Fig. 5

The accumulation of AGEs in adipocytes may explain the inverse association between AGE levels and BMI; high-AGE diets are associated with greater fat consumption and an increased risk of abdominal obesity [55]. RAGE activation also raises circulating inflammatory cytokines while decreasing anti-inflammatory adipokines like adiponectin. IL-6 and leptin are recognized as inflammatory mediators in the presence of obesity [56]. Moreover, adipocyte hypertrophy is associated with enhanced RAGE expression [57]. However, the involvement of sRAGE in the prevention of age-related muscle mass loss must be addressed [58]. As a decoy receptor for AGEs and other inflammatory ligands, sRAGE attributed to the reduced ligand-mediated disruption, preventing AGEs from binding to the cell-bound full-length receptor RAGE [58] and inhibiting the obesogenic effects of AGE-RAGE interaction by diminishing AGES accumulation visceral fat, regulating leptin and Adiponectin release [56], reducing Insulin resistance [58]. AGEs = advanced glycation end products; RAGE = receptor for advanced glycation end products; sRAGE = soluble receptor for advanced glycation end products; IL-1 = interleukin-1; IL-6 = interleukin-6; TNF-α = Tumor Necrosis Factor alpha; BMI = Body mass index; WC = Waist Circumference