There are now accumulating data that aging is associated with a low-grade inflammation, coined InflammAging by Claudio Franceschi (Franceschi et al., 2000). This status reflects an imbalance between the innate and the adaptive immune response. Whereas the pro-inflammatory cytokines such as IL-6, TNF-a are increasing, originating in particular from monocytes/macrophages as those infiltrating the various adipose tissues (Mazurek et al., 2003; Weisberg et al., 2003), those coming from the adaptive immune response are decreasing. In the meantime, as a compensatory mechanism, the anti-inflammatory cytokines originating from Th-2 cells of the adaptive immune response are also increasing. These changes add to the already increased production of pro-inflammatory cytokines by the increased abdominal fat cell mass (Unger, 2003; Eckel et al., 2005; Sharma et al., 2005). Indeed, central fat not only contributes to insulin resistance by direct secretion of pro-inflammatory cytokines, but also by the release of FFA, which, in turn, can stimulate the NFkB activation through the phosphorylation of 1KB via IKK leading to the production of more pro-inflammatory cytokines. Thus, increased pro-inflammatory cytokine levels participate in the development of the insulin resistance. In this context IL-6 was also associated with the frailty syndrome leading to loss of independence and poor prognosis.
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