Low-grade inflammation in insulin resistance associates with bacterial load in adipose tissue

2019 ◽  
Author(s):  
S Tabei ◽  
L Scheffler ◽  
R Chakaroun ◽  
S Ziesche ◽  
A Crane ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Adipose Tissue ◽  
Bacterial Load ◽  
Low Grade ◽  
Low Grade Inflammation

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 Adipose tissue macrophages in aging-associated adipose tissue function

2021 ◽  
Vol 71 (1) ◽  
Author(s):  
Bangchao Lu ◽  
Liang Huang ◽  
Juan Cao ◽  
Lingling Li ◽  
Wenhui Wu ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Adipose Tissue ◽  
Therapeutic Targets ◽  
Visceral Adiposity ◽  
Low Grade ◽  
Recent Advances ◽  
Adipose Tissue Macrophages ◽  
Low Grade Inflammation

Abstract“Inflammaging” refers to the chronic, low-grade inflammation that characterizes aging. Aging, like obesity, is associated with visceral adiposity and insulin resistance. Adipose tissue macrophages (ATMs) have played a major role in obesity-associated inflammation and insulin resistance. Macrophages are elevated in adipose tissue in aging. However, the changes and also possibly functions of ATMs in aging and aging-related diseases are unclear. In this review, we will summarize recent advances in research on the role of adipose tissue macrophages with aging-associated insulin resistance and discuss their potential therapeutic targets for preventing and treating aging and aging-related diseases.

scholarly journals TIR-Domain-Containing Adaptor-Inducing Interferon-β (TRIF) Is Involved in Glucose Metabolism in Adipose Tissue through the Insulin/AKT Signaling Pathway

2020 ◽  
Vol 2020 ◽  
pp. 1-9
Author(s):  
Junling Yang ◽  
Ken-Ichiro Fukuchi
Keyword(s):  
Insulin Resistance ◽  
Adipose Tissue ◽  
Epididymal Adipose Tissue ◽  
Chow Diet ◽  
Low Grade ◽  
Interferon Β ◽  
Tlr Signaling ◽  
Normal Chow ◽  
Low Grade Inflammation

Obesity significantly increases the risk of developing type 2 diabetes mellitus and other metabolic diseases. Obesity is associated with chronic low-grade inflammation in white adipose tissues, which is thought to play an essential role in developing insulin resistance. Many lines of evidence indicate that toll-like receptors (TLRs) and their downstream signaling pathways are involved in development of chronic low-grade inflammation and insulin resistance, which are associated with obesity. Mice lacking molecules positively involved in the TLR signaling pathways are generally protected from high-fat diet-induced inflammation and insulin resistance. In this study, we have determined the effects of genetic deficiency of toll/interleukin-1 receptor-domain-containing adaptor-inducing interferon-β (TRIF) on food intake, bodyweight, glucose metabolism, adipose tissue macrophage polarization, and insulin signaling in normal chow diet-fed mice to investigate the role of the TRIF-dependent TLR signaling in adipose tissue metabolism and inflammation. TRIF deficiency (TRIF−/−) increased food intake and bodyweight. The significant increase in bodyweight in TRIF−/− mice was discernible as early as 24 weeks of age and sustained thereafter. TRIF−/− mice showed impaired glucose tolerance in glucose tolerance tests, but their insulin tolerance tests were similar to those in TRIF+/+ mice. Although no difference was found in the epididymal adipose mass between the two groups, the percentage of CD206+ M2 macrophages in epididymal adipose tissue decreased in TRIF−/− mice compared with those in TRIF+/+ mice. Furthermore, activation of epididymal adipose AKT in response to insulin stimulation was remarkably diminished in TRIF−/− mice compared with TRIF+/+ mice. Our results indicate that the TRIF-dependent TLR signaling contributes to maintaining insulin/AKT signaling and M2 macrophages in epididymal adipose tissue under a normal chow diet and provide new evidence that TLR4-targeted therapies for type 2 diabetes require caution.

Regulation of adipokine secretion byn-3 fatty acids

2010 ◽  
Vol 69 (3) ◽  
pp. 324-332 ◽  
Author(s):  
María J. Moreno-Aliaga ◽  
Silvia Lorente-Cebrián ◽  
J. Alfredo Martínez
Keyword(s):  
Insulin Resistance ◽  
Metabolic Syndrome ◽  
Fatty Acids ◽  
Adipose Tissue ◽  
Physiological Role ◽  
Low Grade ◽  
Protective Effects ◽  
Metabolic Disturbances ◽  
The Metabolic Syndrome ◽  
Low Grade Inflammation

Obesity leads to several chronic morbidities including type 2 diabetes, dyslipidaemia, atherosclerosis and hypertension, which are major components of the metabolic syndrome. White adipose tissue (WAT) metabolism and WAT-derived factors (fatty acids and adipokines) play an important role in the development of these metabolic disturbances. In fact, dysregulated adipokine secretion from the expanded WAT of obese individuals contributes to the development of systemic low-grade inflammation, insulin resistance and metabolic syndrome. Then-3 PUFA EPA and DHA have been widely reported to have protective effects in a range of chronic inflammatory conditions including obesity. In fact,n-3 PUFA have been shown to ameliorate low-grade inflammation in adipose tissue associated with obesity and up-regulate mitochondrial biogenesis and induce beta-oxidation in WAT in mice. Moreover, the ability ofn-3 PUFA to regulate adipokine gene expression and secretion has been observed bothin vitroandin vivoin rodents and human subjects. The present article reviews: (1) the physiological role of adiponectin, leptin and pre-B cell colony-enhancer factor/visfatin, three adipokines with immune-modulatory properties involved in the regulation of metabolism and insulin sensitivity and (2) the actions ofn-3 PUFA on these adipokines focusing on the underlying mechanisms and the potential relationship with the beneficial effects of these fatty acids on obesity-associated metabolic disorders. It can be concluded that the ability ofn-3 PUFA to improve obesity and insulin resistance conditions partially results from the modulation of WAT metabolism and the secretion of bioactive adipokines including leptin, adiponectin and visfatin.

scholarly journals Obesity, Bioactive Lipids, and Adipose Tissue Inflammation in Insulin Resistance

Nutrients ◽  
2020 ◽  
Vol 12 (5) ◽  
pp. 1305 ◽  
Author(s):  
Iwona Kojta ◽  
Marta Chacińska ◽  
Agnieszka Błachnio-Zabielska
Keyword(s):  
Insulin Resistance ◽  
Type 2 Diabetes ◽  
Adipose Tissue ◽  
Biologically Active ◽  
Bioactive Molecules ◽  
Low Grade ◽  
Bioactive Lipids ◽  
Chain Acyl ◽  
Low Grade Inflammation

Obesity is a major risk factor for the development of insulin resistance and type 2 diabetes. The exact mechanism by which adipose tissue induces insulin resistance is still unclear. It has been demonstrated that obesity is associated with the adipocyte dysfunction, macrophage infiltration, and low-grade inflammation, which probably contributes to the induction of insulin resistance. Adipose tissue synthesizes and secretes numerous bioactive molecules, namely adipokines and cytokines, which affect the metabolism of both lipids and glucose. Disorders in the synthesis of adipokines and cytokines that occur in obesity lead to changes in lipid and carbohydrates metabolism and, as a consequence, may lead to insulin resistance and type 2 diabetes. Obesity is also associated with the accumulation of lipids. A special group of lipids that are able to regulate the activity of intracellular enzymes are biologically active lipids: long-chain acyl-CoAs, ceramides, and diacylglycerols. According to the latest data, the accumulation of these lipids in adipocytes is probably related to the development of insulin resistance. Recent studies indicate that the accumulation of biologically active lipids in adipose tissue may regulate the synthesis/secretion of adipokines and proinflammatory cytokines. Although studies have revealed that inflammation caused by excessive fat accumulation and abnormalities in lipid metabolism can contribute to the development of obesity-related insulin resistance, further research is needed to determine the exact mechanism by which obesity-related insulin resistance is induced.

scholarly journals Adipokine inflammation and insulin resistance: the role of glucose, lipids and endotoxin

2012 ◽  
Vol 216 (1) ◽  
pp. T1-T15 ◽  
Author(s):  
M K Piya ◽  
P G McTernan ◽  
S Kumar
Keyword(s):  
Insulin Resistance ◽  
Adipose Tissue ◽  
Human Adipose Tissue ◽  
Dietary Factors ◽  
Positive Energy ◽  
Low Grade ◽  
Positive Energy Balance ◽  
Secretory Tissue ◽  
The Impact ◽  
Low Grade Inflammation

Adipose tissue is an active endocrine organ, and our knowledge of this secretory tissue, in recent years, has led us to completely rethink how our body functions and becomes dysregulated with weight gain. Human adipose tissue appears to act as a multifunctional secretory organ with the capacity to control energy homoeostasis through peripheral and central regulation of energy homoeostasis. It also plays an important role in innate immunity. However, the capability to more than double its original mass to cope with positive energy balance in obesity leads to many pathogenic changes. These changes arise within the adipose tissue as well as inducing secondary detrimental effects on other organs like muscle and liver, including chronic low-grade inflammation mediated by adipocytokines (adipokine inflammation). This inflammation is modulated by dietary factors and nutrients including glucose and lipids, as well as gut bacteria in the form of endotoxin or LPS. The aim of this current review is to consider the impact of nutrients such as glucose and lipids on inflammatory pathways, specifically within adipose tissue. Furthermore, how nutrients such as these can influence adipokine inflammation and consequently insulin resistance directly through their effects on secretion of adipocytokines (TNFα, IL6 and resistin) as well as indirectly through increases in endotoxin is discussed.

Adipose tissue inflammation and insulin resistance: all obese humans are not created equal

2010 ◽  
Vol 430 (2) ◽  
pp. e1-e4 ◽  
Author(s):  
Marie-Soleil Gauthier ◽  
Neil B. Ruderman
Keyword(s):  
Insulin Resistance ◽  
Adipose Tissue ◽  
Obese Individual ◽  
Low Grade ◽  
Key Factors ◽  
Insulin Resistant ◽  
The Metabolic Syndrome ◽  
Biochemical Journal ◽  
Visceral Adipose ◽  
Low Grade Inflammation

In recent years, it has become widely accepted that obesity is characterized by a chronic low-grade inflammation of adipose tissue that predisposes affected individuals to insulin resistance, Type 2 diabetes and other disorders associated with the metabolic syndrome. On the other hand, a subset of obese individuals appears to be protected against insulin resistance and the disorders to which it predisposes. The comparison between such insulin-sensitive and insulin-resistant obese individuals offers a unique opportunity to identify key factors that either contribute to or prevent the development of insulin resistance in humans, without the confounding effect of a major difference in fat mass. In the previous issue of the Biochemical Journal, Barbarroja et al. reported that insulin-sensitive obese individuals show less inflammation in their visceral adipose tissue than a group of insulin-resistant subjects matched for BMI (body mass index). This finding reinforces the concept that inflammation in adipose tissue may be a cause of insulin resistance in most obese individuals, although it does not prove it. Further studies will be required for this purpose, as well as to identify the pathogenetic factors that determine whether or not adipose tissue of an obese individual becomes inflamed.

scholarly journals NK cells in human visceral adipose tissue contribute to obesity‐associated insulin resistance through low‐grade inflammation

2020 ◽  
Vol 10 (6) ◽  
Author(s):  
Kristiaan Wouters ◽  
Yvo H.A.M. Kusters ◽  
Mitchell Bijnen ◽  
Suzan Wetzels ◽  
Xiaodi Zhang ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Adipose Tissue ◽  
Nk Cells ◽  
Visceral Adipose Tissue ◽  
Low Grade ◽  
Visceral Adipose ◽  
Low Grade Inflammation
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