Therefore, it is plausible to suggest that a sustained high luminal concentration of glucose due to high sugar, per se, induces the upregulation of TLR2 expression in the small intestine and, consequently, may lead to chronic intestinal permeability, hyperglycaemia [52,57] and, metabolic endotoxemia [8], which may contribute to the onset and progression of obesity. This evidence concerns the gene TLR2 and obesity due to melanocortin 4 receptor deficiency.