title: Nutrition, intestinal permeability, and blood ethanol levels are altered in patients with nonalcoholic fatty liver disease (NAFLD).
abstract: BACKGROUND
  A role of an altered dietary pattern (e.g., a diet rich in sugar) but also alterations at the level of the intestinal barrier have repeatedly been discussed to be involved in the development and progression of nonalcoholic fatty liver disease (NAFLD).
  
  
  OBJECTIVE
  To determine if the nutritional intake, intestinal flora, and permeability and the development of NAFLD are related in humans.
  
  
  METHODS
  Ten controls and 20 patients with NAFLD ranging from simple steatosis to steatohepatitis were included in the study. Bacterial overgrowth, orocecal transit time, and intestinal permeability were assessed. Alcohol, endotoxin, and plasminogen activator inhibitor (PAI-) 1 concentration were determined in plasma. Nutritional intake was assessed using a dietary history.
  
  
  RESULTS
  Despite no differences in the prevalence of bacterial overgrowth and in the orocecal transit time, intestinal permeability, alcohol, and endotoxin levels in plasma were significantly higher in patients with NAFLD than in controls. Similar results were also found for PAI-1 plasma concentrations. Patients with NAFLD had a significantly higher intake of protein, total carbohydrates, and mono- as well as disaccharides than controls. PAI-1, endotoxin, and ALT plasma levels were positively related to total protein and carbohydrate intake.
  
  
  CONCLUSIONS
  Taken together, our results indicate that intestinal permeability, endogenous alcohol synthesis, and nutritional intake are markedly altered in patients with NAFLD.
authors.affiliation: Department of Nutritional Medicine, University of Hohenheim, Stuttgart, Germany. volynets@uni-hohenheim.de
authors.forename: Valentina
authors.initials: V
authors.lastname: Volynets
authors.forename: Markus A
authors.initials: MA
authors.lastname: Küper
authors.forename: Stefan
authors.initials: S
authors.lastname: Strahl
authors.forename: Ina B
authors.initials: IB
authors.lastname: Maier
authors.forename: Astrid
authors.initials: A
authors.lastname: Spruss
authors.forename: Sabine
authors.initials: S
authors.lastname: Wagnerberger
authors.forename: Alfred
authors.initials: A
authors.lastname: Königsrainer
authors.forename: Stephan C
authors.initials: SC
authors.lastname: Bischoff
authors.forename: Ina
authors.initials: I
authors.lastname: Bergheim
mesh_terms: D000328:Adult; D016022:Case-Control Studies; D004040:Dietary Carbohydrates / Q000494:pharmacology; D004044:Dietary Proteins / Q000494:pharmacology; D018450:Disease Progression; D004731:Endotoxins / Q000097:blood; D000431:Ethanol / Q000097:blood*; D005234:Fatty Liver / Q000097:blood* / Q000503:physiopathology*; D005260:Female; D006801:Humans; D007422:Intestines / Q000382:microbiology / Q000502:physiology*; D008297:Male; D065626:Non-alcoholic Fatty Liver Disease; D009752:Nutritional Status / Q000502:physiology*; D010539:Permeability / Q000187:drug effects; D017395:Plasminogen Activator Inhibitor 1 / Q000097:blood
chemical_list: D004040:Dietary Carbohydrates; D004044:Dietary Proteins; D004731:Endotoxins; D017395:Plasminogen Activator Inhibitor 1; D000431:Ethanol