Key result
Obesity induces chronic inflammation via adipose remodeling, contributing to metabolic and autoimmune disorders.
Why the study?
Obesity and associated chronic inflammation lead to metabolic and autoimmune disorders, and a better understanding of these mechanisms could yield new treatments.
Understanding the mechanisms of obesity-induced chronic inflammation may provide new therapeutic targets for metabolic and autoimmune disorders.
May guide anti-inflammatory strategies in obese patients; leaves open whether targeting these pathways improves outcomes.
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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Artemniak-Wojtowicz et al. (2021) conducted a review in Obesity and chronic inflammation. Obesity was evaluated. Obesity induces chronic, low-grade inflammation through adipose tissue remodeling, immune cell infiltration, and altered adipokine secretion, contributing to metabolic and autoimmune disorders.
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