Active spice-derived components can inhibit inflammatory responses of adipose tissue in obesity by suppressing inflammatory actions of macrophages and release of monocyte chemoattractant protein-1 from adipocytes

Life Sciences ◽  
2007 ◽  
Vol 80 (10) ◽  
pp. 926-931 ◽  
Author(s):  
Hae-Mi Woo ◽  
Ji-Hye Kang ◽  
Teruo Kawada ◽  
Hoon Yoo ◽  
Mi-Kyung Sung ◽  
...  
Keyword(s):  
Adipose Tissue ◽  
Inflammatory Responses ◽  
Monocyte Chemoattractant Protein 1 ◽  
Monocyte Chemoattractant ◽  
Monocyte Chemoattractant Protein

scholarly journals Monocyte Chemoattractant Protein-1 Deficiency Fails to Restrain Macrophage Infiltration Into Adipose Tissue

Diabetes ◽  
2008 ◽  
Vol 57 (5) ◽  
pp. 1254-1261 ◽  
Author(s):  
E. A. Kirk ◽  
Z. K. Sagawa ◽  
T. O. McDonald ◽  
K. D. O'Brien ◽  
J. W. Heinecke
Keyword(s):  
Adipose Tissue ◽  
Macrophage Infiltration ◽  
Monocyte Chemoattractant Protein 1 ◽  
Monocyte Chemoattractant ◽  
Monocyte Chemoattractant Protein

Monocyte chemoattractant protein-1 secreted by adipose tissue induces direct lipid accumulation in hepatocytes

Hepatology ◽  
2008 ◽  
Vol 48 (3) ◽  
pp. 799-807 ◽  
Author(s):  
Sophie Clément ◽  
Cristiana Juge-Aubry ◽  
Antonino Sgroi ◽  
Stéphanie Conzelmann ◽  
Valerio Pazienza ◽  
...  
Keyword(s):  
Adipose Tissue ◽  
Lipid Accumulation ◽  
Monocyte Chemoattractant Protein 1 ◽  
Monocyte Chemoattractant ◽  
Monocyte Chemoattractant Protein

scholarly journals Monocyte Chemoattractant Protein-1 in Subcutaneous Abdominal Adipose Tissue: Characterization of Interstitial Concentration and Regulation of Gene Expression by Insulin

2007 ◽  
Vol 92 (7) ◽  
pp. 2688-2695 ◽  
Author(s):  
Giuseppe Murdolo ◽  
Ann Hammarstedt ◽  
Madeléne Sandqvist ◽  
Martin Schmelz ◽  
Christian Herder ◽  
...  
Keyword(s):  
Gene Expression ◽  
Adipose Tissue ◽  
Regulation Of Gene Expression ◽  
Whole Body ◽  
Mrna Levels ◽  
Abdominal Adipose Tissue ◽  
Monocyte Chemoattractant Protein 1 ◽  
Monocyte Chemoattractant ◽  
Monocyte Chemoattractant Protein ◽  
Adipose Organ

Abstract Context: The chemokine monocyte chemoattractant protein-1 (MCP-1) is implicated in obesity-associated chronic inflammation, insulin resistance, and atherosclerosis. Objectives: The objectives of this study were to: 1) characterize the interstitial levels and the gene expression of MCP-1 in the sc abdominal adipose tissue (SCAAT), 2) elucidate the response of MCP-1 to acute hyperinsulinemia, and 3) determine the relationship between MCP-1 and arterial stiffness. Design: Nine lean (L) and nine uncomplicated obese (OB) males were studied in the fasting state and during a euglycemic-hyperinsulinemic clamp combined with the microdialysis technique. Interstitial and serum MCP-1 (iMCP-1 and sMCP-1, respectively) levels, pulse wave analysis, and SCAAT biopsies were characterized at baseline and after hyperinsulinemia. Results: OB showed elevated sMCP-1 (P < 0.01) but similar iMCP-1 levels as compared with L. Basal iMCP-1 concentrations were considerably higher than sMCP-1 (P < 0.0001), and a gradient between iMCP-1 and sMCP-1 levels was maintained throughout the hyperinsulinemia. At baseline, SCAAT gene expression profile revealed a “co-upregulation” of MCP-1, MCP-2, macrophage inflammatory protein-1α, and CD68 in OB, and whole-body glucose disposal inversely correlated with the MCP-1 gene expression. After hyperinsulinemia, MCP-1 and MCP-2 mRNA levels significantly increased in L, but not in OB. Finally, sMCP-1 excess in the OB positively correlated with the stiffer vasculature. Conclusions: These observations demonstrate similar interstitial concentrations and a differential gene response to hyperinsulinemia of MCP-1 in the SCAAT from L and OB individuals. In human obesity, we suggest the SCAAT MCP-1 gene overexpression as a biomarker of an “inflamed” adipose organ and impaired glucose metabolism.

Angiotensin II induces monocyte chemoattractant protein-1 expression via a nuclear factor-κB-dependent pathway in rat preadipocytes

2006 ◽  
Vol 291 (4) ◽  
pp. E771-E778 ◽  
Author(s):  
Kyoichiro Tsuchiya ◽  
Takanobu Yoshimoto ◽  
Yuki Hirono ◽  
Toru Tateno ◽  
Toru Sugiyama ◽  
...  
Keyword(s):  
Gene Expression ◽  
Adipose Tissue ◽  
Luciferase Assay ◽  
Ang Ii ◽  
Monocyte Chemoattractant Protein 1 ◽  
Monocyte Chemoattractant ◽  
Monocyte Chemoattractant Protein ◽  
Dependent Pathway

Both monocyte chemoattractant protein-1 (MCP-1), a member of chemokine family, and angiotensinogen, a precursor of angiotensin (ANG) II, are produced by adipose tissue and increased in obese state. MCP-1 has been shown to decrease insulin-stimulated glucose uptake and several adipogenic genes expression in adipocytes in vitro, suggesting its pathophysiological significance in obesity. However, the pathophysiological interaction between MCP-1 and ANG II in adipose tissue remains unknown. The present study was undertaken to investigate the potential mechanisms by which ANG II affects MCP-1 gene expression in rat primary cultured preadipocytes and adipose tissue in vivo. ANG II significantly increased steady-state MCP-1 mRNA levels in a time- and dose-dependent manner. The ANG II-induced MCP-1 mRNA and protein expression was completely abolished by ANG II type 1 (AT1)-receptor antagonist (valsartan). An antioxidant/NF-κB inhibitor (pyrrolidine dithiocarbamate) and an inhibitor of 1κB-α phosphorylation (Bay 11-7085) also blocked ANG II-induced MCP-1 mRNA expression. ANG II induced translocation of NF-κB p65 subunit from cytoplasm to nucleus by immunocytochemical study. Luciferase assay using reporter constructs containing MCP-1 promoter region revealed that two NF-κB binding sites in its enhancer region were essential for the ANG II-induced promoter activities. Furthermore, basal mRNA and protein of MCP-1 during preadipocyte differentiation were significantly greater in preadipocytes than in differentiated adipocytes, whose effect was more pronounced in the presence of ANG II. Exogenous administration of ANG II to rats led to increased MCP-1 expression in epididymal, subcutaneous, and mesenteric adipose tissue. In conclusion, our present study demonstrates that ANG II increases MCP-1 gene expression via ANG II type 1 receptor-mediated and NF-κB-dependent pathway in rat preadipocytes as well as adipose MCP-1 expression in vivo. Thus the augmented MCP-1 expression by ANG II in preadipocytes may provide a new link between obesity and cardiovascular disease.

scholarly journals A Unique Role of Monocyte Chemoattractant Protein 1 among Chemokines in Adipose Tissue of Obese Subjects

2005 ◽  
Vol 90 (10) ◽  
pp. 5834-5840 ◽  
Author(s):  
Ingrid Dahlman ◽  
Maria Kaaman ◽  
Tommy Olsson ◽  
Garry D. Tan ◽  
Alex S. T. Bickerton ◽  
...  
Keyword(s):  
Adipose Tissue ◽  
Unique Role ◽  
Monocyte Chemoattractant Protein 1 ◽  
Monocyte Chemoattractant ◽  
Monocyte Chemoattractant Protein ◽  
Obese Subjects

scholarly journals Protease-activated receptor 1 activation is necessary for monocyte chemoattractant protein 1–dependent leukocyte recruitment in vivo

2008 ◽  
Vol 205 (8) ◽  
pp. 1739-1746 ◽  
Author(s):  
Daxin Chen ◽  
Adam Carpenter ◽  
Joel Abrahams ◽  
Rachel C. Chambers ◽  
Robert I. Lechler ◽  
...  
Keyword(s):  
Inflammatory Responses ◽  
Mouse Heart ◽  
Protease Activated Receptors ◽  
Chemokine Production ◽  
Monocyte Chemoattractant Protein 1 ◽  
Cell Recruitment ◽  
Monocyte Chemoattractant ◽  
Monocyte Chemoattractant Protein ◽  
Protease Activated Receptor 1

Thrombin, acting through a family of protease-activated receptors (PARs), is known to amplify inflammatory responses, but the in vivo importance of PARs in inflammation is not fully appreciated. In a mouse heart-to-rat transplant model, where it is possible to distinguish graft (mouse) from systemic (rat) chemokines, we show that donor PAR-1 is required to generate the local monocyte chemoattractant protein (MCP)-1 needed to recruit rat natural killer cells and macrophages into the hearts. We have confirmed the importance of this mechanism in a second model of thioglycollate-induced peritonitis and also show that PAR-1 is important for the production of MCP-3 and MCP-5. Despite the presence of multiple other mediators capable of stimulating chemokine production in these models, these data provide the first evidence that thrombin and PAR activation are required in vivo to initiate inflammatory cell recruitment.

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