Abstract
Background: Pediatric metabolic-associated fatty liver disease (MAFLD) is a global health problem, with lifestyle modification as its major therapeutic strategy. Rigorous characterization of dietary content on MAFLD in children is lacking. We hypothesized an objectively measured healthier diet would positively modulate MAFLD. Methods: Diet was assessed using the Nutrition Data System for Research in children enrolled from 10 tertiary clinical centers to determine the Healthy Eating Index (HEI, 0-100) and individual food components. Results: In all, 119 children were included (13.3 ± 2.7 y), 80 (67%) male, 67 (18%) White, and 90 (76%) Hispanic, with an average body mass index Z-score of 2.2 ± 0.5. Diet was classified as low HEI < 47.94 (n = 39), mid HEI ≥ 47.94 and < 58.89 (n = 41), or high HEI ≥ 58.89 (n = 39). Children with high HEI (healthier diet) had lower body weight (p = 0.005) and more favorable lipids. Mean serum triglycerides for low, mid, and high HEI were 163, 148, and 120 mg/dL, respectively; p = 0.04 mid versus high, p = 0.01 low versus high. Mean HDL was 38, 41 and 43 mg/dL; p = 0.02 low vs high. Less severe steatosis was noted with added sugar ≤ 10% of calories (p = 0.03). Higher lobular inflammation is associated with a higher percentage of calories from fat (OR (95% CI) = 0.95 (0.91-1.00), p = 0.04). Conclusions: In children with MAFLD, high HEI is associated with lower body weight and more favorable lipids, while added sugar and fat intake has individual histologic features. Differential consumption of major dietary components may modify both metabolic risk factors and histologic liver injury, highlighting the importance of objective diet assessments in children with MAFLD.
Original language | English (US) |
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Pages (from-to) | e0320 |
Journal | Hepatology Communications |
Volume | 7 |
Issue number | 12 |
DOIs | |
State | Published - Dec 2023 |
Funding
The Nonalcoholic Steatohepatitis Clinical Research Network (NASH CRN) is supported by the National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK) (grants U01DK061713, U01DK061718, U01DK061728, U01DK061732, U01DK061734, U01DK 061737, U01DK061738, U01DK061730, U24DK061 730). Additional support is received from the National Center for Advancing Translational Sciences (NCATS) (grants UL1TR000077, UL1TR000150, UL1TR000424, UL1TR000006, UL1TR000448, UL1TR000040, UL1 TR000100, UL1TR000004, UL1TR000423, UL1TR00 0454). Ajay Jain had funding through the National Institutes of Health [NIH-1R01DK131136-01, NIH-R21AI169487-01]. The other authors received no additional funding. Please Note: CyNCh: The CyNCh trial was conducted by the NASH CRN and supported in part by the Intramural Research Program of the National Cancer Institute and by a Collaborative Research and Development Agreement (CRADA) between NIDDK and Raptor Pharmaceuticals. The authors thank the National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK) for its support of the NASH CRN and this research. The content is solely the responsibility of the authors and does not necessarily represent the official views of the National Institutes of Health.
ASJC Scopus subject areas
- Hepatology