scholarly journals Study of TNF-α, IL-6 and Insulin Resistance in Type 2 Diabetes Mellitus at Vidharbha Region

2021 ◽  
pp. 534-539
Author(s):  
Ankita Kondhalkar ◽  
Rajan Barokar ◽  
Prajakta Warjukar ◽  
Roshan Kumar Jha
Keyword(s):  
Insulin Resistance ◽  
Diabetic Patients ◽  
Low Grade ◽  
Immunological Parameters ◽  
Insulin Synthesis ◽  
Immunological Markers ◽  
Chronic Hyperglycemia ◽  
Hematological Markers ◽  
Tnf Α ◽  
Low Grade Inflammation

Background: DM is a metabolic condition caused by deficiencies in insulin synthesis, insulin action, or both. It is characterised by chronic hyperglycemia and glycosuria, as well as abnormalities in carbohydrate, fat, and protein metabolism. Diabetes and its complications are believed to be caused by a variety of causes. Genetics, diet, sedentary lifestyle, perinatal causes, age, and obesity are among them.  The relationship and interaction of various risk factors with disease severity is still unknown, so the aim of the proposed study was to determine the possible relationship between biochemical markers glycosylated haemoglobin, lipid profile, insulin resistance, and immunological markers TNF- and IL-6, in order to suggest appropriate measures to reduce the country's diabetes burden. Materials and Methods: A total of 300 people were chosen for the study after visiting Shalinitai Meghe hospital in Nagpur for a health check-up. The three groups were contained in this area. Results: Both biochemical and immunological parameters rose in managed diabetic patients and significantly increased in uncontrolled diabetic patients, according to the report, but values did not differ between groups 1. Conclusion: Low-grade inflammation and inflammatory mediator upregulation have been suggested to play a role in T2DM etiology. TNF- and IL-6 have a positive connection with T2DM and insulin sensitivity, according to our data. These can be used as T2DM biomarkers in the early stages of the disease. To help doctors monitor and treat T2DM successfully, more research on a larger spectrum of pro and anti-inflammatory cytokines (mediators) in conjunction with other biochemical, immunoassay, and hematological markers is needed.

IL-6 as a Surrogate Biomarker: The IL-6 Clinical Value for the Diagnosis of Insulin Resistance and Type 2 Diabetes.

2021 ◽  
pp. 1-13
Keyword(s):  
Insulin Resistance ◽  
Type 2 Diabetes ◽  
Molecular Mechanisms ◽  
Diagnostic Value ◽  
Low Grade ◽  
Clinical Value ◽  
Insulin Resistant ◽  
Tnf Α ◽  
Low Grade Inflammation

1. Abstract Insulin Resistance is the leading cause of Type 2 diabetes mellitus (T2D). It occurs as a result of lipid disorders and increased levels of circulating free fatty acids (FFAs). FFAs accumulate within the insulin sensitive tissues such as muscle, liver and adipose tissues exacerbating different molecular mechanisms. Increased levels fatty acid has been documented to be strongly associated with insulin resistant states and obesity causing inflammation that eventually causes type 2-diabetes. Among the biomarkers that are accompanying low grade inflammation include IL-1β, IL-6 and TNF-α. The current review point out the importance of measuring the inflammatory biomarkers especially focusing on the conductance and measurement for IL-6 as a screening laboratory test and its diagnostic value in clinical practice.

Angiotensin blockade in diabetic patients decreases insulin resistance-associated low-grade inflammation

2010 ◽  
Vol 41 (6) ◽  
pp. 652-658 ◽  
Author(s):  
Maria G. Pavlatou ◽  
George Mastorakos ◽  
Alexandra Margeli ◽  
Evangelia Kouskouni ◽  
Nicholas Tentolouris ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Diabetic Patients ◽  
Low Grade ◽  
Angiotensin Blockade ◽  
Low Grade Inflammation

scholarly journals The association between obesity and fluid intelligence impairment is mediated by chronic low-grade inflammation

2014 ◽  
Vol 112 (10) ◽  
pp. 1724-1734 ◽  
Author(s):  
Eirini C. Spyridaki ◽  
Panagiotis Simos ◽  
Pavlina D. Avgoustinaki ◽  
Eirini Dermitzaki ◽  
Maria Venihaki ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Fluid Intelligence ◽  
Leisure Time Physical Activity ◽  
Resistance Index ◽  
Low Grade ◽  
Model Assessment ◽  
Inverse Association ◽  
Published Evidence ◽  
Activity Measurements ◽  
Low Grade Inflammation

Published evidence suggests that obesity impairs cognition. Development of chronic low-grade inflammation (CLGI) represents the earliest consequence of obesity. The present study investigated the association between obesity and fluid intelligence impairment and assessed the potential mediating role of CLGI and psychological (depression/anxiety symptoms), lifestyle (exercise) and physiological (metabolic dysfunction indices) factors in this association. Clinically healthy participants (n 188), grouped as per BMI, underwent cognitive (General Ability Measure for Adults), psychological (Beck Depression Inventory-II and State-Trait Anxiety Inventory) and activity (Godin leisure-time physical activity) measurements. Biochemical parameters included the following: (a) indices of CLGI (high-sensitivity C-reactive protein, erythrocyte sedimentation rate and fibrinogen); (b) insulin resistance (Homeostasis Model Assessment of Insulin Resistance index); (c) adiposity (plasma adiponectin). An inverse association between elevated BMI and fluid intelligence was observed, with obese participants displaying significantly poorer performance compared with age-matched normal-weight peers. Structural equation modelling results were consistent with a negative impact of obesity on cognition that was mediated by CLGI. The results of the present study support the hypothesis that reduced general cognitive ability is associated with obesity, an adverse effect mainly mediated by obesity-associated activation of innate immunity.

scholarly journals Adipose tissue inflammation and metabolic dysfunction: a clinical perspective

2013 ◽  
Vol 15 (1) ◽  
Author(s):  
Charmaine S. Tam ◽  
Leanne M. Redman
Keyword(s):  
Insulin Resistance ◽  
Adipose Tissue ◽  
Low Grade ◽  
Metabolic Dysfunction ◽  
Adipose Tissue Inflammation ◽  
Tissue Inflammation ◽  
Proinflammatory Mediators ◽  
Low Grade Inflammation

AbstractObesity is characterized by a state of chronic low-grade inflammation due to increased immune cells, specifically infiltrated macrophages into adipose tissue, which in turn secrete a range of proinflammatory mediators. This nonselective low-grade inflammation of adipose tissue is systemic in nature and can impair insulin signaling pathways, thus, increasing the risk of developing insulin resistance and type 2 diabetes. The aim of this review is to provide an update on clinical studies examining the role of adipose tissue in the development of obesity-associated complications in humans. We will discuss adipose tissue inflammation during different scenarios of energy imbalance and metabolic dysfunction including obesity and overfeeding, weight loss by calorie restriction or bariatric surgery, and conditions of insulin resistance (diabetes, polycystic ovarian syndrome).

scholarly journals Osteopontin Expression in Human and Murine Obesity: Extensive Local Up-Regulation in Adipose Tissue but Minimal Systemic Alterations

Endocrinology ◽  
2007 ◽  
Vol 149 (3) ◽  
pp. 1350-1357 ◽  
Author(s):  
Florian W. Kiefer ◽  
Maximilian Zeyda ◽  
Jelena Todoric ◽  
Joakim Huber ◽  
René Geyeregger ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Adipose Tissue ◽  
Plasma Concentrations ◽  
Morbidly Obese ◽  
Low Grade ◽  
Obese Patients ◽  
Multifunctional Protein ◽  
Inflammatory Processes ◽  
Low Grade Inflammation

Obesity is associated with a chronic low-grade inflammation characterized by macrophage infiltration of adipose tissue (AT) that may underlie the development of insulin resistance and type 2 diabetes. Osteopontin (OPN) is a multifunctional protein involved in various inflammatory processes, cell migration, and tissue remodeling. Because these processes occur in the AT of obese patients, we studied in detail the regulation of OPN expression in human and murine obesity. The study included 20 morbidly obese patients and 20 age- and sex-matched control subjects, as well as two models (diet-induced and genetic) of murine obesity. In high-fat diet-induced and genetically obese mice, OPN expression was drastically up-regulated in AT (40 and 80-fold, respectively) but remained largely unaltered in liver (<2-fold). Moreover, OPN plasma concentrations remained unchanged in both murine models of obesity, suggesting a particular local but not systemic importance for OPN. OPN expression was strongly elevated also in the AT of obese patients compared with lean subjects in both omental and sc AT. In addition, we detected three OPN isoforms to be expressed in human AT and, strikingly, an obesity induced alteration of the OPN isoform expression pattern. Analysis of AT cellular fractions revealed that OPN is exceptionally highly expressed in AT macrophages in humans and mice. Moreover, OPN expression in AT macrophages was strongly up-regulated by obesity. In conclusion, our data point toward a specific local role of OPN in obese AT. Therefore, OPN could be a critical regulator in obesity induced AT inflammation and insulin resistance.

scholarly journals PCOS without hyperandrogenism is associated with higher plasma Trimethylamine N-oxide levels

2020 ◽  
Vol 20 (1) ◽  
Author(s):  
Jiayu Huang ◽  
Lin Liu ◽  
Chunyan Chen ◽  
Ying Gao
Keyword(s):  
Insulin Resistance ◽  
Polycystic Ovary ◽  
Predictive Biomarker ◽  
Normal Weight ◽  
Inflammatory Factors ◽  
Low Grade ◽  
Model Assessment ◽  
Increased Risk ◽  
Homeostatic Model Assessment ◽  
Low Grade Inflammation

Abstract Background Polycystic ovary syndrome (PCOS) is an endocrine and metabolic disorder, and its pathogenesis is still under debate. Trimethylamine-N-oxide (TMAO) is a small, organic compound generated by the gut microbiome with a hypothesized relation to insulin resistance (IR) and low-grade inflammation in PCOS. By comparing plasma TMAO levels in non-PCOS participants and PCOS patients without hyperandrogenism (HA), we aimed to determine whether plasma TMAO levels correlate with PCOS without HA and to analyze their relationship with low-grade inflammation and IR. Methods A total of 27 PCOS patients without HA and 23 non-PCOS participants were enrolled in this study and subdivided into “nonobese” and “obese” arms for each group. Levels of plasma TMAO were quantified, and basic clinical characteristics and plasma biomarkers of inflammation were assessed. Results First, plasma TMAO levels, insulin levels and homeostatic model assessment of insulin resistance (HOMA-IR) values were higher in PCOS patients without HA, especially in the obese subgroup. Second, the levels of the inflammatory factors interleukin (IL)-17A, IL-18 and interferon gamma (IFN-γ) were significantly increased in obese PCOS patients without HA. Third, plasma TMAO levels were associated with body mass index (BMI) in the normal-weight groups, and the obese groups had higher fasting plasma insulin (FINS) and HOMA-IR values. Finally, logistic regression showed that the plasma levels of TMAO and luteinizing hormone/follicle-stimulating hormone (LH/FSH) were independent predictors of PCOS and indicated an increased risk of PCOS. Conclusions Elevated plasma TMAO levels may be associated with the pathogenesis of PCOS without HA and correlated with increased systemic inflammation. Further studies are needed to determine the suitability of TMAO as a predictive biomarker and to identify possible therapies for PCOS.

Difficulty in Improving Malnutrition and Low-grade Inflammation in Diabetic Patients on Peritoneal Dialysis

2008 ◽  
Vol 12 (6) ◽  
pp. 475-483 ◽  
Author(s):  
Sung-Won Park ◽  
Jung-Ju Seo ◽  
Ho-Sang Bae ◽  
Jong-Yeon Kim ◽  
Chan-Duck Kim ◽  
...  
Keyword(s):  
Peritoneal Dialysis ◽  
Diabetic Patients ◽  
Low Grade ◽  
Low Grade Inflammation
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