title: [The role of inflammation in the development of insulin resistance in type 2 diabetes].
abstract: Insulin resistance observed in type 2 diabetes or obesity is closely associated with a state of low-grade inflammation. The gene expressions of numerous inflammatory mediators, such as proinflammatory cytokines, are increased in adipose tissues of human and animal models of obesity or type 2 diabetes. These inflammatory mediators inhibit insulin signaling with several mechanisms, such as serine-phosphorylation of IRS-1, the induction of SOCS3 and the activation of JNK or NFkappaB signaling in insulin-target tissues. They are mainly produced by the classically-activated macrophages, termed M1 macrophages, in obese adipose tissues. In contrast, alternatively-activated macrophages, termed M2 macrophages, are observed even in the non-obese adipose tissues. The activation of PPAR signaling is highly associated with the alternative activation of myeloid cells.
authors.affiliation: First Department of Internal Medicine, University of Toyama.
authors.forename: Isao
authors.initials: I
authors.lastname: Usui
authors.forename: Kazuyuki
authors.initials: K
authors.lastname: Tobe
mesh_terms: D003924:Diabetes Mellitus, Type 2 / Q000503:physiopathology*; D006801:Humans; D007249:Inflammation / Q000503:physiopathology*; D007333:Insulin Resistance; D008264:Macrophages / Q000502:physiology