MiR-130b promotes obesity associated adipose tissue inflammation and insulin resistance in diabetes mice through alleviating M2 macrophage polarization via repression of PPAR-γ

2016 ◽  
Vol 180 ◽  
pp. 1-8 ◽  
Author(s):  
Min Zhang ◽  
Zhongqi Zhou ◽  
Jinguang Wang ◽  
Shufa Li
Keyword(s):  
Insulin Resistance ◽  
Adipose Tissue ◽  
Macrophage Polarization ◽  
M2 Macrophage ◽  
Adipose Tissue Inflammation ◽  
Tissue Inflammation ◽  
Ppar Γ ◽  
Diabetes Mice ◽  
M2 Macrophage Polarization

scholarly journals Role of RAGE in obesity-induced adipose tissue inflammation and insulin resistance

2021 ◽  
Vol 7 (1) ◽  
Author(s):  
Ziqian Feng ◽  
Zuoqin Du ◽  
Xin Shu ◽  
Luochen Zhu ◽  
Jiaqi Wu ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Adipose Tissue ◽  
Insulin Signaling ◽  
Macrophage Polarization ◽  
Chow Diet ◽  
Cell Trafficking ◽  
Adipose Tissue Inflammation ◽  
Blood Monocytes ◽  
Adipose Tissues ◽  
Tissue Inflammation

AbatractObesity is known to be associated with adipose tissue inflammation and insulin resistance. Importantly, in obesity, the accumulation of proinflammatory macrophages in adipose tissue correlates with insulin resistance. We hypothesized that the receptor for advanced glycation end products (RAGE) and associated ligands are involved in adipose tissue insulin resistance, and that the activation of the AGE–RAGE axis plays an important role in obesity-associated inflammation. C57BL/6J mice (WT) and RAGE deficient (RAGE−/−) mice were fed a high fat diet (HFD) and subjected to glucose and insulin tolerance tests. Epdidymal adipose tissue (eAT) was collected and adipose stromal vascular cells isolated using flow cytometry. Visceral adipose tissue macrophage polarization was assessed by quantitative real time PCR. Immunoblotting was performed to evaluate the insulin signaling in adipose tissues. In additional studies, cell trafficking was assessed by injecting labeled blood monocytes into recipient mice. RAGE−/− mice displayed improved insulin sensitivity and glucose tolerance, accompanied by decreased body weight and eAT mass. Exogenous methylglyoxal (MGO) impaired insulin-stimulated AKT signaling in adipose tissues from WT mice fed a normal chow diet, but not in RAGE−/− mice. In contrast, in obese mice, treatment with MGO did not reduce insulin-induced phosphorylation of AKT in WT-HFD mice. Moreover, insulin-induced AKT phosphorylation was found to be impaired in adipose tissue from RAGE−/−-HFD mice. RAGE−/− mice displayed improved inflammatory profiles and evidence for increased adipose tissue browning. This observation is consistent with the finding of reduced plasma levels of FFA, glycerol, IL-6, and leptin in RAGE−/− mice compared to WT mice. Collectively the data demonstrate that RAGE-mediated adipose tissue inflammation and insulin-signaling are potentially important mechanisms that contribute to the development of obesity-associated insulin resistance.

Angiopoietin-like 8 Improves Insulin Resistance and Attenuates Adipose Tissue Inflammation in Diet-Induced Obese Mice

2018 ◽  
Vol 128 (05) ◽  
pp. 290-296 ◽  
Author(s):  
Deng Luo ◽  
Xiaolin Chen ◽  
Wenqiang Yang ◽  
Wenzhuo Ran ◽  
Zhongyuan Wen
Keyword(s):  
Insulin Resistance ◽  
Adipose Tissue ◽  
Mrna Expression ◽  
M2 Macrophage ◽  
Dependent Manner ◽  
Adipose Tissue Inflammation ◽  
Obese Mice ◽  
Tissue Inflammation ◽  
M1 Macrophage ◽  
Dose Dependent

AbstractAngiopoietin-like 8 (ANGPTL8) is closely linked to obesity-associated metabolic diseases and insulin resistance. The aim of the current study was to investigate the ability of ANGPTL8 to reverse insulin resistance in obese mice. The administration of ANGPTL8 reduced weight gain and improved glucose tolerance in mice with diet-induced obesity. In addition, ANGPTL8 administration modified macrophage infiltration, reduced monocyte chemoattractant protein-1 (MCP-1) and interleukin-1β(IL-1β) levels, and increased adiponectin gene expression in inguinal white adipose tissue (iWAT). Moreover, the exposure of a cultured peritoneal macrophage line to ANGPTL8 reduced the mRNA expression of M1 macrophage markers (TNF-α and IL-1β) upon stimulation with lipopolysaccharides in a dose-dependent manner. By contrast, when incubated with IL-4, exposure of macrophages to ANGPTL8 increased the mRNA expression of M2 macrophage markers (Arg1 and Chi3l3) in a dose-dependent manner. Collectively, the results of the present study demonstrated that treatment with ANGPTL8 can attenuate adipose tissue inflammation through regulation of macrophage polarization, and thus, it could be useful for improving insulin resistance.

scholarly journals Interferon Tau Alleviates Obesity-Induced Adipose Tissue Inflammation and Insulin Resistance by Regulating Macrophage Polarization

PLoS ONE ◽  
2014 ◽  
Vol 9 (6) ◽  
pp. e98835 ◽  
Author(s):  
Wei Ying ◽  
Srikanth Kanameni ◽  
Cheng-An Chang ◽  
Vijayalekshmi Nair ◽  
Stephen Safe ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Adipose Tissue ◽  
Macrophage Polarization ◽  
Adipose Tissue Inflammation ◽  
Interferon Tau ◽  
Tissue Inflammation

FNDC5 attenuates adipose tissue inflammation and insulin resistance via AMPK-mediated macrophage polarization in obesity

Metabolism ◽  
2018 ◽  
Vol 83 ◽  
pp. 31-41 ◽  
Author(s):  
Xiao-Qing Xiong ◽  
Zhi Geng ◽  
Bing Zhou ◽  
Feng Zhang ◽  
Ying Han ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Adipose Tissue ◽  
Macrophage Polarization ◽  
Adipose Tissue Inflammation ◽  
Tissue Inflammation

scholarly journals IL-1 family members in the pathogenesis and treatment of metabolic disease: Focus on adipose tissue inflammation and insulin resistance

Cytokine ◽  
2015 ◽  
Vol 75 (2) ◽  
pp. 280-290 ◽  
Author(s):  
Dov B. Ballak ◽  
Rinke Stienstra ◽  
Cees J. Tack ◽  
Charles A. Dinarello ◽  
Janna A. van Diepen
Keyword(s):  
Metabolic Disease ◽  
Insulin Resistance ◽  
Adipose Tissue ◽  
Family Members ◽  
Adipose Tissue Inflammation ◽  
Tissue Inflammation ◽  
Disease Focus

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 Glucose-6-Phosphate Dehydrogenase Deficiency Improves Insulin Resistance With Reduced Adipose Tissue Inflammation in Obesity

Diabetes ◽  
2016 ◽  
Vol 65 (9) ◽  
pp. 2624-2638 ◽  
Author(s):  
Mira Ham ◽  
Sung Sik Choe ◽  
Kyung Cheul Shin ◽  
Goun Choi ◽  
Ji-Won Kim ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Adipose Tissue ◽  
Dehydrogenase Deficiency ◽  
Adipose Tissue Inflammation ◽  
Tissue Inflammation ◽  
Glucose 6 Phosphate Dehydrogenase
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