Non-alcoholic fatty liver disease (NAFLD) and non-alcoholic steatohepatitis (NASH) are of growing concern with an estimated 75 - 100 million people diagnosed with NAFLD in the United States. Excessive fructose consumption may be associated with human NAFLD development and increased prevalence (1, 2). Indeed, increased fructose intake promotes fatty liver, obesity and inflammation in animal models (1). Fructose interacts with the gut microbiota to aid in NAFLD/NASH progression (3). This is important since dietary composition is able to influence gut microbial genera (4), and these changes may influence gut permeability. However, the mechanism by which fructose promotes gut permeability is unknown.