scholarly journals Acute exercise induces a phenotypic switch in adipose tissue macrophage polarization in diet-induced obese rats

Obesity ◽  
2013 ◽  
Vol 21 (12) ◽  
pp. 2545-2556 ◽  
Author(s):  
Alexandre G. Oliveira ◽  
Tiago G. Araujo ◽  
Bruno M. Carvalho ◽  
Dioze Guadagnini ◽  
Guilherme Z. Rocha ◽  
...  
Keyword(s):  
Adipose Tissue ◽  
Acute Exercise ◽  
Macrophage Polarization ◽  
Phenotypic Switch ◽  
Tissue Macrophage ◽  
Adipose Tissue Macrophage ◽  
Obese Rats

scholarly journals Obesity induces a phenotypic switch in adipose tissue macrophage polarization

2007 ◽  
Vol 117 (1) ◽  
pp. 175-184 ◽  
Author(s):  
Carey N. Lumeng ◽  
Jennifer L. Bodzin ◽  
Alan R. Saltiel
Keyword(s):  
Adipose Tissue ◽  
Macrophage Polarization ◽  
Phenotypic Switch ◽  
Tissue Macrophage ◽  
Adipose Tissue Macrophage

scholarly journals Role of microRNA in CB1 antagonist–mediated regulation of adipose tissue macrophage polarization and chemotaxis during diet-induced obesity

2019 ◽  
Vol 294 (19) ◽  
pp. 7669-7681 ◽  
Author(s):  
Pegah Mehrpouya-Bahrami ◽  
Kathryn Miranda ◽  
Narendra P. Singh ◽  
Elizabeth E. Zumbrun ◽  
Mitzi Nagarkatti ◽  
...  
Keyword(s):  
Adipose Tissue ◽  
Macrophage Polarization ◽  
Tissue Macrophage ◽  
Adipose Tissue Macrophage ◽  
Diet Induced Obesity ◽  
Cb1 Antagonist

Adipose tissue macrophage polarization by intermittent hypoxia in a mouse model of OSA: Effect of tumor microenvironment

2015 ◽  
Vol 361 (2) ◽  
pp. 233-239 ◽  
Author(s):  
Isaac Almendros ◽  
Alex Gileles-Hillel ◽  
Abdelnaby Khalyfa ◽  
Yang Wang ◽  
Shelley X. Zhang ◽  
...  
Keyword(s):  
Adipose Tissue ◽  
Tumor Microenvironment ◽  
Mouse Model ◽  
Intermittent Hypoxia ◽  
Macrophage Polarization ◽  
Tissue Macrophage ◽  
Adipose Tissue Macrophage

scholarly journals Telmisartan Improves Insulin Resistance and Modulates Adipose Tissue Macrophage Polarization in High-Fat-Fed Mice

Endocrinology ◽  
2011 ◽  
Vol 152 (5) ◽  
pp. 1789-1799 ◽  
Author(s):  
Shiho Fujisaka ◽  
Isao Usui ◽  
Yukiko Kanatani ◽  
Masashi Ikutani ◽  
Ichiro Takasaki ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Adipose Tissue ◽  
Insulin Sensitivity ◽  
Macrophage Polarization ◽  
High Fat ◽  
Adipose Tissues ◽  
Tissue Macrophage ◽  
Adipose Tissue Macrophage ◽  
Visceral Adipose

Diet-induced obesity is reported to induce a phenotypic switch in adipose tissue macrophages from an antiinflammatory M2 state to a proinflammatory M1 state. Telmisartan, an angiotensin II type 1 receptor blocker and a peroxisome proliferator-activated receptor-γ agonist, reportedly has more beneficial effects on insulin sensitivity than other angiotensin II type 1 receptor blockers. In this study, we studied the effects of telmisartan on the adipose tissue macrophage phenotype in high-fat-fed mice. Telmisartan was administered for 5 wk to high-fat-fed C57BL/6 mice. Insulin sensitivity, macrophage infiltration, and the gene expressions of M1 and M2 markers in visceral adipose tissues were then examined. An insulin- or a glucose-tolerance test showed that telmisartan treatment improved insulin resistance, decreasing the body weight gain, visceral fat weight, and adipocyte size without affecting the amount of energy intake. Telmisartan reduced the mRNA expression of CD11c and TNF-α, M1 macrophage markers, and significantly increased the expressions of M2 markers, such as CD163, CD209, and macrophage galactose N-acetyl-galactosamine specific lectin (Mgl2), in a quantitative RT-PCR analysis. A flow cytometry analysis showed that telmisartan decreased the number of M1 macrophages in visceral adipose tissues. In conclusion, telmisartan improves insulin sensitivity and modulates adipose tissue macrophage polarization to an antiinflammatory M2 state in high-fat-fed mice.

scholarly journals Fetuin-A regulates adipose tissue macrophage content and activation in insulin resistant mice through MCP-1 and iNOS: Involvement of IFNγ-JAK2-STAT1 pathway

2021 ◽  
Author(s):  
Dipanjan Chattopadhyay ◽  
Snehasis Das ◽  
Suktara Guria ◽  
Soumyadeep Basu ◽  
Sutapa Mukherjee
Keyword(s):  
Adipose Tissue ◽  
Macrophage Polarization ◽  
Interferon Γ ◽  
Adipose Tissue Inflammation ◽  
Fetuin A ◽  
Monocyte Chemoattractant Protein 1 ◽  
Tissue Inflammation ◽  
Tissue Macrophage ◽  
Adipose Tissue Macrophage ◽  
Anti Inflammatory

In the context of obesity-induced adipose tissue inflammation, migration of macrophages and their polarization from predominantly anti-inflammatory to proinflammatory subtype is considered a pivotal event in the loss of adipose insulin sensitivity. Two major chemoattractants, monocyte chemoattractant protein-1 (MCP-1) and Fetuin A (FetA), have been reported to stimulate macrophage migration into inflamed adipose tissue instigating inflammation. Moreover, FetA could notably modulate macrophage polarization, yet the mechanism(s) is unknown. The present study was undertaken to elucidate the mechanistic pathway involved in the actions of FetA and MCP-1 in obese adipose tissue. We found that FetA knockdown in high fat diet (HFD) fed mice could significantly subdue the augmented MCP-1 expression and reduce adipose tissue macrophage (ATM) content thereby indicating that MCP-1 is being regulated by FetA. Additionally, knockdown of FetA in HFD mice impeded the expression of inducible nitric oxide synthase (iNOS) reverting macrophage activation from mostly proinflammatory to anti-inflammatory state. It was observed that the stimulating effect of FetA on MCP-1 and iNOS was mediated through interferon γ (IFNγ) induced activation of JAK2-STAT1-NOX4 pathway. Furthermore, we detected that the enhanced IFNγ expression was accounted by the stimulatory effect of FetA upon the activities of both cJun and JNK. Taken together, our findings revealed that obesity-induced FetA acts as a master upstream regulator of adipose tissue inflammation by regulating MCP-1 and iNOS expression through JNK-cJun-IFNγ-JAK2-STAT1 signaling pathway. This study opened a new horizon in understanding the regulation of ATM content and activation in conditions of obesity-induced insulin resistance.

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