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Capsaicin, a spicy component of hot peppers, modulates adipokine gene expression and protein release from obese‐mouse adipose tissues and isolated adipocytes, and suppresses the inflammatory responses of adipose tissue macrophages
Author(s) -
Kang Ji-Hye,
Kim Chu-Sook,
Han In-Seob,
Kawada Teruo,
Yu Rina
Publication year - 2007
Publication title -
febs letters
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.593
H-Index - 257
eISSN - 1873-3468
pISSN - 0014-5793
DOI - 10.1016/j.febslet.2007.07.082
Subject(s) - adipokine , adipose tissue , endocrinology , inflammation , adiponectin , medicine , proinflammatory cytokine , capsaicin , adipose tissue macrophages , leptin , macrophage , adipocyte , chemistry , white adipose tissue , obesity , insulin resistance , receptor , biochemistry , in vitro
Adipokines are involved in the obesity‐induced chronic inflammatory response that plays a crucial role in the development of obesity‐related pathologies such as type II diabetes and atherosclerosis. We here demonstrate that capsaicin, a naturally occurring phytochemical, can suppress obesity‐induced inflammation by modulating adipokine release from and macrophage behavior in obese mice adipose tissues. Capsaicin inhibited the expressions of IL‐6 and MCP‐1 mRNAs and protein release from the adipose tissues and adipocytes of obese mice, whereas it enhanced the expression of the adiponectin gene and protein. The action of capsaicin is associated with NF‐κB inactivation and/or PPARγ activation. Moreover, capsaicin suppressed not only macrophage migration induced by the adipose tissue‐conditioned medium, but also macrophage activation to release proinflammatory mediators. Capsaicin may be a useful phytochemical for attenuating obesity‐induced inflammation and obesity‐related complications.