title: Toll-like receptor 2/4 links to free fatty acid-induced inflammation and β-cell dysfunction.
abstract: T2D is a metabolic and inflammatory disease characterized by deteriorating β-cell function and increased levels of inflammatory cytokines. Low-grade inflammation and innate immune system activation lead to β-cell failure. Recently, SFAs have been proposed as triggers of metabolism-associated inflammation through the TLR family of PRRs. In this review, recent progress in defining the molecular basis of FFA-associated TLR2/4 activation and signaling in β-cell dysfunction and apoptosis is summarized. Furthermore, we highlight links between TLRs and diabetic complications, insulin resistance, and autophagy. This knowledge may facilitate novel strategies to abrogate inflammation in T2D.
authors.affiliation: 1.Shanghai First People's Hospital, Shanghai Jiao Tong University, 100 Haining Rd., Shanghai, 200080, China. pyongde@hotmail.com.
authors.forename: Jiajing
authors.initials: J
authors.lastname: Yin
authors.forename: Yongde
authors.initials: Y
authors.lastname: Peng
authors.forename: Jingcheng
authors.initials: J
authors.lastname: Wu
authors.forename: Yufan
authors.initials: Y
authors.lastname: Wang
authors.forename: Lili
authors.initials: L
authors.lastname: Yao
mesh_terms: D000818:Animals; D017209:Apoptosis; D048909:Diabetes Complications / Q000378:metabolism; D003924:Diabetes Mellitus, Type 2 / Q000188:drug therapy / Q000276:immunology / Q000378:metabolism; D005227:Fatty Acids / Q000378:metabolism*; D006801:Humans; D007249:Inflammation / Q000276:immunology* / Q000378:metabolism*; D007333:Insulin Resistance; D050417:Insulin-Secreting Cells / Q000276:immunology / Q000378:metabolism*; D015398:Signal Transduction; D051195:Toll-Like Receptor 2 / Q000037:antagonists & inhibitors / Q000378:metabolism*; D051197:Toll-Like Receptor 4 / Q000037:antagonists & inhibitors / Q000378:metabolism*
chemical_list: D005227:Fatty Acids; D051195:Toll-Like Receptor 2; D051197:Toll-Like Receptor 4
keywords: FFA; TLR 2/4; apoptosis; autophagy; type 2 diabetes