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. 2018 Sep 19;10(9):1329.
doi: 10.3390/nu10091329.

Non-Alcoholic Fatty Liver Disease in Overweight Children: Role of Fructose Intake and Dietary Pattern

Anika Nier  1 , Annette Brandt  2 , Ina Barbara Conzelmann  3 , Yelda Özel  4 , Ina Bergheim  5
Affiliations

Non-Alcoholic Fatty Liver Disease in Overweight Children: Role of Fructose Intake and Dietary Pattern

Anika Nier et al. Nutrients. .

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.

Keywords: NAFLD; children; dietary intervention; dietary pattern; fructose; overweight.

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Conflict of interest statement

The authors declare no conflicts of interest. The funders had no role in the design of the study; in the collection, analyses, or interpretation of data; in the writing of the manuscript, and in the decision to publish the results.

Figures

Figure 1
Figure 1
Study design of the feasibility study assessing the effect of a moderate dietary intervention focusing only on the reduction of fructose intake (−50%) on the health status of overweight children with non-alcoholic fatty liver disease (NAFLD).
Figure 2
Figure 2
(a) Body mass index (BMI), (b) BMI standard deviation score (BMI-SDS), (c) energy, (d) total fructose intake (free fructose and fructose derived from sucrose), and (e) physical and (f) sedentary activities of normal-weight (NW) children, overweight children without NAFLD (OW), and overweight children with NAFLD (NAFLD). Data are means ± standard error of the mean (SEM), * p < 0.05 overweight children in comparison to overweight children with NAFLD; NW children were not included in the statistical analysis, but are shown for comparison. Underreporters were excluded from the analysis.
Figure 3
Figure 3
(a) Plasma active plasminogen activator inhibitor 1 (PAI-1), (b) interleukin 6 (IL-6), (c) serum c-reactive protein (CRP), (d) tumor necrosis factor α (TNFα), (e) endotoxin, (f) lipopolysaccharide-binding protein (LBP) plasma concentrations of normal-weight (NW) children, overweight children without NAFLD (OW), and overweight children with NAFLD (NAFLD). Data are means ± SEM; * p < 0.05 overweight children in comparison to overweight children with NAFLD; NW children were not included in the statistical analysis, but are shown for comparison. Underreporters were excluded from the analysis.
Figure 3
Figure 3
(a) Plasma active plasminogen activator inhibitor 1 (PAI-1), (b) interleukin 6 (IL-6), (c) serum c-reactive protein (CRP), (d) tumor necrosis factor α (TNFα), (e) endotoxin, (f) lipopolysaccharide-binding protein (LBP) plasma concentrations of normal-weight (NW) children, overweight children without NAFLD (OW), and overweight children with NAFLD (NAFLD). Data are means ± SEM; * p < 0.05 overweight children in comparison to overweight children with NAFLD; NW children were not included in the statistical analysis, but are shown for comparison. Underreporters were excluded from the analysis.
Figure 4
Figure 4
(a) Plasma endotoxin, (b) serum IL-6, and (c) plasma TNFα concentrations of children with NAFLD enrolled in the control (Control) and intervention (Intervention) group at baseline (baseline) and at the end of the study (EoS). Data are means ± SEM; # p < 0.05 values at baseline between both groups; NW children were not included in the statistical analysis, but are shown for comparison. Underreporters were excluded from the analysis.
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