Dietary fructose and intestinal barrier: potential risk factor in the pathogenesis of nonalcoholic fatty liver disease

Abstract 

Worldwide, not only the prevalence of obesity has increased dramatically throughout the last three decades but also the incidences of co-morbid conditions such as diabetes type 2 and liver disease have increased. The ‘hepatic manifestation of the metabolic syndrome’ is called nonalcoholic fatty liver disease (NAFLD) and comprises a wide spectrum of stages of liver disease ranging from simple steatosis to liver cirrhosis. NAFLD of different stages is found in ∼30% of adults and ∼20% in the US population. Not just a general overnutrition but also an elevated intake of certain macronutrients such as fat and carbohydrates and herein particularly fructose has been claimed to be risk factors for the development for NAFLD; however, the etiology of this disease is still unknown. The present review outlines some of the potential mechanisms associated with the development of NAFLD and fructose intake with a particular focus on the role of the intestinal barrier functions.

Abbreviations: GLUT-5, glucose transporter 5, HFSC, high-fructose corn syrup, HGF, hepatocyte growth factor, LBP, lipopolysaccharide binding protein, MTP, microsomal triglyceride transport protein, NAFLD, nonalcoholic fatty liver disease, NASH, nonalcoholic steatohepatitis, NFκB, nuclear factor kappaB, PAI-1, plasminogen activator inhibitor 1, TLR-4, toll-like receptor 4, TNFα, tumor necrosis factor alpha, VLDL, very-low-density lipoprotein

Keywords: NAFLD, Endotoxin, Fructose, Intestinal barrier