In conclusion, we may suggest that the loss of TLR2 in conventionalized mice results in a reminiscent phenotype of metabolic syndrome, characterized by a clear difference in the gut microbiota, which induces insulin resistance, subclinical inflammation associated with ER stress, glucose intolerance, and later obesity, which is reproduced in WT by microbiota transplantation and can be reversed using antibiotics. Here, TLR2 is linked to metabolic syndrome.