Increased endotoxemia, which results from this trans- and paracellular intestinal translocation, triggers a slight increase in plasmatic levels of proinflammatory cytokines such as interleukin-6 (Il-6) and tumor necrosis factor-α (TNF-α) [5] and therefore participates in the onset of a low-grade metabolic inflammation. The gene discussed is IL6; the disease is serum lipopolysaccharide activity.