Comunicaciones a congresos, conferencias…(Fac Farmacia y Nutrición)
Permanent URI for this collectionhttps://hdl.handle.net/10171/70316
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Results
- Maresin 1 exerts a tissue-specific regulation of adipo-hepato-myokines in diet-induced obese mice and modulates adipokine expression in cultured human adipocytes in basal and inflammatory conditions(2023) Laiglesia-González, L.M. (Laura María); Moreno-Aliaga, M. J. (María Jesús); Arbones-Mainar, J.M. (José M.); Burgos, M. (Miguel); Gonzalez-Muniesa, P. (Pedro); Martínez-Fernández, L. (Leyre); Sainz, N. (Neira)This study analyses the effects of Maresin 1 (MaR1), a docosahexaenoic acid (DHA)-derived specialized proresolving lipid mediator with anti-inflammatory and insulin-sensitizing actions, on the expression of adipokines, including adiponectin, leptin, dipeptidyl peptidase 4 (DPP-4), cardiotrophin-1 (CT-1), and irisin (FNDC5), both in vitro and in in vivo models of obesity. The in vivo effects of MaR1 (50 & mu;g/kg, 10 days, oral gavage) were evaluated in epididymal adipose tissue (eWAT), liver and muscle of diet-induced obese (DIO) mice. Moreover, two models of human differentiated primary adipocytes were incubated with MaR1 (1 and 10 nM, 24 h) or with a combination of tumor necrosis factor-& alpha; (TNF-& alpha;, 100 ng/mL) and MaR1 (1-200 nM, 24 h) and the expression and secretion of adipokines were measured in both models. MaR1-treated DIO mice exhibited an increased expression of adiponectin and Ct-1 in eWAT, increased expression of Fndc5 and Ct-1 in muscle and a decreased expression of hepatic Dpp-4. In human differentiated adipocytes, MaR1 increased the expression of ADIPONECTIN, LEPTIN, DPP4, CT-1 and FNDC5. Moreover, MaR1 counteracted the downregulation of ADIPONECTIN and the upregulation of DPP-4 and LEPTIN observed in adipocytes treated with TNF-& alpha;. Differential effects for TNF-& alpha; and MaR1 on the expression of CT-1 and FNDC5 were observed between both models of human adipocytes. In conclusion, MaR1 reverses the expression of specific adipomyokines and hepatokines altered in obese mice in a tissue-dependent manner. Moreover, MaR1 regulates the basal expression of adipokines in human adipocytes and counteracts the alterations of adipokines expression induced by TNF-& alpha; in vitro. These actions could contribute to the metabolic benefits of this lipid mediator.
- Effects of glucosinolate-enriched red radish (Raphanus sativus) on in vitro models of intestinal microbiota and metabolic syndrome-related functionalities(2023) Rosés, C. (Carles); Barceló, A. (Anna); Milagro-Yoldi, F.I. (Fermín Ignacio); Carvajal, M. (Micaela); Tomás-Cobos, L. (Lidia); Gallego, E. (Elisa); Garcia-Ibañez, P. (Paula); Agudelo, A. (Agatha)The gut microbiotaprofile is determined by diet composition, andtherefore this interaction is crucial for promoting specific bacterialgrowth and enhancing the health status. Red radish (Raphanus sativus L.) contains severalsecondary plant metabolites that can exert a protective effect onhuman health. Recent studies have shown that radish leaves have ahigher content of major nutrients, minerals, and fiber than roots,and they have garnered attention as a healthy food or supplement.Therefore, the consumption of the whole plant should be considered,as its nutritional value may be of greater interest. The aim of thiswork is to evaluate the effects of glucosinolate (GSL)-enriched radishwith elicitors on the intestinal microbiota and metabolic syndrome-relatedfunctionalities by using an in vitro dynamic gastrointestinalsystem and several cellular models developed to study the GSL impacton different health indicators such as blood pressure, cholesterolmetabolism, insulin resistance, adipogenesis, and reactive oxygenspecies (ROS). The treatment with red radish had an influence on short-chainfatty acids (SCFA) production, especially on acetic and propionicacid and many butyrate-producing bacteria, suggesting that consumptionof the entire red radish plant (leaves and roots) could modify thehuman gut microbiota profile toward a healthier one. The evaluationof the metabolic syndrome-related functionalities showed a significantdecrease in the gene expression of endothelin, interleukin IL-6, andcholesterol transporter-associated biomarkers (ABCA1 and ABCG5), suggestingan improvement of three risk factors associated with metabolic syndrome.The results support the idea that the use of elicitors on red radishcrops and its further consumption (the entire plant) may contributeto improving the general health status and gut microbiota profile.
- Crosstalk between gut microbiota and epigenetic markers in obesity development: relationship between ruminococcus, BMI, and MACROD2/SEL1L2 methylation(2023) Martinez, J.A. (José Alfredo); Riezu-Boj, J.I. (José Ignacio); Milagro-Yoldi, F.I. (Fermín Ignacio); Salas-Pérez, F. (Francisca); Silveira-Assmann, T. (Taís); Ramos-López, O. (Omar)Changes in gut microbiota composition and in epigenetic mechanisms have been proposed to play important roles in energy homeostasis, and the onset and development of obesity. However, the crosstalk between epigenetic markers and the gut microbiome in obesity remains unclear. The main objective of this study was to establish a link between the gut microbiota and DNA methylation patterns in subjects with obesity by identifying differentially methylated DNA regions (DMRs) that could be potentially regulated by the gut microbiota. DNA methylation and bacterial DNA sequencing analysis were performed on 342 subjects with a BMI between 18 and 40 kg/m(2). DNA methylation analyses identified a total of 2648 DMRs associated with BMI, while ten bacterial genera were associated with BMI. Interestingly, only the abundance of Ruminococcus was associated with one BMI-related DMR, which is located between the MACROD2/SEL1L2 genes. The Ruminococcus abundance negatively correlated with BMI, while the hypermethylated DMR was associated with reduced MACROD2 protein levels in serum. Additionally, the mediation test showed that 19% of the effect of Ruminococcus abundance on BMI is mediated by the methylation of the MACROD2/SEL1L2 DMR. These findings support the hypothesis that a crosstalk between gut microbiota and epigenetic markers may be contributing to obesity development.