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• W2018490897 abstract "Obesity, in particular android obesity, has strong associations with cardiovascular disease through mechanisms possibly linking the metabolic disorder to a low-grade inflammation [1, 2] and a prothrombotic hypofibrinolytic condition [3]. Indeed, adipose tissue represents a source of several molecules, including plasminogen activator inhibitor-1 (PAI-1) [4]. Moreover, visceral adipose tissue has a higher capacity to produce PAI-1 than subcutaneous adipose tissue [4]. Obesity is also accompanied by oxidative stress [2, 5]. Using several mouse models of obesity, Furukawa et al. [5] recently demonstrated that increased oxidative stress in accumulated fat leads to dysregulated production of adipocytokines. In particular, in cultured adipocytes oxidative stress enhanced PAI-1 mRNA expression [5]. Treatment of obese mice with a NADPH oxidase inhibitor reduced ROS production in adipose tissue and attenuated the dysregulation of adipocytokines [5]. These considerations prompted us to investigate the relationship between oxidative stress and PAI-1 levels in obese healthy women. To this purpose, we performed a cross sectional comparison of urinary 8-iso-prostaglandin (PG)F2α (an in vivo marker of oxidative stress) excretion rates and plasma PAI-1 levels in 46 women: 21 with android obesity; 15 with gynoid obesity; 10 non-obese women served as controls (Table 1). All women were recruited at the University of Chieti after they had provided written informed consent. The study was approved by the Medical Ethics Committee of the University Medical School. Women had to be in good general health and physical condition. Exclusion criteria were: clinical cardiovascular disease, diabetes mellitus, smoking, hypercholesterolemia, hypertension, hormonal contraception or replacement therapy, treatment with corticosteroids or non-steroidal anti-inflammatory drugs and vitamin supplements. Women were also excluded if they were pregnant or had delivered in the previous 6 months. PAI-1 antigen was determined by ELISA (Imubind PAI-1 ELISA kit; American Diagnostica, Greenwich, CT, USA). Urinary 8-iso-PGF2α excretion rates were determined by a previously described radioimmunoassay [6]. Statistical analysis was performed by appropriate statistics using a computer software package (Statistica 6.0, StatSoft Inc.,). Data are presented as mean ± SD or median and interquartile range (IQR; 25th to 75th percentile). Only P-values <0.05 were regarded as statistically significant. PAI-1 levels were significantly higher in women with android obesity compared with either gynoid obese or non-obese women (Table 1). Oxidative stress, as reflected by urinary 8-iso-PGF2α excretion, was enhanced in android obesity, whereas no differences were observed between gynoid obese and non-obese women (Table 1). Spearman rank correlation analysis of the values measured in all 46 women showed the presence of a relationship between PAI-1 levels and urinary 8-iso-PGF2α excretion rates (ρ = 0.474, P < 0.001) and either body mass index (BMI, ρ = 0.676, P < 0.0001) or waist-to-hip ratio (WHR, ρ = 0.381, P < 0.01). These results were confirmed in a subgroup analysis of obese, but not in non-obese women. Thus, to better analyze the relationship of PAI-1 levels with all other variables, a multivariate linear regression analysis including age, BMI, WHR, total cholesterol, LDL and HDL-cholesterol, triglyceride levels and urinary 8-iso-PGF2α excretion rates was performed. The final model obtained by backward stepping revealed that urinary 8-iso-PGF2α excretion rates (β = 0.64, P < 0.002) were independently related to PAI-1, but only in android obese women. These results are consistent with previous findings of increased oxidative stress and PAI-1 levels in obesity [2, 3]. Moreover, they show, for the first time, a direct correlation between PAI-1 and urinary 8-iso-PGF2α and a close relationship between these analytical variables and android obesity, which is independent of other variables. The two groups of obese women were in fact comparable for age, overall obesity (BMI), systolic and diastolic blood pressure and plasma lipid levels. Thus, from the present results, a key involvement of urinary 8-iso-PGF2α in the enhancement of PAI-1 levels associated with android obesity may be hypothesized. Although the origin of PAI-1 overproduction in obese women remains to be established, our observations are in agreement with the observation that increased oxidative stress in cultured adipocytes is able to enhance PAI-1 mRNA expression [5]. The close relationship of increased PAI-1 levels with android obesity is also consistent with the finding that visceral fat has a higher capacity to produce PAI-1 than subcutaneous adipose tissue [4]. Prospective studies have shown that an elevated PAI-1 activity independently predicts cardiovascular events [4], suggesting that elevated levels of PAI-1 may contribute to establish a prothrombotic condition. To date, normalization of impaired fibrinolysis has not been among the primary goals of pharmacological treatment in patients with android obesity and the metabolic syndrome. However, some of the drugs that are currently used for the treatment of the metabolic syndrome may also distinctly modify impaired fibrinolysis [4]. Here, we provide the first evidence of a close relationship between android obesity, increased PAI-1 levels and urinary 8-iso-PGF2α, suggesting that increased oxidative stress may represent a biochemical link between android obesity and an increased risk for cardiovascular disease. Hence, the redox state in adipose tissue might represent a potentially useful target in new therapies against obesity-associated metabolic syndrome." @default.
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• W2018490897 title "Increased plasminogen activator inhibitor‐1 levels in android obesity: correlation with oxidative stress" @default.
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• W2018490897 doi "https://doi.org/10.1111/j.1538-7836.2005.01395.x" @default.
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