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Glucose Control And The Inflammatory Response

A Role Of The Adaptive Immune System In Glucose Homeostasis

A Role Of The Adaptive Immune System In Glucose Homeostasis

Abstract Objective The immune system, including the adaptive immune response, has recently been recognized as having a significant role in diet-induced insulin resistance. In this study, we aimed to determine if the adaptive immune system also functions in maintaining physiological glucose homeostasis in the absence of diet-induced disease. Research design and methods SCID mice and immunocompetent control animals were phenotypically assessed for variations in metabolic parameters and cytokine profiles. Additionally, the glucose tolerance of SCID and immunocompetent control animals was assessed following introduction of a high-fat diet. Results SCID mice on a normal chow diet were significantly insulin resistant relative to control animals despite having less fat mass. This was associated with a significant increase in the innate immunity-stimulating cytokines granulocyte colony-stimulating factor, monocyte chemoattractant protein 1 (MCP1), and MCP3. Additionally, the SCID mouse phenotype was exacerbated in response to a high-fat diet as evidenced by the further significant progression of glucose intolerance. Conclusions These results support the notion that the adaptive immune system plays a fundamental biological role in glucose homeostasis, and that the absence of functional B and T cells results in disruption in the concentrations of various cytokines associated with macrophage proliferation and recruitment. Additionally, the absence of functional B and T cells is not protective against diet-induced pathology. This is an Open Access article distributed in accordance with the terms of the Creative Commons Attribution (CC BY 4.0) license, which permits others to distribute, remix, adapt and build upon this work, for commercial use, provided the original work is properl Continue reading >>

Glucose And Palmitate Differentially Regulate Pfkfb3/ipfk2 And Inflammatory Responses In Mouse Intestinal Epithelial Cells

Glucose And Palmitate Differentially Regulate Pfkfb3/ipfk2 And Inflammatory Responses In Mouse Intestinal Epithelial Cells

The gene PFKFB3 encodes for inducible 6-phosphofructo-2-kinase, a glycolysis-regulatory enzyme that protects against diet-induced intestine inflammation. However, it is unclear how nutrient overload regulates PFKFB3 expression and inflammatory responses in intestinal epithelial cells (IECs). In the present study, primary IECs were isolated from small intestine of C57BL/6J mice fed a low-fat diet (LFD) or high-fat diet (HFD) for 12 weeks. Additionally, CMT-93 cells, a cell line for IECs, were cultured in low glucose (LG, 5.5 mmol/L) or high glucose (HG, 27.5 mmol/L) medium and treated with palmitate (50 mol/L) or bovine serum albumin (BSA) for 24 hr. These cells were analyzed for PFKFB3 and inflammatory markers. Compared with LFD, HFD feeding decreased IEC PFKFB3 expression and increased IEC proinflammatory responses. In CMT-93 cells, HG significantly increased PFKFB3 expression and proinflammatory responses compared with LG. Interestingly, palmitate decreased PFKFB3 expression and increased proinflammatory responses compared with BSA, regardless of glucose concentrations. Furthermore, HG significantly increased PFKFB3 promoter transcription activity compared with LG. Upon PFKFB3 overexpression, proinflammatory responses in CMT-93 cells were decreased. Taken together, these results indicate that in IECs glucose stimulates PFKFB3 expression and palmitate contributes to increased proinflammatory responses. Therefore, PFKFB3 regulates IEC inflammatory status in response to macronutrients. It is well established that inactivity and overnutrition are major determinants in the development of obesity and contribute to obesity-related metabolic diseases such as type 2 diabetes, fatty liver disease and inflammatory atherosclerosis 1 , 2 , 3 , 4 , 5 . High saturated fat intake is Continue reading >>

Metabolic, Stress, And Inflammatory Biomarker Responses To Glucose Administration In Fischer-344 Rats: Intraperitoneal Vs. Oral Delivery - Sciencedirect

Metabolic, Stress, And Inflammatory Biomarker Responses To Glucose Administration In Fischer-344 Rats: Intraperitoneal Vs. Oral Delivery - Sciencedirect

Metabolic, stress, and inflammatory biomarker responses to glucose administration in Fischer-344 rats: intraperitoneal vs. oral delivery Author links open overlay panel ShinjiniPilona Metabolic effects of anthropogenic chemicals are a focus of environmental health research due to the significant public health implications. Conventional glucose tolerance tests (GTTs) do not generally examine multiple metabolic, inflammatory, and endocrine factors; however, responses to exogenous glucose can provide insight into mode-of-action and disease processes, and warrant consideration in developing models for toxicological assessment. GTTs were conducted on male Fischer-344 rats to 1) assess the feasibility of measuring multiple analytes in small sample volumes; 2) monitor analyte response; and 3) determine whether route of glucose delivery (oral, OGTT vs. intraperitoneal, IPGTT, 2g/kg) modified responses. Plasma samples (0, 30, 60, 90, 120min post-glucose administration) were analyzed for triglycerides; hormones involved in glucose regulation (insulin, glucagon, glucagon-like peptide (GLP)-1)), energy homeostasis (ghrelin, leptin), and stress response (corticosterone); cytokines (TNF, IL-6); and markers of endothelial dysfunction (VEGF, PAI-1). Glucose peaked at 30min during the IPGTT but not the OGTT (p<0.001), a trend paralleled by insulin, while triglycerides decreased following the IPGTT (transient) and the OGTT (sustained). GLP-1 was transiently decreased while ghrelin and leptin levels increased progressively during the IPGTT alone. Corticosterone was increased during both the IPGTT (sustained) and OGTT (transient). TNF and VEGF were unchanged, while PAI-1 and IL-6 were not detected. Increasing the oral glucose dose to 3g/kg did not significantly alter profiles. Results con Continue reading >>

Glucose Control And The Inflammatory Response

Glucose Control And The Inflammatory Response

Hyperglycemia is common after cardiac surgery in both diabetic and nondiabetic patients and is associated with increased morbidity and mortality. Association between nadir hematocrit levels on cardiopulmonary bypass (CPB) and postoperative hyperglycemia is not clear. This study was carried out to determine the relationship between nadir hematocrit during CPB and postoperative hyperglycemia in nondiabetic patients.Records of 200 nondiabetic patients undergoing coronary artery bypass grafting operation were retrospectively reviewed. In the first analysis, patients were divided into two subgroups according to the presence or absence of hyperglycemia. Further analysis was made after dividing the patients into 3 subgroups according to nadir hematocrit levels on CPB (less than 20%; 20% to 25%; greater than or equal to 25%).Compared to patients without hyperglycemia, patients with postoperative hyperglycemia had significantly lower preoperative hematocrit levels (p = 0.004) and were associated with lower nadir hematocrit levels during CPB (p= 0.002). Peak intensive care unit blood glucose levels and number of blood transfusions were significantly higher in patients with nadir hematocrit levels less than 20. (p<0.001 and p<0.001 respectively). Logistic regression analysis demonstrated that nadir hematocrit levels less than 20% (OR 2.9, p=0.009) and allogenic blood transfusion (OR 1.5, p=0.003) were independently associated with postoperative hyperglycemia.Nadir hematocrit levels on CPB less than 20% and allogenic blood transfusions were independently associated with postoperative hyperglycemia in nondiabetic patients. Patients with a nadir hematocrit levels less than 20 % during CPB should be closely monitored for hyperglycemia in the perioperative period. BackgroundThe aim of Continue reading >>

Reporting On Glucose Control Metrics In The Intensive Care Unit

Reporting On Glucose Control Metrics In The Intensive Care Unit

Reporting on Glucose Control Metrics in the Intensive Care Unit European Endocrinology, 2015;11(2):758 DOI: The diabetes of injury typically associated with critical illness has recently been thoroughly revisited and much better characterised following major therapeutic advances. The occurrence of severe hyperglycaemia, moderate hypoglycaemia or high glycaemic variability has been associated with an increased mortality and rate of complications in large independent cohorts of acutely ill patients. Hence, current guidelines advocate the prevention and avoidance of each of these three dysglycaemic domains, and the use of a common metrics for a quantitative description of dysglycaemic events, such as the proportion of time spent in the target glycaemic range as a unifying variable. Using a common language will help to face the future challenges, including the definition of the most appropriate blood glucose (BG) target according to the category of admission, the time interval from the initial injury and the medical history. The clinical testing of technological improvements in the monitoring systems and the therapeutic algorithms should be assessed using the same metrics. Keywords: Critically ill, stress hyperglycaemia, diabetes of injury, stress response, insulin, blood glucose, continuous glucose monitoring (CGM) Disclosure: Rafael Machado Tironi and Jean-Charles Preiser have no conflicts of interest to declare. No funding was received for the publication of this article. Open Access: This article is published under the Creative Commons Attribution Noncommercial License, which permits any non-commercial use, distribution, adaptationand reproduction provided the original author(s) and source are given appropriate credit. Received: June 17, 2015 Accepted July 16, 2015 Cor Continue reading >>

[full Text] Hypoglycemic Agents And Potential Anti-inflammatory Activity | Jir

[full Text] Hypoglycemic Agents And Potential Anti-inflammatory Activity | Jir

Editor who approved publication: Dr Ning Quan Vishal Kothari,1 John A Galdo,2 Suresh T Mathews3 1Department of Nutrition and Dietetics, Boshell Diabetes and Metabolic Diseases Research Program, Auburn University, Auburn, 2Department of Pharmacy Practice, 3Department of Nutrition and Dietetics, Samford University, Birmingham, AL, USA Abstract: Current literature shows an association of diabetes and secondary complications with chronic inflammation. Evidence of these immunological changes include altered levels of cytokines and chemokines, changes in the numbers and activation states of various leukocyte populations, apoptosis, and fibrosis during diabetes. Therefore, treatment of diabetes and its complications may include pharmacological strategies to reduce inflammation. Apart from anti-inflammatory drugs, various hypoglycemic agents have also been found to reduce inflammation that could contribute to improved outcomes. Extensive studies have been carried out with thiazolidinediones (peroxisome proliferator-activated receptor- agonist), dipeptidyl peptidase-4 inhibitors, and metformin (AMP-activated protein kinase activator) with each of these classes of compounds showing moderate-to-strong anti-inflammatory action. Sulfonylureas and alpha glucosidase inhibitors appeared to exert modest effects, while the injectable agents, insulin and glucagon-like peptide-1 receptor agonists, may improve secondary complications due to their anti-inflammatory potential. Currently, there is a lack of clinical data on anti-inflammatory effects of sodiumglucose cotransporter type 2 inhibitors. Nevertheless, for all these glucose-lowering agents, it is essential to distinguish between anti-inflammatory effects resulting from better glucose control and effects related to intrinsic anti-inf Continue reading >>

Inflammation And Oxidative Stress In Cardiac Surgery Patients Treated To Intensive Versus Conservative Glucose Targets

Inflammation And Oxidative Stress In Cardiac Surgery Patients Treated To Intensive Versus Conservative Glucose Targets

The Journal of Clinical Endocrinology & Metabolism Inflammation and Oxidative Stress in Cardiac Surgery Patients Treated to Intensive Versus Conservative Glucose Targets Search for other works by this author on: Joseph B. Whitehead Department of Surgery, Emory University, Atlanta, Georgia 30303 Search for other works by this author on: Joseph B. Whitehead Department of Surgery, Emory University, Atlanta, Georgia 30303 Search for other works by this author on: Joseph B. Whitehead Department of Surgery, Emory University, Atlanta, Georgia 30303 Search for other works by this author on: The Journal of Clinical Endocrinology & Metabolism, Volume 102, Issue 1, 1 January 2017, Pages 309315, David Reyes-Umpierrez, Georgia Davis, Saumeth Cardona, Francisco J. Pasquel, Limin Peng, Sol Jacobs, Priyathama Vellanki, Maya Fayfman, Sonya Haw, Michael Halkos, Robert A. Guyton, Vinod H. Thourani, Guillermo E. Umpierrez; Inflammation and Oxidative Stress in Cardiac Surgery Patients Treated to Intensive Versus Conservative Glucose Targets, The Journal of Clinical Endocrinology & Metabolism, Volume 102, Issue 1, 1 January 2017, Pages 309315, We aimed to determine (a) longitudinal changes of inflammatory and oxidative stress markers and (b) the association between markers of inflammation and perioperative complications in coronary artery bypass surgery (CABG) patients treated with intensive vs conservative blood glucose (BG) control. Patients with diabetes (n = 152) and without diabetes with hyperglycemia (n = 150) were randomized to intensive (n = 151; BG: 100140 mg/dL) or to conservative (n = 151; BG: 141180 mg/dL) glycemic targets. Plasma cortisol, high-sensitivity C-reactive protein (hsCRP), tumor necrosis factor-, interleukin-6 (IL-6), thiobarbituric acid-reactive substances, and 2-7- Continue reading >>

The Effect Of Various Intake Levels Of Soybean Oil On Blood Glucose And Inflammation In Mice

The Effect Of Various Intake Levels Of Soybean Oil On Blood Glucose And Inflammation In Mice

The effect of various intake levels of soybean oil on blood glucose and inflammation in mice ?Mathematical formulae have been encoded as MathML and are displayed in this HTML version using MathJax in order to improve their display. Uncheck the box to turn MathJax off. This feature requires Javascript. Click on a formula to zoom. The effects of various intake levels of soybean oil on carbohydrate metabolism and inflammation in mice were studied. Mice were supplied with different diets, in which soybean oil provided 5, 10, 15, 20, 25, and 30% of total energy. Blood glucose indices, blood fat indices, inflammatory factors, and gene expression of insulin receptor substrates 1 and 2 Insulin receptor substrate 1 (IRS1) and Insulin receptor substrate 2 (IRS2) were analyzed. The results showed that higher intake of soybean oil can lead to excessive weight gain, higher levels of fasting blood glucose and serum insulin, increased levels of tumor necrosis factor-, interleukin 6, hyper-sensitive C-reactive protein, and reduced expression of IRS1 and IRS2 mRNA. Primarily, we found that reduced intake of soybean oil led to a similar trend to that of a high soybean oil diet. The optimal intake of soybean oil, as supplied in the diet, was about 1520%. KEYWORDS: Soybean oil , intake , fasting blood glucose , inflammatory factors Metabolic syndrome comprises a mix of symptoms of interrelated risk factors of metabolic origin that have been proven to predict a higher risk of obesity, high blood pressure, atherosclerotic cardiovascular disease, as well as type II diabetes mellitus (Goulart etal., 2017 ; Imran etal., 2017 ). In comparison to people without metabolic syndrome, the risk of chronic diseases, such as cancer, cardiovascular disease, type II diabetes, and chronic inflammation is Continue reading >>

Direct Relationship Between Inflammation And Glucose Levels

Direct Relationship Between Inflammation And Glucose Levels

Scientists at Galileo Pharmaceuticals, Inc. have demonstrated a direct relationship between inflammation and glucose levels. Through its recently established metabolic disease program, Galileo confirmed in preclinical models that inhibiting lipoxygenases, known mediators of inflammatory response, significantly lowers blood glucose levels in animal models of diabetes. "Metabolic disease is a health concern of near-epidemic proportions, particularly in the US," said Lloyd M. Kunimoto, president and chief executive officer of Galileo Pharmaceuticals, Inc. "We are encouraged by our initial study, which confirms the role of inflammation in the regulation of carbohydrate and lipid metabolism, and validates our proprietary drug discovery platform using Conserved Inflammatory Pathway (CIP) modulators to treat a wide variety of important diseases such as asthma, arthritis, diabetes, and other diseases mediated by inflammation." In a paper presented today at the Therapeutic Approaches to Obesity and Related Disorders conference in Washington DC, Galileo scientists demonstrated that administration of a proprietary dual 5- and 15-lipoxygenase inhibitor reduced resting glucose levels by approximately 20% in the db/db mouse model of diabetes without affecting insulin levels. This compares favorably with the reduction obtained by the administration of rosiglitazone, a widely-prescribed treatment for type 2 diabetes that acts by sensitizing cells to insulin. Additional presentation of these data will be made in October at SMi's 7th Annual Diabetes meeting in London. "Our goals are to identify novel mechanisms for controlling glucose levels via the regulation of inflammatory processes, and to develop drug candidates that are based on these mechanisms," said David Liebowitz, MD, PhD, chi Continue reading >>

Diabetes And Inflammation

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 >>

Stress Hyperglycemia: An Essential Survival Response!

Stress Hyperglycemia: An Essential Survival Response!

In 1878, Claude Bernard described hyperglycemia during hemorrhagic shock [1]; and it is now well known that acute illness or injury may result in hyperglycemia, insulin resistance and glucose intolerance, collectively termed stress hyperglycemia. Numerous studies in both ICU and hospitalized non-ICU patients have demonstrated a strong association between stress hyperglycemia and poor clinical outcomes, including mortality, morbidity, length of stay, infections and overall complications [2–5]. This association is well documented for both the admission as well as the mean glucose level during the hospital stay. Based on these data clinicians, researchers and policy makers have assumed this association to be causal with the widespread adoption of protocols and programs for tight or intensive in-hospital glycemic control. However, a critical appraisal of the data has consistently demonstrated that attempts at intensive glycemic control in both ICU and non-ICU patients do not improve health care outcomes [6–8]. Indeed, NICE-SUGAR, a large randomized, multi-center trial performed in 6,104 ICU patients, demonstrated that intensive glucose control (81 to 108 mg/dl) increased mortality when compared to conventional glucose control [9]. Although NICE-SUGAR targeted a blood glucose between 144 and 180 mg/dL, there is no evidence that targeting an even more tolerant level between 180 and 220 mg/dL would not, in fact, have been better (or worse). This information suggests that the degree of hyperglycemia is related to the severity of the disease and is an important prognostic marker. This is, however, not a cause and effect relationship. Indeed, Green and colleagues [10] demonstrated that hyperglycemia was not predictive of mortality in non-diabetic adults with sepsis after corr Continue reading >>

The Hyperglycemia-induced Inflammatory Response In Adipocytes

The Hyperglycemia-induced Inflammatory Response In Adipocytes

The Hyperglycemia-induced Inflammatory Response in Adipocytes Departments of Cell Biology, Pathology, and **Medicine, and the Diabetes Research and Training Center, Albert Einstein College of Medicine, Bronx, New York 10461, the Departments of Medicine and Physiology and Banting and Best Diabetes Center, University of Toronto, Toronto, Ontario M5G 1X5, Canada, the ABR-Affinity BioReagents, Golden, Colorado 80403, and the Pacific Northwest Research Institute and Department of Pharmacology, University of Washington, Seattle, Washington 98122 To whom correspondence should be addressed. Tel.: 718-430-2928; Fax: 718-430-8574; E-mail: scherer{at}aecom.yu.edu. Hyperglycemia is a major independent risk factor for diabetic macrovascular disease. The consequences of exposure of endothelial cells to hyperglycemia are well established. However, little is known about how adipocytes respond to both acute as well as chronic exposure to physiological levels of hyperglycemia. Here, we analyze adipocytes exposed to hyperglycemia both in vitro as well as in vivo. Comparing cells differentiated at 4 mm to cells differentiated at 25 mm glucose (the standard differentiation protocol) reveals severe insulin resistance in cells exposed to 25 mm glucose. A global assessment of transcriptional changes shows an up-regulation of a number of mitochondrial proteins. Exposure to hyperglycemia is associated with a significant induction of reactive oxygen species (ROS), both in vitro as well as in vivo in adipocytes isolated from streptozotocin-treated hyperglycemic mice. Furthermore, hyperglycemia for a few hours in a clamped setting will trigger the induction of a pro-inflammatory response in adipose tissue from rats that can effectively be reduced by co-infusion of N-acetylcysteine (NAC). ROS level Continue reading >>

Diabetes And Infection: Is There A Link? €“ A Mini-review

Diabetes And Infection: Is There A Link? €“ A Mini-review

Fax +41 61 306 12 34 E-Mail [email protected] www.karger.com Clinical Section / Mini-Review Gerontology 2013;59:99–104 DOI: 10.1159/000345107 Sylvia Knapp Center for Molecular Medicine of the Austrian Academy of Sciences, and Division of Infectious Diseases and Tropical Medicine, Department of Medicine 1, Medical University of Vienna, Vienna , Austria Diabetes mellitus is one of the leading causes of mor- bidity worldwide and is anticipated to rise substantially over the next decades. While type 2 diabetes used to be mainly a disease of the elderly, early-onset diabetes is increasingly diagnosed in young adults in industrial- ized countries. In 2011, the diabetes incidence was re- ported to be 26.9% for people older than 65 years in the USA and as high as 11.3% for people older than 20 years [1] . Since Western diet and obesity are spreading rap- idly around the globe, the number of young diabetic in- dividuals is anticipated to further increase in the near future. Diabetes is associated with several complications, in- cluding vascular diseases and renal failure, that ultimate- ly impact the overall survival of these patients. It is fur- thermore a common belief that people with diabetes are generally more susceptible to infections. The difficulties associated with estimating the actual risk of infection in diabetic patients are mainly due to the fact that diabetes is not solely a disturbance of glucose metabolism but in- stead a chronic inflammatory condition characterized by multiple alterations in lipid profiles and neuropathy as well as chronic vascular and renal diseases, with each of these changes having been reported to alter the response to pathogens. Therefore, it seems near impossible to con- Key Words Diabetes � Infection � Neutrophil function Continue reading >>

Diabetes Prolongs The Inflammatory Response To A Bacterial Stimulus Through Cytokine Dysregulation - Sciencedirect

Diabetes Prolongs The Inflammatory Response To A Bacterial Stimulus Through Cytokine Dysregulation - Sciencedirect

Volume 123, Issue 1 , July 2004, Pages 87-92 Author links open overlay panel GhadaNaguib HeshamAl-Mashat TesfahunDesta Dana T.Graves Diabetes has been identified as an important risk factor for infection. But relatively little is known about how diabetes alters the inflammatory response to bacteria. The objective of this study was to investigate how diabetes affects hostbacteria interactions by focusing on the inflammatory response in a connective tissue setting. Diabetic (db/db) and control (db/+) mice were inoculated with Porphyromonas gingivalis, a pathogen associated with bite wounds and periodontal disease. The response was measured histologically or by the expression of inflammatory cytokines. By quantitative histologic analysis, there was little difference between the diabetic and control mice on day 1. On day 3, however, the inflammatory infiltrate had subsided in the control group, whereas it had not in the diabetic group (p<0.05). Similar results were noted at the molecular level by the persistent expression of tumor necrosis factor- (TNF-) and the chemokines MCP-1 and MIP-2. The importance of TNF in this process was demonstrated by reversal of the prolonged chemokine expression by specific inhibition of TNF with Enbrel. These results indicate that cytokine dysregulation associated with prolonged TNF expression represents a mechanism through which bacteria may induce a more damaging inflammatory response in diabetic individuals. Continue reading >>

Profile Of The Immune And Inflammatory Response In Individuals With Prediabetes And Type 2 Diabetes

Profile Of The Immune And Inflammatory Response In Individuals With Prediabetes And Type 2 Diabetes

OBJECTIVE The inflammatory and immune systems are altered in type 2 diabetes. Here, the aim was to profile the immune and inflammatory response in subjects with prediabetes and diabetes in a large population-representative sample. RESEARCH DESIGN AND METHODS In total, 15,010 individuals were analyzed from the population-based Gutenberg Health Study. Glucose status was classified according to HbA1c concentration and history of diagnosis. All samples were analyzed for white blood cells (WBCs), granulocytes, lymphocytes, monocytes, platelets, C-reactive protein (CRP), albumin, fibrinogen, and hematocrit. Interleukin-18 (IL-18), IL-1 receptor antagonist (IL-1RA), and neopterin concentrations were determined in a subcohort. RESULTS In total, 7,584 men and 7,426 women were analyzed (range 35–74 years), with 1,425 and 1,299 having prediabetes and diabetes, respectively. Biomarkers showed varying dynamics from normoglycemic via subjects with prediabetes to subjects with diabetes: 1) gradual increase (WBCs, granulocytes, monocytes, IL-1RA, IL-18, and fibrinogen), 2) increase with subclinical disease only (lymphocytes and CRP), 3) increase from prediabetes to diabetes only (neopterin), and 4) no variation with glucose status (hematocrit). The strongest relative differences were found for CRP, IL-1RA, and fibrinogen concentrations. Several inflammatory and immune markers were associated with the glucose status independent from cardiovascular risk factors and comorbidities, varied with disease severity and the presence of disease-specific complications in the diabetes subcohort. CONCLUSIONS The inflammatory and immune biomarker profile varies with the development and progression of type 2 diabetes. Markers of inflammation and immunity enable differentiation between the early prec Continue reading >>

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