dc.creatorBatista, M. L., Jr.
dc.creatorPeres, S. B.
dc.creatorMcDonald, M. E.
dc.creatorAlcântara, Paulo Sérgio Martins de
dc.creatorOlivan, M.
dc.creatorOtoch, José Pinhata
dc.creatorFarmer, S. R.
dc.creatorSeelaender, Marilia Cerqueira Leite
dc.date.accessioned2013-11-06T19:27:06Z
dc.date.accessioned2018-07-04T16:22:01Z
dc.date.available2013-11-06T19:27:06Z
dc.date.available2018-07-04T16:22:01Z
dc.date.created2013-11-06T19:27:06Z
dc.date.issued2012
dc.identifierCYTOKINE, LONDON, v. 57, n. 1, supl. 1, Part 1, pp. 9-16, JAN, 2012
dc.identifier1043-4666
dc.identifierhttp://www.producao.usp.br/handle/BDPI/42712
dc.identifier10.1016/j.cyto.2011.10.008
dc.identifierhttp://dx.doi.org/10.1016/j.cyto.2011.10.008
dc.identifier.urihttp://repositorioslatinoamericanos.uchile.cl/handle/2250/1634897
dc.description.abstractCancer cachexia is a multifaceted syndrome whose aetiology is extremely complex and is directly related to poor patient prognosis and survival. Changes in lipid metabolism in cancer cachexia result in marked reduction of total fat mass, increased lipolysis, total oxidation of fatty acids, hyperlipidaemia, hypertriglyceridaemia, and hypercholesterolaemia. These changes are believed to be induced by inflammatory mediators, such as tumour necrosis factor-alpha (TNF-alpha) and other factors. Attention has recently been drawn to the current theory that cachexia is a chronic inflammatory state, mainly caused by the host's reaction to the tumour. Changes in expression of numerous inflammatory mediators, notably in white adipose tissue (WAT), may trigger several changes in WAT homeostasis. The inhibition of adipocyte differentiation by PPAR gamma is paralleled by the appearance of smaller adipocytes, which may partially account for the inhibitory effect of PPAR gamma on inflammatory gene expression. Furthermore, inflammatory modulation and/or inhibition seems to be dependent on the IKK/NF-kappa B pathway, suggesting that a possible interaction between NF-kappa B and PPAR gamma is required to modulate WAT inflammation induced by cancer cachexia. In this article, current literature on the possible mechanisms of NF-kappa B and PPAR gamma regulation of WAT cells during cancer cachexia are discussed. This review aims to assess the role of a possible interaction between NF-kappa B and PPAR gamma in the setting of cancer cachexia as well as its significant role as a potential modulator of chronic inflammation that could be explored therapeutically. Crown Copyright (C) 2011 Published by Elsevier Ltd. All rights reserved.
dc.languageeng
dc.publisherACADEMIC PRESS LTD- ELSEVIER SCIENCE LTD
dc.publisherLONDON
dc.relationCYTOKINE
dc.rightsCopyright ACADEMIC PRESS LTD- ELSEVIER SCIENCE LTD
dc.rightsclosedAccess
dc.subjectCANCER CACHEXIA
dc.subjectINFLAMMATION
dc.subjectWHITE ADIPOSE TISSUE
dc.subjectNF-KAPPA B
dc.subjectPPAR GAMMA
dc.titleAdipose tissue inflammation and cancer cachexia: Possible role of nuclear transcription factors
dc.typeArtículos de revistas


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