N-3 Polyunsaturated Fatty Acids and Inflammation in Obesity: Local Effect and Systemic Benefit

Figure 1

Alteration occurring in adipose tissue when it suffers from excessive TAG accumulation. In the face of chronic overnutrition, excessive adipose tissue expansion is initiated and dominated by adipocyte hypertrophy, whereas adipocyte number becomes fixed with obese individuals achieving a higher plateau. Activated adipocytes trigger production of proinflammatory mediators, together with resident immune cells, exerting functions in an endocrine and paracrine fashion. Infiltration of immune cells is secondary consequence followed by adipocyte activation. Mature adipocytes promote diapedesis of monocytes through microvascular endothelial cells, facilitating monocyte-derived macrophages accumulation. Progressive recruitment of immune cells underpins inflammation in AT by enhancing proinflammatory mediator secretion. Additionally, obese state pathologically accelerates AT remodeling featured by ECM overproduction, necrotic adipocyte, and hypoxia, along with dysregulation in fatty acid fluxes. Macrophages are predominantly localized around dead adipocytes. Sensibly, lean individuals exhibit higher ratios of M2:M1 macrophages, Th1:Th2 T cells. With the development of obesity, major shift in the above cell ratios favors a modest inflammation status (originality is inspired by previous review written by Evan D. Rosen and Bruce M. Spiegelman. Based on former illustration focusing on recruitment of immune cells, more detail and latest information are injected into the figure).