It was shown 1) that LPS, through TLR4 and CD14, participates to the low-grade inflammation observed during the metabolic diseases and aggravating the diseases and it was called endotoxemia [82, 83] and peptidoglycans through NOD2 can modulate colonization and intestinal inflammation influencing the sensitivity to insulin [84]; 2) the importance of dietary fibers and the SCFA production in the metabolism regulation through a GLP-1-dependant mechanism [85–88] and 3) the role of secondary biliary acid through TGR5 and FXR [81, 89, 90]. This evidence concerns the gene GCG and metabolic disease.