IL6 and metabolic disease: The underlying mechanism linking increased intestinal permeability with metabolic diseases is likely the translocation of sub-clinical levels of gut-derived bacterial products such as lipopolysaccharide (LPS) from the intestinal lumen into the blood stream, activating immune responses and resulting in low-grade inflammation characterised by increased levels of C-reactive protein and cytokines such as tumour necrosis factor alpha (TNFα) and interleukin-6 (IL-6) [10,12].