The role of inflammation in the development of insulin resistance in type 2 diabetes
Usui, I.; Tobe, K.
Nihon Rinsho. Japanese Journal of Clinical Medicine 69(3): 555-562
2011
ISSN/ISBN: 0047-1852 PMID: 21400856 Document Number: 651688
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.