Nutrition, Intestinal Permeability, and Blood Ethanol Levels Are Altered in Patients with Nonalcoholic Fatty Liver Disease (NAFLD)
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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).
To determine if the nutritional intake, intestinal flora, and permeability and the development of NAFLD are related in humans.
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.
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.
Taken together, our results indicate that intestinal permeability, endogenous alcohol synthesis, and nutritional intake are markedly altered in patients with NAFLD.
KeywordsIntestinal barrier PAI-1 Carbohydrate Protein Ethanol Endotoxin
Body mass index
Diastolic blood pressure
High-performance-anion-exchange chromatography with pulsed amperometric detection
Lipopolysaccharide binding protein
Monounsaturated fatty acids
Nonalcoholic fatty liver disease
Orocecal transit time
Plasminogen activator inhibitor 1
Polyunsaturated fatty acids
Systolic blood pressure
Standard error of mean
Saturated fatty acids
Small intestinal bacterial overgrowth
Toll-like receptor 4
Tumor necrosis factor alpha
We would like to thank Prof. Dr. J.C. Bode and Prof. Dr. K.-P. Maier for their advice and the accompanying evaluation of the liver status of patients and controls included in the study. We further would like to thank Drs. C. Schäfer and K. Dirks for their assistance with the recruitment of patients for the study. We also would like to thank Prof. Dr. A. Heyar for his technical support with the determination of lactulose and mannitol concentrations in urine samples. This study was supported by a grant from the Center of Nutritional Medicine Hohenheim/Tübingen (PIs: AK and IB).
Conflict of interest
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