Abstract
Obesity and its two major comorbidities, insulin resistance and type 2 diabetes, represent worldwide health issues whose incidence is predicted to steadily rise in the coming years. Obesity is characterized by an accumulation of fat in metabolic tissues resulting in chronic inflammation. It is now largely accepted that adipose tissue inflammation underlies the etiology of these disorders. Adipose tissue macrophages (ATMs) represent the most enriched immune fraction in hypertrophic, chronically inflamed adipose tissue, and these cells play a key role in diet-induced type 2 diabetes and insulin resistance. ATMs are triggered by the continuous influx of dietary lipids, among other stimuli; however, how these lipids metabolically activate ATM depends on their nature, composition and localization. This review will discuss the fate and molecular programs elicited within obese ATMs by both exogenous and endogenous lipids, as they mediate the inflammatory response and promote or hamper the development of obesity-associated insulin resistance and type 2 diabetes.
Highlights
Once considered a high-income nation problem, obesity has all but tripled in the last 50 years, reaching pandemic proportions
The central role of AT in maintaining whole-body homeostasis is evidenced during obesity, as ectopic fatty acid (FA) and cholesterol (Chol) accumulation in cell types other than adipocytes leads to metabolic dysfunction
As it occurs in lysosomes, is mainly achieved by the action of LIPA, whose deficiency and overexpression have been shown to alter immune and metabolic (insulin signaling, very low-density lipoproteins (VLDL) metabolism, Adipose tissue macrophages (ATMs) lipid content, polyunsaturated fatty acid (PUFA) release and lipid mediator synthesis) homeostasis [52,53,54]
Summary
Once considered a high-income nation problem, obesity has all but tripled in the last 50 years, reaching pandemic proportions. MMe ATMs present significant changes in their intrinsic metabolism, including lipid mobilization (i.e., lysosomal catabolism, storage within lipid droplets (LDs) and efflux) and utilization (i.e., free fatty acids (FFA)/Chol synthesis and oxidation for energy production or membrane incorporation) [9,10,11]. On this account, the emerging fields of lipidomics and metabolomics have proven key in the study of ATM function in regard to individual lipid species. The object of this review is to discuss he current knowledge regarding ATM metabolic activation by dietary lipids
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