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Associations Between Eating Patterns and Risk of Metabolic Dysfunction-Associated Steatotic...
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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 August 2026 | Viewed by 1307

Special Issue Editor

Dr. Catherine Cohen

E-Mail Website
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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Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All submissions that pass pre-check are peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 250 words) can be sent to the Editorial Office for assessment.

Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. Nutrients is an international peer-reviewed open access semimonthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 2900 CHF (Swiss Francs). Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

Keywords

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

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Published Papers (2 papers)

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Research

15 pages, 290 KB  
Article
Dietary Patterns, Hepatic Fat Fraction, and the Role of Genotype
by Kyle Salmon, Catherine C. Cohen, Leslie Lange, Dana Dabelea and Wei Perng
Nutrients 2026, 18(7), 1087; https://doi.org/10.3390/nu18071087 - 28 Mar 2026
Viewed by 64
Abstract
Background/Objectives: We aimed to identify eating habits associated with hepatic fat fraction (HFF) and assess effect modification by an established genetic variant for fatty liver disease, PNPLA3 rs738409, among 381 general-risk adolescents. Methods: Dietary intake was assessed using the Block Kids [...] Read more.
Background/Objectives: We aimed to identify eating habits associated with hepatic fat fraction (HFF) and assess effect modification by an established genetic variant for fatty liver disease, PNPLA3 rs738409, among 381 general-risk adolescents. Methods: Dietary intake was assessed using the Block Kids Food Frequency Questionnaire and HFF was measured via magnetic resonance imaging (MRI) at age ~16 years. We first characterized naturally occurring dietary patterns using principal component analysis followed by reduced-rank regression with HFF as the response variable to identify a dietary pattern that is both relevant to the population and associated with HFF. Next, we investigated associations of the dietary pattern with HFF using linear regression models that accounted for maternal gestational diabetes, education, and prenatal smoking and child sex, age, Tanner stage, and BMI. Finally, we tested for a dietary pattern and PNPLA3 rs738409 interaction and stratified by genotype if P-interaction < 0.05. Results: The participants were 16.7 ± 1.2 years (range: 12.6–19.6 years). Half were female (50.4%) and 52.0% identified as non-Hispanic White. The dietary pattern of interest was composed of vegetables, fruit, nuts and seeds, oatmeal, sports bars, crackers and sandwiches, and beef, and was inversely associated with HFF (−0.48 [95% CI: −0.81, −0.16]). Stratified analyses revealed the strongest inverse association observed between the diet pattern score and HFF in the high-risk-variant (GG) group (−2.19 [−4.35, −0.03]), followed by the intermediate-risk (CG) group (−0.43 [−0.77, −0.10]), but not the low-risk (CC) group (−0.32 [−0.77, 0.13]). Conclusions: A diet high in vegetables, fruit, nuts and seeds, oatmeal, sports bars, crackers and sandwiches, and beef—potentially capturing an active, on-the-go lifestyle—is associated with lower HFF during adolescence, especially among individuals at genetic risk. Full article
(This article belongs to the Special Issue Associations Between Eating Patterns and Risk of Metabolic Dysfunction-Associated Steatotic Liver Disease)
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
Cited by 1 | Viewed by 879
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
(This article belongs to the Special Issue Associations Between Eating Patterns and Risk of Metabolic Dysfunction-Associated Steatotic Liver Disease)
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