Abstract

The role of nutrition and diet in the development of non-alcoholic fatty liver disease (NAFLD) is still not fully understood. In the present study, we determined if dietary pattern and markers of intestinal permeability differ between overweight children with and without NAFLD. In addition, in a feasibility study, we assessed the effect of a moderate dietary intervention only focusing on nutrients identified to differ between groups on markers of intestinal barrier function and health status. Anthropometric data, dietary intake, metabolic parameters, and markers of inflammation, as well as of intestinal permeability, were assessed in overweight children (n = 89, aged 5–9) and normal-weight healthy controls (n = 36, aged 5–9). Sixteen children suffered from early signs of NAFLD, e.g., steatosis grade 1 as determined by ultrasound. Twelve children showing early signs of NAFLD were enrolled in the intervention study (n = 6 intervention, n = 6 control). Body mass index (BMI), BMI standard deviation score (BMI-SDS), and waist circumference were significantly higher in NAFLD children than in overweight children without NAFLD. Levels of bacterial endotoxin, lipopolysaccharide-binding protein (LBP), and proinflammatory markers like interleukin 6 (IL-6) and tumor necrosis factor α (TNFα) were also significantly higher in overweight children with NAFLD compared to those without. Total energy and carbohydrate intake were higher in NAFLD children than in those without. The higher carbohydrate intake mainly resulted from a higher total fructose and glucose intake derived from a significantly higher consumption of sugar-sweetened beverages. When counseling children with NAFLD regarding fructose intake (four times, 30–60 min within 1 year; one one-on-one counseling and three group counselings), neither alanine aminotransferase (ALT) nor aspartate aminotransferase (AST) activity in serum changed; however, diastolic blood pressure (p < 0.05) and bacterial endotoxin levels (p = 0.06) decreased markedly in the intervention group after one year. Similar changes were not found in uncounseled children. Our results suggest that a sugar-rich diet might contribute to the development of early stages of NAFLD in overweight children, and that moderate dietary counseling might improve the metabolic status of overweight children with NAFLD.

Highlights

  • Non-alcoholic fatty liver disease (NAFLD) comprises a wide spectrum of diseases ranging from simple steatosis afflicted with fat accumulation to steatohepatitis, fibrosis, and even cirrhosis or hepatocellular carcinoma [1]

  • Whether or not general overnutriton or the intake of a specific dietary pattern is critical in the development of non-alcoholic fatty liver disease (NAFLD) and associated intestinal barrier dysfunction is yet to be fully clarified. Starting from this background, the aim of the present study was to determine if the dietary pattern and lifestyle of overweight children without NAFLD differs from overweight children showing early signs of NAFLD

  • Body weight was significantly higher in overweight children with NAFLD than in those without, while height was similar

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Summary

Introduction

Non-alcoholic fatty liver disease (NAFLD) comprises a wide spectrum of diseases ranging from simple steatosis afflicted with fat accumulation to steatohepatitis, fibrosis, and even cirrhosis or hepatocellular carcinoma [1]. It was shown that obese (ob/ob) mice, and mice fed a diet rich in saturated fats and/or fructose develop liver steatosis and early signs of hepatic inflammation within several weeks [17,18,19] It was repeatedly shown in these dietary models that the development of NAFLD was associated with alterations of intestinal barrier function and elevated bacterial endotoxin levels. In line with these findings, results of our own group and others suggest that, in adults and children with NAFLD, the development of the disease is associated with general overnutriton, and, frequently, an elevated intake of fructose and fat, as well as alterations of markers of intestinal barrier function [10,12,20,21,22]

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