scholarly journals Toll-like receptor 5 in obesity: The role of gut microbiota and adipose tissue inflammation

Obesity ◽  
2015 ◽  
Vol 23 (3) ◽  
pp. 581-590 ◽  
Author(s):  
Satu Pekkala ◽  
Eveliina Munukka ◽  
Lingjia Kong ◽  
Eija Pöllänen ◽  
Reija Autio ◽  
...  
Keyword(s):  
Adipose Tissue ◽  
Gut Microbiota ◽  
Adipose Tissue Inflammation ◽  
Toll Like Receptor ◽  
Tissue Inflammation ◽  
Toll Like Receptor 5

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 The role of glucose-6-phosphate dehydrogenase in adipose tissue inflammation in obesity

Adipocyte ◽  
2017 ◽  
Vol 6 (2) ◽  
pp. 147-153 ◽  
Author(s):  
Yoon Jeong Park ◽  
Sung Sik Choe ◽  
Jee Hyung Sohn ◽  
Jae Bum Kim
Keyword(s):  
Adipose Tissue ◽  
Adipose Tissue Inflammation ◽  
Tissue Inflammation ◽  
Glucose 6 Phosphate Dehydrogenase

scholarly journals Toll-like receptor 4 (TLR4) deficient mice are protected from adipose tissue inflammation in aging

Aging ◽  
2017 ◽  
Vol 9 (9) ◽  
pp. 1971-1982 ◽  
Author(s):  
Amiya K. Ghosh ◽  
Martin O’Brien ◽  
Theresa Mau ◽  
Raymond Yung
Keyword(s):  
Adipose Tissue ◽  
Adipose Tissue Inflammation ◽  
Toll Like Receptor ◽  
Toll Like Receptor 4 ◽  
Tissue Inflammation ◽  
Deficient Mice

scholarly journals The role of uncoupling protein 2 in macrophages and its impact on obesity-induced adipose tissue inflammation and insulin resistance

2020 ◽  
Vol 295 (51) ◽  
pp. 17535-17548
Author(s):  
Xanthe A. M. H. van Dierendonck ◽  
Tiphaine Sancerni ◽  
Marie-Clotilde Alves-Guerra ◽  
Rinke Stienstra
Keyword(s):  
Insulin Resistance ◽  
Adipose Tissue ◽  
Macrophage Activation ◽  
Uncoupling Protein ◽  
Uncoupling Protein 2 ◽  
Adipose Tissue Inflammation ◽  
Tissue Inflammation ◽  
Obesity And Diabetes ◽  
Adipose Tissue Macrophages

The development of a chronic, low-grade inflammation originating from adipose tissue in obese subjects is widely recognized to induce insulin resistance, leading to the development of type 2 diabetes. The adipose tissue microenvironment drives specific metabolic reprogramming of adipose tissue macrophages, contributing to the induction of tissue inflammation. Uncoupling protein 2 (UCP2), a mitochondrial anion carrier, is thought to separately modulate inflammatory and metabolic processes in macrophages and is up-regulated in macrophages in the context of obesity and diabetes. Here, we investigate the role of UCP2 in macrophage activation in the context of obesity-induced adipose tissue inflammation and insulin resistance. Using a myeloid-specific knockout of UCP2 (Ucp2ΔLysM), we found that UCP2 deficiency significantly increases glycolysis and oxidative respiration, both unstimulated and after inflammatory conditions. Strikingly, fatty acid loading abolished the metabolic differences between Ucp2ΔLysM macrophages and their floxed controls. Furthermore, Ucp2ΔLysM macrophages show attenuated pro-inflammatory responses toward Toll-like receptor-2 and -4 stimulation. To test the relevance of macrophage-specific Ucp2 deletion in vivo, Ucp2ΔLysM and Ucp2fl/fl mice were rendered obese and insulin resistant through high-fat feeding. Although no differences in adipose tissue inflammation or insulin resistance was found between the two genotypes, adipose tissue macrophages isolated from diet-induced obese Ucp2ΔLysM mice showed decreased TNFα secretion after ex vivo lipopolysaccharide stimulation compared with their Ucp2fl/fl littermates. Together, these results demonstrate that although UCP2 regulates both metabolism and the inflammatory response of macrophages, its activity is not crucial in shaping macrophage activation in the adipose tissue during obesity-induced insulin resistance.

scholarly journals A Novel Combination of Fruits and Vegetables Prevents Diet-Induced Hepatic Steatosis and Metabolic Dysfunction in Mice

2020 ◽  
Vol 150 (11) ◽  
pp. 2950-2960
Author(s):  
Weimin Guo ◽  
Dayong Wu ◽  
Maria C Dao ◽  
Lijun Li ◽  
Erin D Lewis ◽  
...  
Keyword(s):  
Adipose Tissue ◽  
Weight Gain ◽  
Gut Microbiota ◽  
Hepatic Steatosis ◽  
Fruits And Vegetables ◽  
Causal Relation ◽  
Adipose Tissue Inflammation ◽  
Tissue Inflammation ◽  
Freeze Dried ◽  
Underlying Mechanisms

ABSTRACT Background Epidemiological studies suggest that higher fruits and vegetables (F&V) consumption correlates with reduced risk of hepatic steatosis, yet evidence for causality and the underlying mechanisms is lacking. Objectives We aimed to determine the causal relation between F&V consumption and improved metabolic disorders in mice fed high-fat (HF) (Experiment-1) or normal-fat (Experiment-2) diets and its underlying mechanisms. Methods Six-week-old male C57BL/6J mice were randomly grouped and fed diets supplemented at 0%–15% (wt:wt) with a freeze-dried powder composed of 24 commonly consumed F&V (human equivalent of 0–9 servings/d) for 20 wk. In Experiment-1, mice were fed an HF (45% kcal fat) diet with 0% (HF0), 5%, 10%, or 15% (HF15) F&V or a matched low-fat control diet (10% kcal fat). In Experiment-2, mice were fed an AIN-93 diet (basal) (B, 16% kcal fat) with 0% (B0), 5%, 10%, or 15% (B15) F&V supplementation. Body weight and composition, food intake, hepatic steatosis, inflammation, ceramide levels, sphingomyelinase activity, and gut microbiota were assessed. Results In Experiment-1, mice fed the HF15 diet had lower weight gain (17.9%), hepatic steatosis (48.4%), adipose tissue inflammation, blood (24.6%) and liver (33.9%) ceramide concentrations, and sphingomyelinase activity (38.8%) than HF0 mice (P < 0.05 for all). In Experiment-2, mice fed the B15 diet had no significant changes in weight gain but showed less hepatic steatosis (28.5%), blood and adipose tissue inflammation, and lower blood (30.0%) ceramide concentrations than B0 mice (P < 0.05 for all). These F&V effects were associated with favorable microbiota changes. Conclusions These findings represent the first evidence for a causal role of high F&V intake in mitigating hepatic steatosis in mice. These beneficial effects may be mediated through changes in ceramide and/or gut microbiota, and suggest that higher than currently recommended servings of F&V may be needed to achieve maximum health benefits.

scholarly journals Targeted disruption of the iNOS gene improves adipose tissue inflammation and fibrosis in leptin-deficient ob/ob mice: role of tenascin C

2018 ◽  
Vol 42 (8) ◽  
pp. 1458-1470 ◽  
Author(s):  
S Becerril ◽  
A Rodríguez ◽  
V Catalán ◽  
L Méndez-Giménez ◽  
B Ramírez ◽  
...  
Keyword(s):  
Adipose Tissue ◽  
Adipose Tissue Inflammation ◽  
Targeted Disruption ◽  
Tissue Inflammation ◽  
Tenascin C ◽  
Inos Gene

Role of A 1 and A 2A adenosine receptor agonists in adipose tissue inflammation induced by obesity in mice

2017 ◽  
Vol 799 ◽  
pp. 154-159 ◽  
Author(s):  
Caroline Candida DeOliveira ◽  
Cintia Rabelo e Paiva Caria ◽  
Erica Martins Ferreira Gotardo ◽  
Marcelo Lima Ribeiro ◽  
Alessandra Gambero
Keyword(s):  
Adipose Tissue ◽  
Adenosine Receptor ◽  
Adipose Tissue Inflammation ◽  
Adenosine Receptor Agonists ◽  
Tissue Inflammation ◽  
Receptor Agonists ◽  
Obesity In Mice

Role of the intestinal vitamin D receptor in obesity, adipose tissue inflammation and hepatic lipid accumulation

2017 ◽  
Vol 66 (1) ◽  
pp. S168
Author(s):  
D. Jahn ◽  
D. Dorbath ◽  
A.-K. Schilling ◽  
L. Gildein ◽  
J. Schmitt ◽  
...  
Keyword(s):  
Vitamin D ◽  
Adipose Tissue ◽  
Vitamin D Receptor ◽  
Lipid Accumulation ◽  
Adipose Tissue Inflammation ◽  
Tissue Inflammation ◽  
Hepatic Lipid ◽  
Hepatic Lipid Accumulation

scholarly journals Adipocyte-Derived Lactate Potentiates Obesity-Evoked Adipose Macrophage Inflammation

2021 ◽  
Vol 5 (Supplement_1) ◽  
pp. A40-A41
Author(s):  
Xiaoyan Hannah Hui ◽  
Tianshi Feng
Keyword(s):  
Adipose Tissue ◽  
Lactate Level ◽  
Macrophage Polarization ◽  
Lactate Production ◽  
Physiological Role ◽  
Adipose Tissue Inflammation ◽  
Tissue Inflammation ◽  
Adipose Inflammation

Abstract Introduction: Obesity is characterized by mobilization of macrophage inflammation, which represents the major events of obesity-associated adipose tissue inflammation. . On the other hand, lactate accumulation in adipose tissue long been observed. However, whether elevation of lactate plays an essential role in adipose inflammation is not known. In this study, we sought to examine the intermediary role of lactate in macrophage polarization and adipose inflammation upon obesity. Method: Lactate level and activity of lactate dehydrogense (LDH), the key enzyme of lactate production, were measured by biochemical assays. Adipocyte- and macrophage- specific Ldha knock out mice were constructed by cre-LoxP system to study the physiological role of lactate in diet induced obesity. Macrophage polarization and inflammation were examined by western blotting and Q-PCR. Results: Lactate and LDH activity were selectively upregulated in adipose tissues of obese mice. Adipocyte-, but not macrophage-selective deletion of LDHA, led to a significant improvement of adipose inflammation and metabolic dysfunctions. In vitro experiments showed that the lactate promoted M1 polarization through direct interation and inhibition of the PHD2, which subsequently stabilizes HIF-1alpha. In addition, a positive correlation between adipose lactate level and adipose tissue inflammation was found in obese patients. Conclusion: In obese condition, increased production of lactate from adipocytes enhances adipose tissue inflammation by promoting the proinflammatory polarization of adipose macrophages.

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