“…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.…”