2004
DOI: 10.1053/j.gastro.2004.06.049
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Activation of PPAR γ and δ by conjugated linoleic acid mediates protection from experimental inflammatory bowel disease

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Cited by 355 publications
(373 citation statements)
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References 73 publications
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“…Consistent with this theory, whole-body PPAR-␥ ϩ/Ϫ mice and immune cell-specific PPAR-␥ null mice are more susceptible to autoimmune and intestinal inflammatory diseases (34,37,42). Furthermore, PPAR-␥ activation by synthetic or natural agonists in an inflammatory setting limits the extent of tissue injury (10,11).…”
Section: Discussionmentioning
confidence: 85%
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“…Consistent with this theory, whole-body PPAR-␥ ϩ/Ϫ mice and immune cell-specific PPAR-␥ null mice are more susceptible to autoimmune and intestinal inflammatory diseases (34,37,42). Furthermore, PPAR-␥ activation by synthetic or natural agonists in an inflammatory setting limits the extent of tissue injury (10,11).…”
Section: Discussionmentioning
confidence: 85%
“…Tissue-specific PPAR-␥ fl/fl; MMTV-Cre ϩ (i.e., hemopoietic and epithelial cell-deficient) PPAR-␥ null mice and PPAR-␥ fl/fl; MMTV-Cre Ϫ littermates in a C57BL6/J background were generated by using the Cre-lox recombination system as previously described (37,38). The mice were maintained in the animal facilities at Virginia Polytechnic Institute and State University and used at 6 -8 wk.…”
Section: Micementioning
confidence: 99%
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“…Chronically high intracellular Ca 21 levels can activate calcineurin, which appears to be needed in the conversion to oxidative muscle phenotype (Bigard et al, 2000;Delling et al, 2000). Narkar et al (2008) found that peroxisome proliferator-activated receptor d (PPARd) agonist can increase oxidative myofibres in adult mice, and CLA can act as a ligand for some of PPARs family, such as PPARa, g and d (Meadus et al, 2002;Bassaganya-Riera et al, 2004). Furthermore, Chang (2007) reported that PGC-1a activation, in partnership with nuclear hormone receptors, including PPARs, could increase oxidative capacity in skeletal muscle.…”
Section: Discussionmentioning
confidence: 99%
“…A inibição da ativação de NF-κB também foi observada em células da musculatura lisa da artéria coronária de humanos. A associação com a inibição da produção de prostaglandina resultante do metabolismo do ácido araquidônico via cicloxigenases, também observada nessas células, pode explicar o efeito anti-aterogênico do CLA observado in vivo [139][140][141] .…”
Section: Cla E Receptores Ativados Por Proliferadores De Peroxissomounclassified