Abstract
The adipose tissue has been recognized as an active organ involved in numerous metabolic, hormonal and immunological processes. Obesity and associated chronic inflammation leads to many metabolic and autoimmune disorders. The number of cells, their phenotype and distribution in adipose tissue depends on the degree of obesity. Polarization of macrophages towards M1, neutrophils influx to adipose tissue, activation of Th1 and Th17 cells and increased level of proinflammatory cytokines are characteristic for obesity-induced inflammation. Several mechanisms, such as adipocytes’ hypoxia, oxidative stress, endoplasmic reticulum stress, impairment of PPAR receptors, inflammasomes’ activation and activation of TLR are involved into development of chronic obesity-induced inflammation. A better understanding of this processes can provide new treatments for obesity and related disorders.
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