type-2 diabetes are favorable, despite the progression of diabetic vascular disease [ 7 ]. However, co-administration of pioglitazone and statins provides regression in intima-media thickness and endothelial f Continue reading >>
Role Of Inflammation In Diabetic Complications
Role of inflammation in diabetic complications Correspondence and offprint requests to: J. F. Navarro, Servicio de Nefrologia, Hospital Nvestra Seora de Candelaria, 38010 Santa Cruz de Tenerife, Spain. Email: [email protected] Search for other works by this author on: Nephrology Dialysis Transplantation, Volume 20, Issue 12, 1 December 2005, Pages 26012604, Juan F. Navarro, Carmen Mora; Role of inflammation in diabetic complications, Nephrology Dialysis Transplantation, Volume 20, Issue 12, 1 December 2005, Pages 26012604, cytokines , diabetes , diabetic nephropathy , inflammation , pentoxifylline , tumor necrosis factor- Diabetes mellitus, especially type 2 diabetes, is a public health problem which has reached epidemic proportions due to the rapidly increasing rates of this disease worldwide. Target organ complications, secondary to diabetes, will be one of the most important medical concerns of the coming decades. A clear example is diabetic nephropathy (DN), which has become the single most frequent cause of end-stage renal disease, in other words: a medical catastrophe of worldwide dimensions [ 1 ]. In the last few years, our knowledge of DN and its clinical course, the factors that influence it as well as the progression of renal injury and the possibilities of effective therapeutic approaches have substantially improved. From a pathophysiological point of view, the critical importance of metabolic and haemodynamic factors for the risk of developing DN is clear. However, the intimate mechanisms leading from chronic hyperglycaemia to the development of renal injury are complex and not yet fully unravelled. Diabetes mellitus: an evolving disease. From a metabolic disorder to an inflammatory condition In 1998, a hypothesis was proposed suggesting that l Continue reading >>
Type 2 Diabetes Is An Inflammatory Disease, Say Researchers
Type 2 diabetes is an inflammatory disease, say researchers New research from Denmark adds further weight to the idea that type 2 diabetes is an inflammatory disease. The recently published study describes how in mice, during the very early stages of type 2 diabetes , immune cells called macrophages invade pancreatic tissue, releasing large quantities of cytokines - pro-inflammatory proteins - that help destroy insulin-producing beta cells. More than 360 million people around the world have type 2 diabetes, including around 8% of Americans. The disease can lead to more serious conditions like cardiovascular disease, blindness, loss of limbs, and kidney failure. In people who are healthy and do not have diabetes , the beta cells of the pancreas secrete insulin into the bloodstream - this helps to regulate blood sugar levels which rise after eating. One of the researchers, Dr. Alexander Rosendahl, from the Department of Diabetes Complication Biology at Novo Nordisk A/S, in Malov, says: "The study may provide novel insights allowing development of tailor-made anti-inflammatory based therapies reducing the burden of type 2 patients." Such new treatments could be used to complement existing therapies, for example those that use insulin analogues, he adds. For their study, Dr. Rosendahl and colleagues compared obese mice that spontaneously developed diabetes to normal healthy mice. They observed the mice from a young age, when in early stages of obesity , until after their obesity in adulthood had started to affect multiple organs. They monitored presence of macrophages around the insulin-producing beta cells of the pancreas, and also in the spleen. The advanced cytometric technology they used allowed them to take measurements at the level of single cells. Proinflammatory ma Continue reading >>
Chronic Inflammatory Disorders And Risk Of Type 2 Diabetes Mellitus, Coronary Heart Disease, And Stroke: A Population-based Cohort Study
Journal of the American Heart Association Chronic Inflammatory Disorders and Risk of Type 2 Diabetes Mellitus, Coronary Heart Disease, and Stroke: A Population-Based Cohort Study Alex Dregan, Judith Charlton, Phil Chowienczyk, Martin C. Gulliford King's College London, London & NIHR Biomedical Research Centre at Guy's and St Thomas' NHS Foundation Trust, London, United Kingdom King's College London, London & NIHR Biomedical Research Centre at Guy's and St Thomas' NHS Foundation Trust, London, United Kingdom BackgroundThe study aimed to evaluate whether risks of diabetes and cardiovascular disease (CVD) are elevated across a range of organ-specific and multi-system chronic inflammatory disorders. Methods and ResultsA matched cohort study was implemented in the UK Clinical Practice Research Datalink (CPRD) including participants with severe psoriasis (5,648), mild psoriasis (85,232), bullous skin diseases (4,284), ulcerative colitis (12,203), Crohn's disease (7,628), inflammatory arthritis (27,358), systemic autoimmune disorders (7,472), systemic vasculitis (6,283) and 373,851 matched controls. The main outcome measures were new diagnoses of type 2 diabetes mellitus (T2DM), stroke, or coronary heart disease (CHD). The outcomes were evaluated for each condition in a multiple outcomes model, adjusting for conventional cardiovascular risk factors. Estimates for different inflammatory conditions were pooled in a random effects meta-analysis. There were 4,695 new diagnoses of T2DM, 3,266 for CHD and 1,715 for stroke. The hazards for pooled multiple failure estimate was 1.20 (95% confidence interval (CI), 1.15-1.26). The highest relative hazards were observed in systemic autoimmune disorders (1.32, CI: 1.16-1.44) and systemic vasculitis (1.29, CI: 1.16-1.44). Hazards were incr Continue reading >>
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How Inflammation Makes You Fat And Diabetic (and Vice Versa)
In the previous article in this series, I argued that diabesity is an autoimmune, inflammatory disorder. In this article, we’re going to review the evidence linking inflammation to obesity and type 2 diabetes (T2DM) and learn why inflammation may be the single-most important mechanism driving the diabesity epidemic. The inflammation-diabesity connection is a hot topic in the scientific literature. A Pubmed search for “inflammation diabetes obesity” turns up more than 1,800 articles. The association between these conditions has been known for decades. In fact, more than 100 years ago high doses of salycilates – a class of anti-inflammatory compounds which includes aspirin – were used to treat T2DM. In 1876, a physician named Ebstein found that sodium salycilate could make the symptoms of diabetes completely disappear. (In case you’re wondering why doctors don’t use this therapy today, it fell out of favor due to the serious side effects caused by high doses of salicylates.) Though the association between inflammation and diabesity is well-known, questions remain. Does diabesity cause inflammation, or does inflammation cause diabesity? How and why does the body initiate an inflammatory response to diabesity? Does obesity itself cause inflammation, or is inflammation caused by something secondary to obesity (like high blood sugar or triglycerides)? I’m going to try to answer those questions in this article. Let’s dive in. How inflammation causes diabesity There are several lines of evidence that inflammation directly causes obesity and diabetes. First, inflammation has been shown to precede the development of diabesity. Elevated levels of inflammatory cytokines predict future weight gain, and infusion of inflammatory cytokines into healthy, normal weight Continue reading >>
Put Out The Fire Of Diabetes Inflammation
Inflammation is a vital body function. It fights infection and repairs injury. But inflammation can also cause insulin resistance and diabetes complications. What is inflammation exactly? And how can we make it help us, not hurt us? Inflammation is a miraculous system for fighting invaders: germs, toxic chemicals, anything unwanted. Monica Smith reported here in 2009, that “Inflammation is the body’s natural response to injury and the first step in healing. In its acute form, it can be quite dramatic. Whether you have a virus or a cut, the body sends white blood cells to the site of infection or injury, where they release chemicals to protect you. The most obvious sign of acute inflammation is pain, such as when you have a sore throat; you may also experience fever in the case of an infection, or swelling as your body deals with a traumatic injury.” The immune system brings more red and white blood cells to the area. It opens blood vessel walls so more fluid can come out into the infected or injured parts. It brings healing substances like cholesterol to the area to make patches for damaged areas and help new cells grow. That’s fine for an infected finger, but imagine that process going on day after day in your kidneys, your eyes, or your coronary arteries! Once the invader is defeated, the system should cool down. The active immune cells should go home, leaving a few guardians to watch for the next attack. But that doesn’t always happen. When there’s no cool-down, the tissues stay hot and swollen. When that happens in blood vessels, they can break down or become blocked. Sometimes the inflammation becomes chronic. Chronic inflammation is like having a fire burning in your body. It causes all kinds of damage. “[Chronic low-grade inflammation] seems to play Continue reading >>
Is Systemic Inflammation Related To Islet Autoimmunity?
Type 1 Diabetes: A Chronic Inflammatory Disease of the Islets Type 1 diabetes is a T-cell-mediated autoimmune disease in which autoreactive cytotoxic T-cells recognize a number of antigenic determinants expressed in pancreatic -cells. Similarly to other autoimmune disorders, in type 1 diabetes many components of the inflammatory responses, including CD4+ and CD8+ T-cells, macrophages, dendritic cells, natural killer (NK) cells, cytokines, free oxygen, nitric oxide radicals, etc., contribute to -cell destruction. The observation that in newly diagnosed diabetic patients, islet-infiltrating CD8+ T-cells represent the prevalent cell type of insulitis[ 13 , 14 ] suggests that major histocompatibility complex (MHC) class I-restricted T-cells are likely to be as crucial to the development of autoimmune diabetes in human as they are in the NOD mouse. The autoantigens targeted by autoreactive CD8+ T-cells in NOD mice appear to be insulin[ 15 ] and the islet-specific glucose-6-phosphatase catalytic subunit-related protein (IGRIP).[ 16 ] An intriguing human investigation provided evidence that peptide 10-18 of the insulin B chain is associated with recurrence of autoimmunity and loss of -cell function in islet grafted type 1 diabetic recipients.[ 17 ] Other investigations indicated that islet destruction is caused by proinflammatory autoreactive T-cells, while the tolerant, nondiabetic state is characterized by autoreactive T-cells that secrete the immune suppressive cytokine, IL-10.[ 18 ] The nervous system may also be implicated in initiating the chain of events leading to local inflammation and ultimately autoimmune diabetes. The TRPV1+ pancreatic sensory neurons in NOD mice appear to function as a controller of islet T-cell infiltration and -cell stress despite systemic pres Continue reading >>
Diabetes And Chronic Inflammation Connecting The Dots, Part Un
Nature Medicine has recently featured studies dealing with obesity-related insulin resistance which leads to a type of diabetes, called Type 2 diabetes. Of these papers, one by Pal et al. (Nature Medicine, 18(8):1284, August 2012) highlights some specific aspects of the disease, including prospects for future therapeutics. I found it interesting for various reasons* enough to spur me to write about diabetes in the context of their observations. I shall make it a 2-part series; in the first post, I would talk a bit about diabetes in general, and follow it up with a review of the main findings of their elegant studies. (Full disclosure: I have parents and grandparents who are/were diabetic.) Id probably be hard pressed to find an adult person in an industrialized nation, who hasnt heard of the dreaded metabolic disease, diabetes, short for Diabetes Mellitus or DM. Diabetes is the condition of hyperglycemia (hyper = over the limit; glyc = referring to sugar, generally simple sugars such as glucose; emia = in blood; that is, high blood sugar) with glycosuria (uria = in urine); this means, that the level of sugar in the blood is so much, that the kidney filtration system is overwhelmed and the sugar literally spills into the urine. How does this happen? In the healthy body, Insulin a hormone produced by the -cells of pancreas moves glucose from blood into muscles, fat and liver cells, where they are either used up in form of fuel or stored in a complex form called glycogen. This works in a feed-forward/feed-back loop. More glucose is detected in the blood, more insulin is produced; when the glucose level in blood is normal, Insulin production decreases. Another hormone, glucagon , produced by -cells of pancreas, does the exact opposite function, moving glucose from tissues Continue reading >>
Inflammation, Stress, And Diabetes
Go to: Inflammation, stress, and diabetes Survival of multicellular organisms depends on the ability to fight infection and heal damage and the ability to store energy for times of low nutrient availability or high energy need. Metabolic and immune systems are therefore among the most basic requirements across the animal kingdom, and many nutrient and pathogen-sensing systems have been highly conserved from organisms such as Caenorhabditis elegans and Drosophila to mammals. Perhaps not surprisingly, metabolic and immune pathways have also evolved to be closely linked and interdependent. Many hormones, cytokines, signaling proteins, transcription factors, and bioactive lipids can function in both metabolic and immune roles. In addition to using some of the same cellular machinery, metabolic and immune systems also regulate each other. The normal inflammatory response relies upon metabolic support, and energy redistribution, particularly the mobilization of stored lipid, plays an important role in fighting infection during the acute-phase response (1). The basic inflammatory response thus favors a catabolic state and suppresses anabolic pathways, such as the highly conserved and powerful insulin signaling pathway. The integration of metabolism and immunity, which under normal conditions is beneficial for the maintenance of good health, can become deleterious under conditions of metabolic challenge, as exemplified by the immunosuppression characteristic of malnourished or starving individuals (1–3). Famine has been a prominent hazard to human health throughout history, and for thousands of years the link between infection and poor nutrition has been well recognized. Today this threat is as widespread as ever, and there are approximately 1 billion undernourished individua Continue reading >>
Gut Bacteria And Fat Cells May Interact To Produce “perfect Storm” Of Inflammation That Promotes Diabetes And Other Chronic Disease
Health problems such as obesity, insulin resistance, type 2 diabetes, periodontal disease, stroke, and heart disease are all rooted in inflammation, which must be properly addressed if you wish to be healed Research suggests there’s a connection between certain types of bacteria and body fat that produces a heightened inflammatory response and drives the inflammatory process Superantigens—toxic molecules produced by pathogenic bacteria such as staph—may play a role in the development of type 2 diabetes through their effect on fat cells Your oral health can have a significant impact on your cardiovascular and heart health. In a recent study, improved gum health was shown to significantly slow down the progression of atherosclerosis Periodontal disease is the result of the colonization of certain pathogenic bacteria in your mouth. This bacterial profile is influenced by the microflora in your gut By Dr. Mercola A wide array of health problems, including but not limited to obesity, insulin resistance, type 2 diabetes, periodontal disease, stroke, and heart disease all have inflammation as a part of the disease. The majority of inflammatory diseases start in your gut. Chronic inflammation in your gut can disrupt the normal functioning of many bodily systems. There also appears to be a connection between certain types of bacteria and body fat that produces a heightened inflammatory response and drives the inflammatory process. For example, recent research1 suggests that superantigens—toxic molecules produced by pathogenic bacteria such as staph—may play a role in the development of type 2 diabetes through their effect on fat cells. As reported by the featured article:2 "The idea is that when fat cells (adipocytes) interact with environmental agents -- in this case, Continue reading >>
Anti-inflammatory Agents In The Treatment Of Diabetes And Its Vascular Complications
The association between hyperglycemia and inflammation and vascular complications in diabetes is now well established. Antidiabetes drugs may alleviate inflammation by reducing hyperglycemia; however, the anti-inflammatory effects of these medications are inconsistent and it is unknown whether their beneficial metabolic effects are mediated via modulation of chronic inflammation. Recent data suggest that immunomodulatory treatments may have beneficial effects on glycemia, β-cell function, and insulin resistance. However, the mechanisms underlying their beneficial metabolic effects are not always clear, and there are concerns regarding the specificity, safety, and efficacy of immune-based therapies. Herein, we review the anti-inflammatory and metabolic effects of current antidiabetes drugs and of anti-inflammatory therapies that were studied in patients with type 2 diabetes. We discuss the potential benefit of using anti-inflammatory treatments in diabetes and important issues that should be addressed prior to implementation of such therapeutic approaches. The prevalence of diabetes is on the rise, with 415 million people affected worldwide according to recent data from the International Diabetes Federation (1). This number is predicted to increase further, with 642 million people expected to develop diabetes by 2040. While many factors are known to contribute to the development of diabetes and its complications, the involvement of the immune system in the pathogenesis of metabolic diseases has been gaining interest. It has long been appreciated that inflammation is central to the pathology of the pancreatic islet in type 1 diabetes. However, growing evidence suggests that inflammation also plays an important role in the pathogenesis of type 2 diabetes, including obesit Continue reading >>
Does Inflammation Trigger Insulin Resistance And Diabetes?
Nearly 21 million Americans suffer from type 2 diabetes, and every year 800,000 more are diagnosed. Considering the growing numbers, scientists are trying to fit together the disease’s disparate puzzle pieces. People who acquire it are typically obese, suffer from chronic inflammation and are resistant to insulin, the hormone that removes sugar from the blood and stores it as energy. For years no one has known exactly how the three characteristics are related, if at all. But a handful of recent studies suggest that they are inextricably linked through the actions of specific inflammatory immune cells and a master genetic switch—and the hope is that an understanding of the relations could open the door to new therapeutic opportunities. Several decades ago scientists noticed that people with type 2 diabetes have overly active immune responses, leaving their bodies rife with inflammatory chemicals. In the early 1990s researchers at Harvard University pinpointed one major immune player as TNF-alpha, a chemical secreted by immune cells; such compounds are generally referred to as cytokines. They found high levels of the cytokine in the fat tissue of rats with type 2 diabetes, and when they bred obese rats that could not make the cytokine, diabetes did not develop in the animals. Researchers have since shown that TNF-alpha—and, more generally, inflammation—activates and increases the expression of several proteins that suppress insulin-signaling pathways, making the human body less responsive to insulin and increasing the risk for insulin resistance. So what causes the inflammation? Although type 2 diabetes can develop in patients of normal weight, most scientists agree that “obesity is the driving force,” says Jerrold Olefsky, an endocrinologist at the University Continue reading >>
