ABSTRACT
BACKGROUND: Obesity promotes a low-grade systemic inflammatory state that may act on the lung to exacerbate asthma. There is little information on the relationship between systemic inflammation and lung function in children and adolescents. OBJECTIVES: To explore the relationship among fibrinogen, plasminogen activator inhibitor-1 (PAI-1), lung function in adolescents with the presence of asthma, and/or obesity. METHODS: Totally 178 adolescents (boys and girls) were involved; four groups were divided according to their diagnosis: non-obese and non-asthmatic controls (n = 38), non-obese asthmatics (n = 31), obese non-asthmatics (n = 62), obese asthmatics (n = 47). The levels of PAI-1 and fibrinogen were determined in blood samples. The lung function was evaluated with spirometry by measuring forced expiratory volume in 1 s (FEV1), forced vital capacity (FVC), and forced expiratory flows between 25 and75% (FEF(25-75%)). RESULTS: Compared to healthy controls, obese adolescents with or without asthma show higher levels of fibrinogen (289.2 ± 61.5, 328.4 ± 54.9, and 324.9 ± 68.9 mg/dL, respectively), PAI-1 (36.0 ± 17.3, 53.2 ± 22.3, and 52.6 ± 24.7 ng/mL, respectively), and the reduced FEV1/FVC ratio (87.7 ± 7.7, 81.6 ± 8.6, and 81.7 ± 6.9, respectively). In the whole studied subjects, FEV1/FVC ratio shows significant inverse correlation with PAI-1 (r = -0.185), fibrinogen (r = -0.157), body mass index (BMI; r = -0.303), insulin(r = -0.198), and HOMA (r = -0.173). In the 78 asthmatic subjects, FVC correlates positively with BMI. CONCLUSION: Our data demonstrate that the degree of systemic inflammation and the degree of obesity in the whole studied adolescents groups correlate negatively with lung function, suggesting an obstructive pulmonary pattern. Further studies are needed to identify the pathophysiological mechanism for such association.
Subject(s)
Asthma/physiopathology , Fibrinogen/analysis , Lung/physiopathology , Obesity/physiopathology , Plasminogen Activator Inhibitor 1/blood , Adolescent , Asthma/complications , Body Mass Index , Child , Female , Forced Expiratory Flow Rates , Forced Expiratory Volume , Humans , Inflammation/physiopathology , Male , Obesity/complications , Vital CapacityABSTRACT
Recent studies have shown the effect of perivascular adipose tissue (PVAT) on the regulation of vascular function; however, its role in the model of metabolic syndrome remains unclear. The aim of this study was to examine the effect of losartan on PVAT-derived vascular dysfunction in fructose-induced hypertensive rats. Rats were fed with either water, 10% fructose, or 10% fructose with 10mg/kg losartan for 8 weeks. In the isolated aorta with PVAT and endothelium, contraction induced by norepinephrine (NE) was more potent in fructose-fed rats compared to control rats. Losartan normalized blood pressure, insulin resistance, and NE-induced vasoconstriction in fructose-fed rats. In the aortic rings with/without endothelium and with/without PVAT, losartan could not improve the acetylcholine-induced relaxation in fructose-fed rats. The observation suggested that losartan partly improved the PVAT-associated vascular regulation in fructose-induced hypertensive rats.
Subject(s)
Adipose Tissue/drug effects , Adipose Tissue/physiopathology , Aorta, Thoracic/drug effects , Aorta, Thoracic/physiopathology , Hypertension/drug therapy , Hypertension/physiopathology , Losartan/pharmacology , Acetylcholine/pharmacology , Angiotensin II Type 1 Receptor Blockers/pharmacology , Animals , Disease Models, Animal , Fructose/toxicity , Hypertension/etiology , Male , Metabolic Syndrome/chemically induced , Metabolic Syndrome/complications , Metabolic Syndrome/physiopathology , Norepinephrine/pharmacology , Rats , Rats, Wistar , Vasoconstriction/drug effects , Vasoconstriction/physiology , Vasodilation/drug effects , Vasodilation/physiologyABSTRACT
Asthma and obesity are prevalent disorders, each with a significant impact on the public health. The causality relating obesity and asthma has not been established. The objective of this article is to investigate whether asthma could exacerbate the endothelial activation and to determine the relationship between systemic inflammation and endothelial activation in obese asthmatic children. Eighty-nine children (10-16 years old) were divided according to their diagnosis (asthma, obese nonasthmatic, and obese asthmatic children). Twenty healthy children formed the control group. Three adhesion molecules (E-selectin, sICAM-1, and sVCAM-1) and C-reactive protein (CRP) were measured in serum samples. The levels of sICAM-1 were significantly higher in obese nonasthmatic and obese asthmatic children versus control and lean asthmatic children (414.7+/-154.7, 434.9+/-181.1, 238.6+/-117.8, and 351.2+/-153.5 ng/mL, respectively). No difference was observed between obese nonasthmatic and obese asthmatic groups. No difference of the levels of CRP, E-selectin, and sVCAM-1 was found among the study groups. Correlation analysis showed that E-selectin associated significantly with body mass index (BMI), CRP and the other two adhesion molecules. CRP depended on BMI. sICAM-1 associated with CRP, BMI, and triglycerides. Correlations were verified in multiple regression analysis models in the whole study groups: CRP levels depended on sICAM-1, E-selectin, and sICAM-1 concentrations depended on BMI. Correlations were verified in asthmatic subjects: CRP depended on sICAM-1. These results confirmed the endothelial activation in obese children. Mild nonallergic asthma in our study did not exacerbate the endothelial activation in obese or lean asthmatic children. Significant association between systemic inflammation and endothelial activation was observed in asthmatic children.
