The “Big Bang” in obese fat: events initiating obesity-induced adipose tissue inflammation

摘要: Obesity is associated with the accumulation of pro-inflammatory cells in visceral adipose tissue (VAT), which an important underlying cause insulin resistance and progression to diabetes mellitus type 2 (DM2). Although role cytokines disease development established, initiating events leading immune cell activation remain elusive. Lean predominantly populated regulatory cells, such as eosinophils innate lymphocytes. These maintain homeostasis through excretion cytokines, IL-4, IL-5, IL-13, keep macrophages (ATMs) anti-inflammatory, M2-like state. Diet-induced obesity loss 1 inflammatory responses VAT, characterized by IFN-γ. A key event a shift ATMs toward M1 phenotype. Recent studies show that obesity-induced adipocyte hypertrophy results upregulated surface expression stress markers. Adipose detected local sentinels, NK CD8(+) T produce IFN-γ, driving ATM polarization. rapid VAT follows, inflammation. In this review, we provide overview inflammation, special focus on marks initiation