2016
DOI: 10.1016/j.jnutbio.2016.04.004
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Fish-oil-derived n-3 polyunsaturated fatty acids reduce NLRP3 inflammasome activity and obesity-related inflammatory cross-talk between adipocytes and CD11b+ macrophages

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Cited by 41 publications
(49 citation statements)
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“…A vast literature shows that fish oil and krill oil have potential benefits against chronic disorders such as cardiovascular diseases, endocannabinoid dysregulation, poor infant development, non-alcoholic fatty liver disease, premenstrual syndrome, inflammation and certain cancers [28, 5557]. De Boer et al, suggest that n-3 polyunsaturated fatty acids reduce inflammation, partly by increasing adiponectin and reducing the intensity of adipocyte-macrophage cross-linking, to reduce obesity related diseases [58]. Haider et al, suggested that the preventive effect of krill oil was attributable to the synergistic action among n-3 PUFAs, phospholipids and astaxanthin [28].…”
Section: Discussionmentioning
confidence: 99%
“…A vast literature shows that fish oil and krill oil have potential benefits against chronic disorders such as cardiovascular diseases, endocannabinoid dysregulation, poor infant development, non-alcoholic fatty liver disease, premenstrual syndrome, inflammation and certain cancers [28, 5557]. De Boer et al, suggest that n-3 polyunsaturated fatty acids reduce inflammation, partly by increasing adiponectin and reducing the intensity of adipocyte-macrophage cross-linking, to reduce obesity related diseases [58]. Haider et al, suggested that the preventive effect of krill oil was attributable to the synergistic action among n-3 PUFAs, phospholipids and astaxanthin [28].…”
Section: Discussionmentioning
confidence: 99%
“…Nevertheless, evidence from in vitro and rodent in vivo studies suggests that EPA and DHA can decrease inflammatory adipokine production in adipocytes [ 34 , 35 , 36 , 37 , 38 , 39 , 40 , 41 , 42 , 43 ]. Further, in an in vitro co-culture model of obese AT, we have shown that LC n -3 PUFA reduce the inflammatory cross-talk between adipocytes and (i) macrophages [ 44 , 45 ]; (ii) cluster of differentiation (CD)8 + T cells [ 46 , 47 , 48 ] and (iii) (CD)4 + T cells [ 49 ] via, at least in part, downregulation of inflammatory adipokine synthesis and secretion. As discussed herein, multiple factors contribute to the development of AT dysfunction in obesity, but the focus of this review will include the changes in AT immune cellularity, dysregulation of adipokine secretion, and inflammatory signaling mechanisms in obese AT, while identifying potential targets for n -3 PUFA intervention to mitigate the ensuing metabolic consequences of obesity.…”
Section: Introductionmentioning
confidence: 99%
“…Such activation of the endothelial NLPR inflammasome is due to lysosome membrane permeabilization and cathepsin B release and can be suppressed by lysosome stabilization agents [103]. Thus, the Ad-induced inhibition of NLRP3 inflammasome activation, as recently documented [104] may represent an original and pivotal crosstalk mechanism to mitigate endothelial dysfunctions due to metabolic derangements.…”
Section: Endothelial Dysfunction and Metaflammationmentioning
confidence: 89%