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The evidences have been increasingly accumulated on the implication of inflammatory mediators like tumor necrosis factor-α (TNF-α) and interleukin-6 (IL-6) in the pathological states related to insulin resistance like obesity, type 2 diabetes and atherosclerosis. There seems a link between insulin resistance and these pro-inflammatory agents, secreted by macrophages and adipocytes. Th (helper) cells are differentiated into either Th1 or Th2 phenotypes. It is generally considered that Th1 phenotype is pro-inflammatory whereas Th2 phenotype exerts anti-inflammatory (protective) effects. The upregulation of Th1 phenotype may aggravate these pathologies. One of the adipokines, i.e., adiponectin, and insulin act as anti-inflammatory agents. Insulin also favours the differentiation of Th cells into Th2 phenotype. TNF-α and IL-6 might counter balance the action of insulin by interfering with insulin receptor signalling in these pathological situations. The agonists of PPARα and PPARγ, and n-3 polyunsaturated fatty acids may exert an anti-inflammatory effect by shifting Th1/Th2 balance to Th2 phenotype. The factors, implicated in the secretion of inflammatory mediators are not well known, though the role of glucose-induced oxidative stress has been underlined. In this article, we shed light on the cross-talk between pro- and anti-inflammatory agents in these patho-physiological states related to insulin resistance

Inflammation et immunité : implications dans l’obésité et le diabète de type 2