Fig. 2. Transition from normal to impaired adipose tissue (AT) function and adverse systemic outcomes. AT serves important functions including energy storage, release of metabolites, body insulation, mechanical organ protection, endocrine secretion, and storage of xenobiotics under normal conditions. With a chronic positive energy balance and body weight gain, AT expands due to increased nutrient flux. Adipocytes primarily respond to the higher demand for energy storage by increasing their size (adipocyte hypertrophy). Adipocyte hypertrophy contributes to hypoxia, cellular and tissue stress, altered exosome production and release, and increased production of proinflammatory cytokines (including tumor necrosis factor-α [TNF-α], interleukin [IL]-1β, monocyte chemoattractant protein-1, chemerin, progranulin, plasminogen activator inhibitor-1 [PAI-1]), as well as activation of autophagy and apoptosis (mainly in visceral depots) and increased release of cell-free DNA. AT dysfunction is characterized by altered cellular composition including an increased number of immune cells. Symptoms of AT dysfunction include adipocyte hypertrophy, ectopic AT deposition, and immune cell infiltration of AT. Through different mechanisms including increased lipolysis, higher free fatty acid (FFA) release from AT, reduced glucose uptake, and increased secretion of diabetogenic, atherogenic, and proinflammatory signals, AT dysfunction is linked to endorgan damage. MCP-1, monocyte-chemotactic-protein-1.
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