Green tea extract improves high fat diet-induced hypothalamic inflammation, without affecting the serotoninergic system

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dc.contributor.author Okuda, Marcos H. [UNIFESP]
dc.contributor.author Zemdegs, Juliane C. S. [UNIFESP]
dc.contributor.author Santana, Aline A. de [UNIFESP]
dc.contributor.author Santamarina, Aline B. [UNIFESP]
dc.contributor.author Moreno, Mayara F. [UNIFESP]
dc.contributor.author Hachul, Ana C. L. [UNIFESP]
dc.contributor.author Santos, Bruno dos [UNIFESP]
dc.contributor.author Oller do Nascimento, Claudia M. [UNIFESP]
dc.contributor.author Ribeiro, Eliane B. [UNIFESP]
dc.contributor.author Oyama, Lila M. [UNIFESP]
dc.date.accessioned 2016-01-24T14:37:57Z
dc.date.available 2016-01-24T14:37:57Z
dc.date.issued 2014-10-01
dc.identifier http://dx.doi.org/10.1016/j.jnutbio.2014.05.012
dc.identifier.citation Journal of Nutritional Biochemistry. New York: Elsevier B.V., v. 25, n. 10, p. 1084-1089, 2014.
dc.identifier.issn 0955-2863
dc.identifier.uri http://repositorio.unifesp.br/handle/11600/38290
dc.description.abstract To investigate possible mechanisms of green tea's anti-obesity and anti-diabetic effects in the hypothalamus, the central regulator of metabolism, of mice fed with high-fat diet (HFD), we analyzed proteins of the toll-like receptor 4 (TLR4) pathway and serotoninergic proteins involved in energy homeostasis. Thirty-day-old male Swiss mice were fed with HFD rich in saturated fat and green tea extract (GTE) for 8 weeks. After that, body weight and mass of fat depots were evaluated. Oral glucose tolerance test was performed 3 days prior to euthanasia; serum glucose, insulin and adiponectin were measured in fasted mice. Hypothalamic TLR4 pathway proteins, serotonin receptors 1B and 2C and serotonin transporter were analyzed by Western blotting or enzyme-linked immunosorbent assay. A second set of animals was used to measure food intake in response to fluoxetine, a selective serotonin reuptake inhibitor. Mice fed with HFD had increased body weight and mass of fat depots, impaired oral glucose tolerance, elevated glucose and insulin and decreased adiponectin serum levels. TLR4, I kappa B-alpha, nuclear factor kappa B p50 and interleukin 6 were increased by HFD. Concomitant GTE treatment ameliorated these parameters. the serotoninergic system remained functional after HFD treatment despite a few alterations in protein content of serotonin receptors I B and 2C and serotonin transporter. in summary, the GTE attenuated the deleterious effects of the HFD investigated in this study, partially due to reduced hypothalamic inflammation. (C) 2014 Elsevier Inc. All rights reserved. en
dc.description.sponsorship DSM Nutritional Products Ltd., Basel, Switzerland
dc.description.sponsorship Coordenação de Aperfeiçoamento de Pessoal de Nível Superior (CAPES)
dc.description.sponsorship Conselho Nacional de Desenvolvimento Científico e Tecnológico (CNPq)
dc.description.sponsorship Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)
dc.format.extent 1084-1089
dc.language.iso eng
dc.publisher Elsevier B.V.
dc.relation.ispartof Journal of Nutritional Biochemistry
dc.rights Acesso restrito
dc.subject Green tea extract en
dc.subject High-fat diet en
dc.subject Hypothalamus en
dc.subject Neuroinflammation en
dc.subject Serotonin en
dc.title Green tea extract improves high fat diet-induced hypothalamic inflammation, without affecting the serotoninergic system en
dc.type Artigo
dc.rights.license http://www.elsevier.com/about/open-access/open-access-policies/article-posting-policy
dc.contributor.institution Universidade Federal de São Paulo (UNIFESP)
dc.description.affiliation Universidade Federal de São Paulo, Disciplina Fisiol Nutr, Dept Fisiol, BR-04023062 São Paulo, Brazil
dc.description.affiliationUnifesp Universidade Federal de São Paulo, Disciplina Fisiol Nutr, Dept Fisiol, BR-04023062 São Paulo, Brazil
dc.description.sponsorshipID FAPESP: 2009/14373-8
dc.description.sponsorshipID FAPESP: 2011/16199-5
dc.description.sponsorshipID FAPESP: 2012/03713-5
dc.identifier.doi 10.1016/j.jnutbio.2014.05.012
dc.description.source Web of Science
dc.identifier.wos WOS:000341799200012



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