Adipose tissue inflammation in insulin resistance: review of mechanisms mediating anti-inflammatory effects of omega-3 polyunsaturated fatty acids

Abstract

Obesity is an increasingly costly and widespread epidemic, effecting 1 in 10 adults worldwide. It has been causally linked with both the metabolic syndrome and insulin resistance, both of which are associated with increased chronic inflammation. The exact mechanisms through which inflammation may contribute to both MetS and IR are numerous and their details are still largely unknown. Recently, micro-RNAs (miRNAs) have emerged as potential interventional targets due to their potential preventive roles in the pathogenesis of several diseases, including MetS and obesity. The purpose of this review paper is to discuss some of the known roles of miRNAs as mediators of inflammation-associated obesity and IR and how omega-3 polyunsaturated fatty acids may be used as a nutritional intervention for these disorders.

Keywords: inflammation; obesity; polyunsaturated fatty acids.

Figure 1

Potential pathways linking obesity-induced inflammation with insulin resistance. Different pathways which were proposed to have a role in the development of insulin resistance. This includes production of reactive oxidative species (ROS), activation of the nuclear factor-κappa B (NF-κB) pathway and inactivation of insulin receptor substrate-1 (IRS-1). Solid lines indicate positive relationships and dashed lines indicate negative ones. IL, interleukin; JNK, c-Jun N-terminal kinase; MCP-1, monocyte chemoattractant protein 1; SOCS-3 suppressor of cytokine signaling; TNF, tumor necrosis factor.

Figure 2

Suggested mechanisms of the anti-inflammatory effects of ω–3 polyunsaturated fatty acid (PUFA) by microRNAs (miRNA) in adipocytes. Different miRNAs are involved in adipocytes imbalance and might be targets of anti-inflammatory effects of ω−3 PUFA. ω−3 PUFAs might be regulating the expression of miR-221 and miR-222 in adipogenesis, miR-320 in insulin resistance, miR-103/miR-107 in mitochondrial respiration, miR-223 in M1 macrophages profile, and miR-146 in response to resolvin D1 effects. IL, interleukin; LTB4, leukotriene B4; MCP-1, monocyte chemoattractant protein 1; PGE₂, prostaglandin E2; ROS, reactive oxidative species; TNF, tumor necrosis factor.