Figure 3.

The relationship between obesity‐induced intestinal inflammation and NAFLD. Obesity has been linked to changes in the composition of the human intestinal microbiota. Mechanistically, it activates inflammatory pathways in the gut, thereby changing the intestinal microbiota composition, this process can affect obesity and pro‐inflammatory status. Chronic inflammation in the intestines induces liver toxicity due to gut‐derived toxic products, such as LPS. These products trigger NAFLD by activating the pathway of immune and inflammatory responses, as well as other downstream TLR4, IRAK, JNK, and IKK complexes. Inflammation increases the severity of liver inflammation by enhancing intestinal permeability. Liver damage in nonalcoholic steatohepatitis further increases intestinal permeability and exacerbates intestinal inflammation. The use of prebiotics (which promote the growth of good intestinal flora) and probiotics (living microorganisms) in the gut flora can be beneficial for ameliorating both NAFLD and intestinal inflammation. IKK, I‐kappa B kinase; IRAK, interleukin‐1 receptor associates kinase; JNK, C‐Jun N‐terminal kinase; LPS, lipopolysaccharide; NAFLD, nonalcoholic fatty liver disease; TLR4, toll‐like receptor 4