N-acetylcysteine attenuates TNF-α induced changes in secretion of interleukin-6, plasminogen activator inhibitor-1 and adiponectin from 3T3-L1 adipocytes

Life Sciences ◽  
2006 ◽  
Vol 79 (25) ◽  
pp. 2405-2412 ◽  
Author(s):  
Shunsuke Araki ◽  
Kazushige Dobashi ◽  
Kazuyasu Kubo ◽  
Yukiyo Yamamoto ◽  
Kohtaro Asayama ◽  
...  
Keyword(s):  
Plasminogen Activator ◽  
Interleukin 6 ◽  
Plasminogen Activator Inhibitor ◽  
Plasminogen Activator Inhibitor 1 ◽  
Tnf Α ◽  
Induced Changes ◽  
Activator Inhibitor

Expression of plasminogen activator inhibitor-1 in human adipose tissue: a role for TNF-α?

1999 ◽  
Vol 143 (1) ◽  
pp. 81-90 ◽  
Author(s):  
M. Cigolini ◽  
M. Tonoli ◽  
L. Borgato ◽  
L. Frigotto ◽  
F. Manzato ◽  
...  
Keyword(s):  
Adipose Tissue ◽  
Plasminogen Activator ◽  
Plasminogen Activator Inhibitor ◽  
Human Adipose Tissue ◽  
Plasminogen Activator Inhibitor 1 ◽  
Tnf Α ◽  
Activator Inhibitor

TNF-α and insulin, alone and synergistically, induce plasminogen activator inhibitor-1 expression in adipocytes

1999 ◽  
Vol 276 (6) ◽  
pp. C1391-C1397 ◽  
Author(s):  
Tomohiro Sakamoto ◽  
Janet Woodcock-Mitchell ◽  
Kousuke Marutsuka ◽  
John J. Mitchell ◽  
Burton E. Sobel ◽  
...  
Keyword(s):  
Plasminogen Activator ◽  
Synergistic Effects ◽  
Plasminogen Activator Inhibitor ◽  
Plasminogen Activators ◽  
System Capacity ◽  
Plasminogen Activator Inhibitor 1 ◽  
Tnf Α ◽  
Factor Α ◽  
Activator Inhibitor ◽  
Pai 1

Obesity is associated with hyperinsulinemia and elevated concentrations of tumor necrosis factor-α (TNF-α) in adipose tissue. TNF-α has been implicated as an inducer of the synthesis of plasminogen activator inhibitor-1 (PAI-1), the primary physiological inhibitor of fibrinolysis, mediated by plasminogen activators in cultured adipocytes. To identify mechanism(s) through which TNF-α induces PAI-1, 3T3-L1 preadipocytes were differentiated into adipocytes and exposed to TNF-α for 24 h. TNF-α selectively increased the synthesis of PAI-1 without increasing activity of plasminogen activators. Both superoxide (generated by xanthine oxidase plus hypoxanthine) and hydrogen peroxide were potent inducers of PAI-1, and hydroxyl radical scavengers completely abolished the TNF-α induction of PAI-1. Exposure of adipocytes to TNF-α or insulin alone over 5 days increased PAI-1 production. These agonists exert synergistic effects. Results obtained suggest that TNF-α stimulates PAI-1 production by adipocytes, an effect potentiated by insulin, and that adipocyte generation of reactive oxygen centered radicals mediates the induction of PAI-1 production by TNF-α. Because induction of PAI-1 by TNF-α is potentiated synergistically by insulin, both agonists appear likely to contribute to the impairment of fibrinolytic system capacity typical in obese, hyperinsulinemic patients.

scholarly journals Waist-to-height ratio, inflammation and CVD risk in obese children

2014 ◽  
Vol 17 (10) ◽  
pp. 2378-2385 ◽  
Author(s):  
Josune Olza ◽  
Concepcion M Aguilera ◽  
Mercedes Gil-Campos ◽  
Rosaura Leis ◽  
Gloria Bueno ◽  
...  
Keyword(s):  
Plasminogen Activator ◽  
Plasminogen Activator Inhibitor ◽  
Normal Weight ◽  
Obese Children ◽  
Plasminogen Activator Inhibitor 1 ◽  
Height Ratio ◽  
Cvd Risk ◽  
Tnf Α ◽  
Waist To Height Ratio ◽  
Activator Inhibitor

AbstractObjectiveTo evaluate the association between waist-to-height ratio (WHtR) and specific biomarkers of inflammation, CVD risk and endothelial dysfunction in prepubertal obese children.DesignProspective, multicentre case–control study matched by age and sex.SettingChildren were recruited between May 2007 and May 2010 from primary-care centres and schools in three cities in Spain (Cordoba, Santiago de Compostela and Zaragoza).SubjectsFour hundred and forty-six (223 normal weight and 223 obese) Caucasian prepubertal children aged 6–12 years.ResultsWHtR was higher in the obese than in the normal-weight children. Blood pressure, waist circumference, weight, height, insulin, plasma lipids, leptin, resistin, abnormal neutrophil and monocyte counts, C-reactive protein, IL-6, IL-8, TNF-α, myeloperoxidase, soluble intercellular adhesion molecule-1, selectin and plasminogen activator inhibitor-1 levels were higher in the obese than in the normal-weight group. Adiponectin and HDL-cholesterol were lower and glucose and metalloproteinase-9 showed no differences. Resistin, TNF-α and active plasminogen activator inhibitor-1 were associated with WHtR, a sensitive indicator of central obesity.ConclusionsOur results lead to the hypothesis that changes in biomarker levels of insulin resistance, inflammation and CVD risk before puberty might induce metabolic consequences of obesity in obese children before reaching adulthood.

scholarly journals Defining the Proinflammatory Phenotype Using High Sensitive C-Reactive Protein Levels as the Biomarker

2005 ◽  
Vol 90 (8) ◽  
pp. 4549-4554 ◽  
Author(s):  
Sridevi Devaraj ◽  
Grant O’Keefe ◽  
Ishwarlal Jialal
Keyword(s):  
Cell Adhesion ◽  
Plasminogen Activator ◽  
Body Mass ◽  
Whole Blood ◽  
Plasminogen Activator Inhibitor ◽  
C Reactive Protein ◽  
Plasminogen Activator Inhibitor 1 ◽  
Reactive Protein ◽  
Tnf Α ◽  
Activator Inhibitor

Context: Inflammation is pivotal in atherosclerosis. The prototypic marker of inflammation is C-reactive protein (CRP). Numerous studies have confirmed that high CRP levels in normal volunteers predict cardiovascular events. Objective: The objective of this study was to define proximal and associated abnormalities of the proinflammatory phenotype using CRP levels as the biomarker. Design and Subjects: Two groups of normal, healthy subjects, selected by stringent criteria from an initial cohort of 252, were studied over the period of 12 months. Group 1 included subjects with consistently low CRP (<0.004 μm or <0.5 mg/liter; low CRP group; n = 15). Group 2 included subjects with consistently high CRP (>2.0 or >0.016 μm to <10 mg/liter or <0.085 μm; high CRP group; n = 13). Main Outcome Measures: Fasting blood (50 ml) was obtained, and the following parameters were assayed: high sensitivity CRP, fibrinogen, lipid profile, insulin, whole blood cytokines after stimulation with lipopolysaccharide (LPS; 100 ng/ml for 24 h), soluble cell adhesion molecules, plasminogen activator inhibitor-1, CD40, CD40 ligand, leptin, adiponectin, monocyte chemoattractant protein-1, IL-8, matrix metalloproteinase-3 (MMP-3), and MMP-9. Genomic DNA was obtained from peripheral blood leukocytes, and the TNF-α −308 genotype was determined. Results: The median CRP levels were 0.0018 μm (0.21 mg/liter) and 0.031 μm (3.7 mg/liter) for the low and high groups, respectively. High CRP subjects were older and had significantly higher body mass indexes, triglycerides, insulin, homeostasis model assessment, and leptin levels compared with low CRP subjects. The markers of inflammation, plasminogen activator inhibitor-1, MMP-9, fibrinogen, and vascular cell adhesion molecule-1 levels were significantly higher in the high compared with the low CRP group. LPS-stimulated levels of whole blood IL-1β, IL-6, and TNF were significantly higher, and IL-4 levels were significantly lower in the high CRP group. After age- and body mass index-adjusted analysis of covariance, only plasma MMP-9 levels and LPS-stimulated whole blood IL-1β and TNF levels were significantly higher in the high CRP group. The frequency of the rare A allele at TNF-α −308 was equivalent in high and low CRP groups. Conclusions: A phenotype characterized by increased plasma inflammatory mediators as well as increased LPS-stimulated whole blood TNF-α and IL-1β levels is associated with high plasma CRP levels. This systemic inflammatory phenotype may contribute to vascular inflammation or may reflect inflammation in vessels or at other sites.

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