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Associations Between Eating Patterns and Risk of Metabolic Dysfunction-Associated Steatotic Liver Disease

A special issue of Nutrients (ISSN 2072-6643). This special issue belongs to the section "Nutrition and Metabolism".

Deadline for manuscript submissions: 15 January 2026 | Viewed by 375

Special Issue Editor


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Guest Editor
Lifecourse Epidemiology of Adiposity and Diabetes (LEAD) Center, Colorado School of Public Health, University of Colorado Anschutz Medical Campus, Aurora, CO, USA
Interests: pediatric nutrition; maternal and child health; lifecourse research; body composition; youth-onset metabolic diseases; childhood obesity

Special Issue Information

Dear Colleagues,

This Special Issue will highlight studies examining the link between eating patterns and the risk of metabolic dysfunction-associated steatotic liver disease (MASLD), the most common chronic liver disease worldwide. Alongside obesity and type 2 diabetes, the prevalence of MASLD has increased considerably over recent decades, driven by a complex combination of intrinsic and extrinsic factors, including diet- and nutrition-related risk factors. For this Special Issue, we invite the submission of original research articles how various aspects of diet, nutrition, and eating patterns—including the composition, timing, and frequencies of meals, as well as relative adherence to specific dietary patterns—may affect the onset and progression of MASLD. A better understanding of the role of modifiable, dietary risk factors in the pathogenesis of MASLD could help to guide more effective disease prevention strategies and inform dietary interventions for those at risk of, or living with, MASLD.

Dr. Catherine Cohen
Guest Editor

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Keywords

  • MASLD
  • hepatic steatosis
  • fibrosis
  • dietary assessment
  • nutrition
  • added sugar
  • dietary patterns
  • obesity
  • saturated fat

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Published Papers (1 paper)

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Research

16 pages, 11386 KB  
Article
European Bilberry Extract Ameliorates Dietary Advanced Glycation End Products-Induced Non-Alcoholic Steatohepatitis in Rats via Gut Microbiota and Its Metabolites
by Lihui Shen, Ruijie Cheng, Wenwen Chen, Hongjie Liu, Xinyu Wang, Ruikun He, Xiaoxing Mo and Liegang Liu
Nutrients 2025, 17(24), 3918; https://doi.org/10.3390/nu17243918 - 15 Dec 2025
Viewed by 183
Abstract
Background: Gut dysbiosis is implicated in the pathogenesis of non-alcoholic steatohepatitis (NASH) caused by diets rich in advanced glycation end products (AGEs). European bilberry extract (EBE) exerts a regulatory effect on gut microbiota. Nevertheless, it is still unknown whether EBE influences NASH via [...] Read more.
Background: Gut dysbiosis is implicated in the pathogenesis of non-alcoholic steatohepatitis (NASH) caused by diets rich in advanced glycation end products (AGEs). European bilberry extract (EBE) exerts a regulatory effect on gut microbiota. Nevertheless, it is still unknown whether EBE influences NASH via gut microbiota and their metabolites. This study aimed to investigate the effects and underlying mechanisms of EBE on NASH caused by a long-term AGEs diet. Methods: Rats fed with a high-AGE diet were orally administered with EBE for 80 weeks, and NASH was measured. 16S rRNA analysis and targeted metabolomics were used to detect gut microbiota and SCFA, respectively. The hepatic expression of SCFA receptors and that of the HMGB1/RAGE/NF-κB signaling pathway were detected to investigate the possible molecular mechanism. Results: EBE reduced the accumulation of AGEs in the circulation and liver of high-AGE diet-fed rats. EBE also ameliorated impaired glucose tolerance and insulin sensitivity, liver inflammation, steatosis, fibrosis, and dysfunction in high-AGE-fed rats. EBE reshaped high-AGE diet-induced gut dysbiosis by increasing short-chain fatty acid (SCFA)-producing bacteria and SCFA levels and reducing deleterious bacteria. Mechanistically, EBE promoted the activation of GPR43 and inhibited the activation of downstream HDAC3 and HMGB1/RAGE/NF-κB signaling pathway in the liver of high-AGE diet-fed rats. Additionally, EBE decreased the levels of TNF-α, IL-1β, and IL-6 and increased the level of IL-10 in the liver of high-AGE diet-fed rats. Conclusions: EBE promoted the production of SCFA, which might engage with the GPR43 receptor and inhibited the activation of HDAC3 and HMGB1/RAGE/NF-κB signaling pathway, ultimately alleviating NASH caused by a high-AGE diet. Full article
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