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Lipid Metabolism and Nutritional Status in Patients Metabolic Dysfunction-Associated Steatotic Liver Disease (MASLD)

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

Deadline for manuscript submissions: 25 July 2026 | Viewed by 4393

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Dr. Toshihiro Sakurai

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Faculty of Health Sciences, Hokkaido University, Sapporo 060-0812, Japan
Interests: lipids; lipoproteins; LDL; HDL; lipid hydroperoxide; lipid droplets; mitochondria; oxidative stress; antioxidants; functional foods; lipidomics; non-alcoholic fatty liver disease (NAFLD); non-alcoholic steatohepatitis (NASH)

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Dear Colleagues,

The number of patients with non-alcoholic fatty liver disease (NAFLD), including non-alcoholic steatohepatitis (NASH), is increasing globally. It is believed that the onset of NASH is contributed to by abnormalities in the lipid metabolism and increased oxidative stress. Indeed, the onset of NASH has been linked to various diseases, such as metabolic syndrome, obesity, and diabetes. Most of the diseases may be explained as oxidative stress-related diseases. In recent years, the name and definition of NAFLD/NASH have been revised to MASLD/MASH, and it is attracting attention again. Research into the pathogenesis, prevention, treatment, and biomarkers of the disease has not been completed. To reduce its prevalence, solving these issues is an urgent task.

In this Special Issue of Nutrients, entitled ‘Lipid Metabolism and Nutritional Status in Patients Metabolic Dysfunction-Associated Steatotic Liver Disease (MASLD)’, we would consider and encourage researchers to submit articles that propose strategies for the early detection of MASLD/MASH, elucidate the possible risk factors of MASLD/MASH in vitro or in vivo, or propose possible interventions through physical exercise and nutrition- or food-derived treatments.

Dr. Toshihiro Sakurai
Guest Editor

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Keywords

MASLD
MASH
fibrosis
lipoprotein
oxidized lipoproteins
hydroperoxide
nutrition
prevention
treatment
biomarker

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Research

15 pages, 4543 KB

Open AccessArticle

Acteoside Ameliorates Hepatic Steatosis and Liver Injury in MASLD Mice Through Activation of PINK1/Parkin-Related Mitophagy Markers

by Meili Cong, Xinxin Qi, Hongguang Sun, Xinxuan Zhang, Yunxin Yan, Tao Liu and Jun Zhao

Nutrients 2026, 18(1), 118; https://doi.org/10.3390/nu18010118 - 29 Dec 2025

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Abstract

Objective: Acteoside (ACT) has different pharmacological properties such as antioxidant, hepatoprotective and anti-inflammatory effects. Impaired mitophagy has been recognized as an important pathogenic factor in metabolic dysfunction-associated steatotic liver disease (MASLD). Nevertheless, the possible therapeutic role of ACT in MASLD and the exact effect of ACT on mitophagy regulation are not explored. This study aims to elucidate the therapeutic efficacy of ACT in a high-fat and high-sugar (HFHS) diet-induced mouse model of MASLD and to determine whether its effects are related to the activation of PINK1/Parkin-related mitophagy markers. Methods: C57BL/6J mice were randomly allocated to control, model, rosuvastatin (RSF, 3 mg/kg), and ACT (30, 60, and 120 mg/kg) groups. Following a 14-week continuous intervention, biochemical parameters, liver histology, and mitophagy-related markers were assessed. Results: ACT administration significantly improved serum lipid profiles, liver function and insulin resistance, marked by reduced levels of MDA, IL-6, TNF-α, IL-1β, LDL-C, TC, TG, AST, ALT, HOMA-IR (p < 0.05), while increasing HDL-C and enhancing hepatic GSH-Px and SOD activities (p < 0.05). Histological examination revealed a notable attenuation of hepatic steatosis and lipid accumulation. At the molecular level, ACT promoted mitophagy activation, as indicated by upregulated PINK1, LC3II/I, and Parkin expression and downregulated P62 and p-P62. Electron microscopy further validated the restoration of mitochondrial morphology and reduction in lipid droplets. Conclusions: These results demonstrate that ACT ameliorates MASLD progression by improving metabolic homeostasis, reducing inflammation and oxidative stress, and alleviating PINK1/Parkin-related mitophagy impairment to restore mitophagy homeostasis. Our study highlights the potential of ACT as a new therapeutic agent for MASLD. Full article

(This article belongs to the Special Issue Lipid Metabolism and Nutritional Status in Patients Metabolic Dysfunction-Associated Steatotic Liver Disease (MASLD))

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11 pages, 428 KB

Open AccessArticle

Dihomo-γ-Linolenic Acid Elevation with Desaturase Imbalance in Metabolic Dysfunction-Associated Steatotic Liver Disease in a Japanese Health Checkups Cohort: HOZUGAWA Study, a Multi-Omic, Diet Adjusted Analysis

by Sayaka Kawai, Hiroshi Okada, Hideto Okamoto, Ren Yashiki, Megumi Minamida, Natsuko Shinagawa, Takahiro Ichikawa, Shinta Yamamoto, Noriyuki Kitagawa, Yoshitaka Hashimoto, Ryoichi Sasano, Kunimasa Yagi, Masahide Hamaguchi and Michiaki Fukui

Nutrients 2026, 18(1), 57; https://doi.org/10.3390/nu18010057 - 23 Dec 2025

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Abstract

Background/Objectives: Metabolic dysfunction-associated steatotic liver disease (MASLD) has been linked to dietary fat quality and polyunsaturated fatty-acid metabolism. We evaluated whether dietary n-6 fatty-acid intake, serum dihomo-γ-linolenic acid (DGLA), and desaturase-based indices for Δ5-desaturase (D5D) and Δ6-desaturase (D6D) are associated with MASLD. Methods: We conducted a cross-sectional analysis within the HOZUGAWA health checkup cohort in Japan (n = 289; 100 MASLD, 189 non-MASLD). Participants underwent hepatic ultrasonography, dietary assessment using the Brief Self-Administered Diet History Questionnaire, and fasting serum metabolomics by gas chromatography–mass spectrometry with solid-phase dehydration derivatization. Enzyme indices were defined as the D5D index = arachidonic acid/DGLA and the D6D proxy index = DGLA/linoleic acid (hereafter referred to as the D6D index) because γ-linolenic acid was not measured. Natural-log-transformed D5D index, D6D index, DGLA, and total dietary n-6 fatty-acid intake were entered into multivariable logistic regression models for MASLD adjusted for age, sex, BMI, alcohol intake, and total energy. Results: Compared with non-MASLD, MASLD showed higher serum DGLA, lower D5D index, and higher D6D index (all p ≤ 0.005), with no between-group differences in total energy intake, linoleic acid, total polyunsaturated fatty acids, or total dietary n-6 fatty-acid intake. Higher ln D5D was independently associated with lower odds of MASLD (OR 0.62, 95% CI 0.42–0.86), whereas higher ln D6D index (OR 1.42, 95% CI 1.04–1.95) and ln DGLA (OR 1.62, 95% CI 1.13–2.43) were each positively associated. Total dietary n-6 fatty-acid intake was not independently associated with MASLD. Conclusions: In this Japanese health examination cohort, an imbalance in estimated desaturase activities—lower D5D index and higher D6D index—together with higher serum DGLA was independently associated with MASLD, whereas n-6 intake showed no group difference or independent association. These findings suggest that enzyme-linked endogenous n-6 metabolic status may be more closely related to the MASLD phenotype than intake quantity alone. Full article

(This article belongs to the Special Issue Lipid Metabolism and Nutritional Status in Patients Metabolic Dysfunction-Associated Steatotic Liver Disease (MASLD))

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17 pages, 3215 KB

Open AccessArticle

Matcha Green Tea Improves Cafeteria-Diet-Induced NAFLD by Modulating the Gut Microbiota in Rats

by Ho-Ching Chong, Shu-Ting Tang, Yu-Chieh Tseng, Suh-Ching Yang, Yasuo Watanabe, Shizuo Yamada, Yu-Chen S. H. Yang and Ya-Ling Chen

Nutrients 2025, 17(19), 3051; https://doi.org/10.3390/nu17193051 - 24 Sep 2025

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Abstract

Background: The aim of this study was to investigate the effects of matcha on lipid metabolism, insulin resistance (IR), inflammation, and gut dysbiosis in non-alcoholic fatty liver disease (NAFLD) induced by a cafeteria diet. Methods: Forty-eight 7-week-old male Wistar rats were divided into six groups (n = 8), including a control group (C), C + 0.2% matcha group (C + 0.2%), C + 1% matcha group (C + 1%), cafeteria group (Caf), Caf + 0.2% matcha group (Caf + 0.2%), and Caf + 1% matcha group (Caf + 1%). All rats were sacrificed at the end of the 12th week of the experiment. A one-way analysis of variance (ANOVA), followed by a Fisher’s post hoc test, was used to determine the significant differences among each of the groups. Results: The results indicated that plasma experiment triglycerides (TGs) significantly increased in the Caf group compared to the C group, and significantly decreased TG levels were found in the Caf + 1% group compared to the Caf group. In addition, the liver total cholesterol and TG had significantly increased in the Caf group, while the 0.2% Matcha intervention can mitigate hepatic lipid accumulation. Blood sugar, serum insulin, the homeostasis model assessment of IR (HOMA-IR), and plasma leptin significantly increased in the Caf group and were significantly lower in the Caf + 0.2% and Caf + 1% groups. Hepatic cytokines significantly increased in the Caf group, while, on the other hand, significantly lower concentrations were found in the Caf + 1% group. In addition, beneficial bacteria including Akkermansia, Faecalibacterium, and Parabacteroides increased after matcha supplementation. Conclusions: These results suggested that 12 weeks of a cafeteria diet can induce abnormal lipid metabolism, IR, liver inflammation, and an altered gut microbiotic composition, while both the 0.2% and 1% matcha interventions might regulate obesity, lipid accumulation, IR, and inflammatory responses, and help maintain a healthier gut microbiota, which may then ameliorate the development of NAFLD. Full article

(This article belongs to the Special Issue Lipid Metabolism and Nutritional Status in Patients Metabolic Dysfunction-Associated Steatotic Liver Disease (MASLD))

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