scholarly journals Intermuscular adipose tissue is associated with monocyte chemoattractant protein-1, independent of visceral adipose tissue

2016 ◽  
Vol 49 (6) ◽  
pp. 439-443 ◽  
Author(s):  
Ji-Hee Haam ◽  
Young-Sang Kim ◽  
Hyung Suk Koo ◽  
Juhee Haam ◽  
Nam Kyoung Seo ◽  
...  

2015 ◽  
Vol 4 (11) ◽  
pp. 779-794 ◽  
Author(s):  
Jennifer L. Kaplan ◽  
Melissa A. Marshall ◽  
Chantel C. McSkimming ◽  
Daniel B. Harmon ◽  
James C. Garmey ◽  
...  


2005 ◽  
Vol 153 (6) ◽  
pp. 871-877 ◽  
Author(s):  
Alexis E Malavazos ◽  
Emanuele Cereda ◽  
Lelio Morricone ◽  
Calin Coman ◽  
Massimiliano M Corsi ◽  
...  

Objective: Obesity can be considered a state of chronic, low-grade inflammation. Particularly, visceral adipose tissue (VAT) seems to be an active compartment in pro-inflammatory molecule secretion. Adipocytes and VAT are able to produce large amounts of monocyte chemoattractant protein 1 (MCP-1), a chemokine directly involved in ventricular remodeling. Design: In this study, the possible existence of a correlation between MCP-1, abdominal fat accumulation and echocardiographic abnormalities in uncomplicated obesity was investigated. Methods: Echocardiographic parameters, MCP-1 and C-reactive protein (CRP) levels were assessed in 27 normotensive obese women of fertile age (body mass index 43.5 ± 4.8 kg/m2, mean ± s.d.) and 15 normal weight women. Visceral fat (VAT) in the obese group was assessed by computed tomography. Results: Obese patients had higher MCP-1 (P < 0.0001) and CRP (P < 0.0001) levels than controls. MCP-1 levels were correlated with VAT area (r = 0.57, P < 0.0001), CRP (P < 0.0001), left ventricular mass (LVM) (P < 0.02), LVM indexed for height (P < 0.03), end-diastolic posterior wall (P < 0.005), relative wall thickness (P < 0.01), early diastolic filling wave velocity (P < 0.01), isovolumetric relaxation time (P < 0.001) and deceleration time (P < 0,01). Obese patients with greater amounts of VAT (> 130 cm2) presented higher MCP-1 (P < 0.0001) and CRP levels (P < 0.04) than those with a lower degree of abdominal adiposity. Conclusions: MCP-1 levels and visceral adipose tissue seem to be associated with some morphological and functional echocardiographic abnormalities and support a role for visceral fat in predisposing the subject to cardiac dysfunction, possibly through a low-grade state of inflammation.



Maturitas ◽  
2015 ◽  
Vol 81 (1) ◽  
pp. 225-226
Author(s):  
Young-Sang Kim ◽  
Ji-Hee Haam ◽  
Hyung Yuk Kim ◽  
Moon Jong Kim ◽  
Kwang-Min Kim ◽  
...  


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


Hepatology ◽  
2008 ◽  
Vol 48 (3) ◽  
pp. 799-807 ◽  
Author(s):  
Sophie Clément ◽  
Cristiana Juge-Aubry ◽  
Antonino Sgroi ◽  
Stéphanie Conzelmann ◽  
Valerio Pazienza ◽  
...  


2007 ◽  
Vol 92 (7) ◽  
pp. 2688-2695 ◽  
Author(s):  
Giuseppe Murdolo ◽  
Ann Hammarstedt ◽  
Madeléne Sandqvist ◽  
Martin Schmelz ◽  
Christian Herder ◽  
...  

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 &lt; 0.01) but similar iMCP-1 levels as compared with L. Basal iMCP-1 concentrations were considerably higher than sMCP-1 (P &lt; 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.



2006 ◽  
Vol 291 (4) ◽  
pp. E771-E778 ◽  
Author(s):  
Kyoichiro Tsuchiya ◽  
Takanobu Yoshimoto ◽  
Yuki Hirono ◽  
Toru Tateno ◽  
Toru Sugiyama ◽  
...  

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.



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