The paper presents an experimental study aimed at investigating the mechanism responsible for Bisphenol A adsorption on natural cork, and the role played on process kinetics by the organic matter released from the cork. Obtained data show that natural cork has a good affinity toward Bisphenol A, with removal efficiency being as high as 75% in less than 24 h. The adsorption process is characterized by a fast-initial rate which tends to reduce progressively, and follows a pseudo second order model equation. Statistical physical analysis allows for obtaining a molecular description of the adsorption, which is shown to take place through a single anchorage point, perpendicularly to the adsorbent surface. Nuclear magnetic resonance spectroscopy and florescence analysis reveal that the colloidal organic matter released from the cork interacts with Bisphenol A; it also plays a relevant role in the slowing down of the adsorption rate, as it competes with cork adsorption sites for Bisphenol A. Organic matter is found to be highly heterogenous, presenting at the same time carbohydrates, aromatic and aliphatic domains. Such moieties interact stably with the contaminant in the solution probably due the establishment of dispersive forces (e.g. 蟺-stacking) which sequestrate Bisphenol A into the inner hydrophobic core of the organic matter three-dimensional structure.
Background It is well known that high-fat diet (HFD) feeding causes cardiac inflammation, remodeling, and dysfunction, and that increased fat intake, especially saturated fat, is a major driver of cardiometabolic diseases. Oleoylethanolamide (OEA) is a member of acylethanolamides recognized for its metabolic and anti-inflammatory properties due to the high affinity for different receptors and to its role as a modulator of the endocannabinoid system. OEA effects on the cardiovascular alterations caused by fat overnutrition are still unknown. Purpose The aim of this study was to evaluate the impact of OEA treatment on cardiac metabolic changes induced by HFD in obese mice. Methods Male C57Bl/6J mice were divided into 3 groups: control group (STD) receiving standard chow diet; mice fed with HFD for 20 weeks; HFD group treated with OEA (HFD+OEA 2,5 mg/kg/die i.p.) from week 12 to week 20. Results In HFD mice, OEA treatment reduced body weight measured throughout the experimental period. Before sacrifice, we performed the oral glucose tolerance test (OGTT), where HFD+OEA mice showed an improvement of insulin sensitivity, altered by HFD. HFD feeding led to a significant increase in the production of inflammatory cytokines and chemokines, such as interleukin (IL)-1b, IL-6, the monocyte chemoattractant protein (MCP)1 and the pro-fibrotic marker fibrillin in the cardiac tissue. Conversely, OEA normalized the transcription of the above-mentioned pro-inflammatory mediators in the heart of obese mice. OEA treatment also reduced the gene expressions levels of cardiac fatty acid transporter CD36, that were significantly induced in the heart of HFD-fed mice, and that have been found to be linked to myocardial lipid accumulation. We also evaluated the gene expression levels of the adipokines adiponectin and meteorin-like protein (Metrnl), finding that the increased ventricular expression of both in HFD mice were significantly reduced by OEA. Moreover, OEA treatment induces an increase in AMPK and AKT phosphorylation, whose pathways converge towards the phosphorylation of AS160, a kinase implicated in the translocation of the glucose transporter (GLUT) 4 to the cardiomyocyte membrane, a mechanism involved in the modulation of cardiac glucose metabolism. Since it has been reported that cardiac autophagy is altered in metabolic disorders like obesity, we also studied the effect of OEA in autophagosome formation, and we determined that cardiac protein levels of LC3II, an autophagosomal membrane marker, are markedly increased by OEA treatment. Conclusions Taken together, our results indicate a potential cardioprotective effect of OEA as a molecule able to reduce body weight and body weight gain, to ameliorate glucose disposal improving blood glucose, to restore cardiac metabolic alterations related to obesity, and to decrease proinflammatory and profibrotic markers at cardiac level, induced by HFD. Funding Acknowledgement Type of funding sources: Public Institution(s). Main funding source(s): Fondo de Investigationes Sanitarias, Instituto de Salud Carlos III
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