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 phosphor-ylation of IKB 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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