2016
DOI: 10.1016/j.bbalip.2016.01.004
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Trans10, cis12 conjugated linoleic acid inhibits 3T3-L1 adipocyte adipogenesis by elevating β-catenin levels

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Cited by 19 publications
(13 citation statements)
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“…Accumulating evidence has demonstrated that c9, t11-CLA and t10, c12-CLA, two major isomers of CLA, have excellent biomedical properties for potential use in anticancer applications and for improving immunity, preventing inflammation, reducing obesity by different pathways such as Wnt/beta-catenin pathway, hormone-mediated mitogenic pathway, PPARc, 5-lipoxygenase (5-LOX) pathway and NF-jB pathway [6][7][8][12][13][14][15]. Although there was tremendous potential for the application of CLA isomers, their source of human daily intake was too limited to reach the recommended dosage, 3 g/d, which would be required to observe health benefits in human subjects [16].…”
Section: Resultsmentioning
confidence: 99%
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“…Accumulating evidence has demonstrated that c9, t11-CLA and t10, c12-CLA, two major isomers of CLA, have excellent biomedical properties for potential use in anticancer applications and for improving immunity, preventing inflammation, reducing obesity by different pathways such as Wnt/beta-catenin pathway, hormone-mediated mitogenic pathway, PPARc, 5-lipoxygenase (5-LOX) pathway and NF-jB pathway [6][7][8][12][13][14][15]. Although there was tremendous potential for the application of CLA isomers, their source of human daily intake was too limited to reach the recommended dosage, 3 g/d, which would be required to observe health benefits in human subjects [16].…”
Section: Resultsmentioning
confidence: 99%
“…In all of the possible cis and trans combinations of CLAs, c9, t11-CLA and t10, c12-CLA have been implicated as the most valuable isomers with noteworthy biological activities such as anti-carcinogenic, anti-obese, anti-diabetic and anti-hypertensive activities [4]. For example, it has been reported that c9, t11-CLA could inhibit the proliferation of estrogen receptor positive breast cancer cells by hormonemediated mitogenic pathways, and t10, c12-CLA could ameliorate disorders of glucose and lipid metabolism through PPARc and some other signal pathways [5][6][7][8]. Therefore, how to elevate the production of c9, t11-CLA and t10, c12-CLA has become a hot spot.…”
Section: Introductionmentioning
confidence: 99%
“…To account for our observations, t10,c12‐CLA must either inhibit the ability of c9,t11‐CLA and thiazolidinediones to bind to their mitochondrial targets, or antagonize the activity of PPARγ. While there is no publication describing the effect of t10,c12‐CLA in modulating mitochondrial metabolism, evidence is emerging for t10,c12‐CLA antagonism of activated PPARγ activity (Granlund et al, ; Yeganeh et al, ). Because c9,t11‐CLA and t10,c12‐CLA are equally efficient in activating PPARγ (Granlund et al, ), the outcome cannot be attributed to binding of CLA isomers to PPARγ per se , but alternative pathways activated by CLA (Clément et al, ).…”
Section: Discussionmentioning
confidence: 99%
“…Yeganeh et al showed that CLA-t10,c12 treatment increased the levels of β-catenin and its activity in 3T3-L1 adipocytes. β-catenin binds to PPARγ, and inhibits its activity to prevent the progression of adipogenesis [ 47 , 48 ]. These researches confirmed that CLA inhibited adipocyte adipogenesis via Wnt/β-catenin signalling.…”
Section: Discussionmentioning
confidence: 99%