Role of bioactive lipid mediators in obese adipose tissue inflammation and endocrine dysfunction

Abstract

a b s t r a c tWhite adipose tissue is recognized as an active endocrine organ implicated in the maintenance of metabolic homeostasis. However, adipose tissue function, which has a crucial role in the development of obesity-related comorbidities including insulin resistance and non-alcoholic fatty liver disease, is dysregulated in obese individuals. This review explores the physiological functions and molecular actions of bioactive lipids biosynthesized in adipose tissue including sphingolipids and phospholipids, and in particular fatty acids derived from phospholipids of the cell membrane. Special emphasis is given to polyunsaturated fatty acids of the omega-6 and omega-3 families and their conversion to bioactive lipid mediators through the cyclooxygenase and lipoxygenase pathways. The participation of omega-3-derived lipid autacoids in the resolution of adipose tissue inflammation and in the prevention of obesity-associated hepatic complications is also thoroughly discussed.

The Gut Bacteria-Driven Obesity Development

“…It is now recognized that adipose tissue is not simply a storage depot but rather an active endocrine tissue producing multiple pro-inflammatory proteins, namely adipokines, which increase insulin resistance [66]. …”

Impact of physical exercise on visceral adipose tissue fatty acid profile and inflammation in response to a high-fat diet regimen

“…Obesity is the result of a positive energy intake with low levels of physical activity, interacting or not with genetic factors, which explain at least in part the excess of visceral adiposity accumulation observed in large proportions worldwide (6). Obesity-associated inflammation is locally observed in the expanded VAT (7), but then becomes systemic through the release of several pro-inflammatory mediators, including interleukin (IL)-6 and tumor necrosis factor (TNF)-α, among others (7,8). Therefore, this inflammatory state triggers the secretion of macrophage chemoattractant protein (MCP)-1 by macrophages, which can either sustain a macrophage-like phenotype in undifferentiated precursor cells or diminish the ability of adipocytes to further expand and store lipids, thus supporting a deleterious "vicious cycle" (7,8).…”

“…Obesity-associated inflammation is locally observed in the expanded VAT (7), but then becomes systemic through the release of several pro-inflammatory mediators, including interleukin (IL)-6 and tumor necrosis factor (TNF)-α, among others (7,8). Therefore, this inflammatory state triggers the secretion of macrophage chemoattractant protein (MCP)-1 by macrophages, which can either sustain a macrophage-like phenotype in undifferentiated precursor cells or diminish the ability of adipocytes to further expand and store lipids, thus supporting a deleterious "vicious cycle" (7,8). Some recent studies reported that specific FA, such as saturated fatty acids (SFA) (9,10), monounsaturated fatty acids (11) and n6-polyunsaturated fatty acids (PUFA) (12) are involved in the pathophysiology of inflammation during obesity (1,2,13,14).…”

The Pharmacological Effect of Omega-3 Fatty Acids Prevent Cancer Progression in Colon and Breast Cancer

“…A lot of studies have shown that high omega-3-PUFA to n-6 PUFA is a strategy to prevent diseases. The current western diet is very high in n-6 PUFA and the ratio of n-6 PUFA / n-3 PUFA has risen to up to 20-30:1, pro-inflammatory and pro-thrombotic eicosanoids generated from omega-6 fatty acids are produced in larger quantities than those derived from omega-3 fatty acids [8].…”