The inflammatory phenotype of ob/ob mice originates from the gut microbiota, since changing the gut microbiota using antibiotics lowers endotoxaemia-induced inflammation and metabolic disorders.6, 64, 65 Recently, it has been proposed that this higher endotoxaemia in ob/ob mice and db/db mice was dependent on a disruption of the key tight-junction proteins, ZO-1 and occludin.26 Here we confirm that obese mice exhibit an altered gut barrier, characterised by a disruption of tight-junction proteins. Here, OCLN is linked to metabolic disease.