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Resumen
Scope
This study evaluated the capacity of dietary catechin (C), quercetin (Q), and the combination of both (CQ), to attenuate adipose inflammation triggered by high fructose (HFr) consumption in rats and by tumor necrosis factor alpha (TNF‐α) in 3T3‐L1 adipocytes.
Methods and results
In rats, HFr consumption for 6 wk caused dyslipidemia, insulin resistance, reduced plasma adiponectin, adiposity, and adipose tissue inflammation. Dietary supplementation
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dc.contributor.author | Vazquez Prieto, Marcela Alejandra | |
dc.contributor.author | Bettaieb, Ahmed | |
dc.contributor.author | Rodriguez Lanzi, Cecilia | |
dc.contributor.author | Soto Vargas, Verónica Carolina | |
dc.contributor.author | Perdicaro, Diahann Jeanette | |
dc.contributor.author | Galmarini, Claudio Romulo | |
dc.contributor.author | Haj, Fawaz G. | |
dc.contributor.author | Miatello, Roberto Miguel | |
dc.contributor.author | Oteiza, Patricia I. | |
dc.date.accessioned | 2019-02-27T17:20:41Z | |
dc.date.available | 2019-02-27T17:20:41Z | |
dc.date.issued | 2015-04 | |
dc.identifier.issn | 1613-4125 | |
dc.identifier.issn | 1613-4133 (Online) | |
dc.identifier.other | https://doi.org/10.1002/mnfr.201400631 | |
dc.identifier.uri | http://hdl.handle.net/20.500.12123/4509 | |
dc.description.abstract | Scope This study evaluated the capacity of dietary catechin (C), quercetin (Q), and the combination of both (CQ), to attenuate adipose inflammation triggered by high fructose (HFr) consumption in rats and by tumor necrosis factor alpha (TNF‐α) in 3T3‐L1 adipocytes. Methods and results In rats, HFr consumption for 6 wk caused dyslipidemia, insulin resistance, reduced plasma adiponectin, adiposity, and adipose tissue inflammation. Dietary supplementation with 20 mg/kg/day of C, Q, and CQ improved all these parameters. In 3T3‐L1 adipocytes, C and Q attenuated TNF‐α‐induced elevated protein carbonyls, increased proinflammatory cytokine expression (MCP‐1, resistin), and decreased adiponectin. The protective effects of C and Q on adipose inflammation are in part associated with their capacity to (i) decrease the activation of the mitogen‐activated kinases (MAPKs) JNK and p38; and (ii) prevent the downregulation of PPAR‐γ. In summary, C and Q, and to a larger extent the combination of both, attenuated adipose proinflammatory signaling cascades and regulated the balance of molecules that improve (adiponectin) or impair (TNF‐α, MCP‐1, resistin) insulin sensitivity. Conclusion Together, these findings suggest that dietary Q and C may have potential benefits in mitigating MetS‐associated adipose inflammation, oxidative stress, and insulin resistance. | eng |
dc.format | application/pdf | eng |
dc.language.iso | eng | |
dc.publisher | Wiley | eng |
dc.rights | info:eu-repo/semantics/restrictedAccess | eng |
dc.source | Molecular nutrition and food research 59 (4) : 622-633. (April 2015) | eng |
dc.subject | Catechin | eng |
dc.subject | Catequina | es_AR |
dc.subject | Quercetin | eng |
dc.subject | Quercetina | es_AR |
dc.subject | Adipose Tissue | eng |
dc.subject | Tejido Adiposo | es_AR |
dc.subject | Inflammation | eng |
dc.subject | Inflamación | es_AR |
dc.subject | Flavonoids | eng |
dc.subject | Flavonoides | es_AR |
dc.subject | Fructose | eng |
dc.subject | Fructosa | es_AR |
dc.subject.other | Metabolic Syndrome | eng |
dc.subject.other | Síndrome Metabólico | es_AR |
dc.title | Catechin and quercetin attenuate adipose inflammation in fructose‐fed rats and 3T3‐L1 adipocytes | eng |
dc.type | info:ar-repo/semantics/artículo | es_AR |
dc.type | info:eu-repo/semantics/article | eng |
dc.type | info:eu-repo/semantics/publishedVersion | eng |
dc.description.origen | EEA La Consulta | es_AR |
dc.description.fil | Fil: Vazquez Prieto, Marcela Alejandra. Universidad Nacional de Cuyo. Facultad de Ciencias Médicas. Area de Fisiología Patológica; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico- Mendoza. Instituto de Medicina y Biología Experimental de Cuyo; Argentina | es_AR |
dc.description.fil | Fil: Bettaieb, Ahmed. University of California. Department of Nutrition; Estados Unidos | es_AR |
dc.description.fil | Fil: Rodriguez Lanzi, Cecilia. Universidad Nacional de Cuyo. Facultad de Ciencias Médicas. Area de Fisiología Patológica; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico- Mendoza. Instituto de Medicina y Biología Experimental de Cuyo; Argentina | es_AR |
dc.description.fil | Fil: Soto Vargas, Verónica Carolina. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - Mendoza. Instituto de Biología Agrícola de Mendoza. Universidad Nacional de Cuyo. Facultad de Ciencias Agrarias. Instituto de Biología Agrícola de Mendoza; Argentina | es_AR |
dc.description.fil | Fil: Perdicaro, Diahann Jeanette. Universidad Nacional de Cuyo. Facultad de Ciencias Médicas. Area de Fisiología Patológica; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico- Mendoza. Instituto de Medicina y Biología Experimental de Cuyo; Argentina | es_AR |
dc.description.fil | Fil: Galmarini, Claudio Romulo. Instituto Nacional de Tecnología Agropecuaria (INTA). Estación Experimental Agropecuaria La Consulta; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentina. Universidad Nacional de Cuyo. Facultad de Ciencias Agrarias; Argentina | es_AR |
dc.description.fil | Fil: Haj, Fawaz G. University of California. Department of Nutrition; Estados Unidos. University of California. Department of Internal Medicine; Estados Unidos | es_AR |
dc.description.fil | Fil: Miatello, Roberto Miguel. Universidad Nacional de Cuyo. Facultad de Ciencias Médicas. Area de Fisiología Patológica; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico- Mendoza. Instituto de Medicina y Biología Experimental de Cuyo; Argentina | es_AR |
dc.description.fil | Fil: Oteiza, Patricia I. University of California. Department of Nutrition; Estados Unidos. University of California. Department of Environmental Toxicology; Estados Unidos | es_AR |
dc.subtype | cientifico |
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