Dietary Influences on Gut Microbiota and Their Role in Metabolic Dysfunction-Associated Steatotic Liver Disease (MASLD) DOI Open Access
Sevag Hamamah,

Oana C. Iatcu,

Mihai Covașă

et al.

Nutrients, Journal Year: 2024, Volume and Issue: 17(1), P. 143 - 143

Published: Dec. 31, 2024

Metabolic dysfunction-associated steatotic liver disease (MASLD) is a major contributor to liver-related morbidity, cardiovascular disease, and metabolic complications. Lifestyle interventions, including diet exercise, are first line in treating MASLD. Dietary approaches such as the low-glycemic-index Mediterranean diet, ketogenic intermittent fasting, high fiber diets have demonstrated potential addressing dysfunction underlying this condition. The development progression of MASLD closely associated with taxonomic shifts gut microbial communities, relationship well-documented literature. Given importance primary treatment for MASLD, it important understand how microbiota their byproducts mediate favorable outcomes induced by healthy dietary patterns. Conversely, changes conferred unhealthy patterns Western may induce dysbiosis influence through promoting hepatic inflammation, up-regulating lipogenesis, dysregulating bile acid metabolism, increasing insulin resistance, causing oxidative damage hepatocytes. Although emerging evidence has identified links between microbiota, significant gaps remain understanding specific roles, metabolite pathways, host interactions, causal relationships. Therefore, review aims provide mechanistic insights into role microbiota-mediated processes analysis both contribution pathophysiology. By better elucidating interplay nutrients, processes, onset work identify new opportunities targeted interventions treat efficiently.

Language: Английский

Contributing roles of mitochondrial dysfunction and hepatocyte apoptosis in liver diseases through oxidative stress, post-translational modifications, inflammation, and intestinal barrier dysfunction DOI Creative Commons
Karli R. LeFort, Wiramon Rungratanawanich, Byoung‐Joon Song

et al.

Cellular and Molecular Life Sciences, Journal Year: 2024, Volume and Issue: 81(1)

Published: Jan. 12, 2024

Abstract This review provides an update on recent findings from basic, translational, and clinical studies the molecular mechanisms of mitochondrial dysfunction apoptosis hepatocytes in multiple liver diseases, including but not limited to alcohol-associated disease (ALD), metabolic dysfunction-associated steatotic (MASLD), drug-induced injury (DILI). While ethanol-inducible cytochrome P450-2E1 (CYP2E1) is mainly responsible for oxidizing binge alcohol via microsomal ethanol system, it also metabolizing many xenobiotics, pollutants, chemicals, drugs, specific diets abundant n-6 fatty acids, into toxic metabolites organs, liver, causing pathological insults through organelles such as mitochondria endoplasmic reticula. Oxidative imbalances (oxidative stress) promote covalent modifications lipids, proteins, nucleic acids enzymatic non-enzymatic mechanisms. Excessive changes stimulate various post-translational (PTMs) transcription factors, histones. Increased PTMs proteins inactivate enzymes involved reduction oxidative species, acid metabolism, mitophagy pathways, leading dysfunction, energy depletion, apoptosis. Unique other organelles, control signaling cascades bioenergetics (fat metabolism), inflammation, apoptosis/necrosis hepatocytes. When homeostasis shifted, these pathways become altered or shut down, likely contributing death with activation inflammation hepatic stellate cells, fibrosis cirrhosis. will encapsulate how contributes hepatocyte several types diseases order provide recommendations targeted therapeutics.

Language: Английский

Citations

35
Lipopolysaccharide binding protein resists hepatic oxidative stress by regulating lipid droplet homeostasis DOI Creative Commons
Qilun Zhang, Xuting Shen, Xin Yuan

et al.

Nature Communications, Journal Year: 2024, Volume and Issue: 15(1)

Published: April 13, 2024

Abstract Oxidative stress-induced lipid accumulation is mediated by droplets (LDs) homeostasis, which sequester vulnerable unsaturated triglycerides into LDs to prevent further peroxidation. Here we identify the upregulation of lipopolysaccharide-binding protein (LBP) and its trafficking through as a mechanism for modulating LD homeostasis in response oxidative stress. Our results suggest that LBP induces controlling lipid-redox lipid-capture activity, sorting LDs. N-acetyl-L-cysteine treatment reduces LBP-mediated phospholipid/triglycerides competition Peroxiredoxin 4, redox state sensor regulates shuttle from Furthermore, chronic stress upregulates expression, leading insulin resistance obesity. findings contribute understanding role regulating against cellular peroxidative injury. These insights could inform development redox-based therapies alleviating metabolic dysfunction.

Language: Английский

Citations

16
Gut microbiota contributes to bisphenol A-induced maternal intestinal and placental apoptosis, oxidative stress, and fetal growth restriction in pregnant ewe model by regulating gut-placental axis DOI Creative Commons
Hao Zhang,

Xia Zha,

Bei Zhang

et al.

Microbiome, Journal Year: 2024, Volume and Issue: 12(1)

Published: Feb. 17, 2024

Abstract Background Bisphenol A (BPA) is an environmental contaminant with endocrine-disrupting properties that induce fetal growth restriction (FGR). Previous studies on pregnant ewes revealed BPA exposure causes placental apoptosis and oxidative stress (OS) decreases efficiency, consequently leading to FGR. Nonetheless, the response of gut microbiota its role in aggravating BPA-mediated apoptosis, autophagy, mitochondrial dysfunction, endoplasmic reticulum (ERS), OS maternal placenta intestine are unclear ovine model gestation. Results Two ewe groups ( n = 8/group) were given either a subcutaneous (sc) injection corn oil (CON group) or (5 mg/kg/day) dissolved (BPA once daily, from day 40 110 The colonic digesta ileum tissue samples collected measure biomarkers ERS, OS. To investigate link between BPA-induced FGR ewes, transplantation (GMT) was conducted two mice 10/group) 0 18 gestation after removing their intestinal by antibiotics. results indicated aggravates ERS function injury ileum, dysbiosis ewes. GMT attributed resulting exposure. Conclusions Our findings indicate underlying gut-placental axis behind OS, further provide novel insights into modulating balance through medication probiotics, functioning via axis, alleviate gut-derived impairment

Language: Английский

Citations

11
Non-Pharmacological Approach to Diet and Exercise in Metabolic-Associated Fatty Liver Disease: Bridging the Gap between Research and Clinical Practice DOI Open Access
Hassam Ali, Muhammad Shahzil, Vishali Moond

et al.

Journal of Personalized Medicine, Journal Year: 2024, Volume and Issue: 14(1), P. 61 - 61

Published: Jan. 1, 2024

This review provides a practical and comprehensive overview of non-pharmacological interventions for metabolic-associated fatty liver disease (MASLD), focusing on dietary exercise strategies. It highlights the effectiveness coffee consumption, intermittent fasting, Mediterranean ketogenic diets in improving metabolic health. The emphasizes importance combining aerobic resistance training as critical approach to reducing fat increasing insulin sensitivity. Additionally, it discusses synergy between diet enhancing parameters role gut microbiota MASLD. paper underscores need holistic, individualized approach, integrating diet, exercise, health, patient motivation. also long-term benefits minimal risks lifestyle compared side effects pharmacological surgical options. calls personalized treatment strategies, continuous education, further research optimize therapeutic outcomes MASLD management.

Language: Английский

Citations

10
Portal hypertension in patients with nonalcoholic fatty liver disease: Current knowledge and challenges DOI Creative Commons
Anita Madir, Ivica Grgurević, Emmanuel Tsochatzis

et al.

World Journal of Gastroenterology, Journal Year: 2024, Volume and Issue: 30(4), P. 290 - 307

Published: Jan. 26, 2024

Portal hypertension (PH) has traditionally been observed as a consequence of significant fibrosis and cirrhosis in advanced non-alcoholic fatty liver disease (NAFLD). However, recent studies have provided evidence that PH may develop earlier stages NAFLD, suggesting there are additional pathogenetic mechanisms at work addition to fibrosis. The early development NAFLD is associated with hepatocellular lipid accumulation ballooning, leading the compression sinusoids. External intra-luminal obstacles cause mechanical forces such strain, shear stress elevated hydrostatic pressure turn activate mechanotransduction pathways, resulting endothelial dysfunction spatial distribution histological functional changes periportal perisinusoidal areas lobule considered responsible for pre-sinusoidal component patients NAFLD. Thus, current diagnostic methods hepatic venous gradient (HVPG) measurement tend underestimate portal (PP) patients, who might decompensate below HVPG threshold 10 mmHg, which most relevant indicator clinically (CSPH). This creates further challenges finding reliable method stratify prognostic risk this population patients. In theory, guided by endoscopic ultrasound overcome limitations avoiding influence component, but more investigations needed test its clinical utility indication. Liver spleen stiffness combination platelet count currently best-validated non-invasive approach diagnosing CSPH varices needing treatment. Lifestyle change remains cornerstone treatment together correcting components metabolic syndrome, using nonselective beta blockers, whereas emerging candidate drugs require robust confirmation from trials.

Language: Английский

Citations

10
The role of mitophagy in metabolic diseases and its exercise intervention DOI Creative Commons

Shaokai Tang,

Yuanwen Geng,

Qinqin Lin

et al.

Frontiers in Physiology, Journal Year: 2024, Volume and Issue: 15

Published: Jan. 29, 2024

Mitochondria are energy factories that sustain life activities in the body, and their dysfunction can cause various metabolic diseases threaten human health. Mitophagy, an essential intracellular mitochondrial quality control mechanism, maintain cellular homeostasis by removing damaged mitochondria participating developing diseases. Research has confirmed exercise regulate mitophagy levels, thereby exerting protective effects This article reviews role of diseases, on mitophagy, potential mechanisms exercise-regulated intervention providing new insights for future basic clinical research interventions to prevent treat

Language: Английский

Citations

8
Caffeic acid ameliorates metabolic dysfunction-associated steatotic liver disease via alleviating oxidative damage and lipid accumulation in hepatocytes through activating Nrf2 via targeting Keap1 DOI
Jinyu Zhang, Hao Ouyang,

Xin-Nan Gu

et al.

Free Radical Biology and Medicine, Journal Year: 2024, Volume and Issue: 224, P. 352 - 365

Published: Aug. 28, 2024

Language: Английский

Citations

8
Thyme, oregano, and rosemary: herbs and food supplements for the management of metabolic associated fatty liver disease DOI
Hamza Elbouny, Ayoub Amssayef,

Rania Benjamaa

et al.

Nutrire, Journal Year: 2025, Volume and Issue: 50(1)

Published: Jan. 6, 2025

Language: Английский

Citations

1
Reviewing MAESTRO-NASH and the implications for hepatology and health systems in implementation/accessibility of Resmetirom DOI Creative Commons
Paul Brennan, Christopher J. Kopka,

Leire Agirre-Garrido

et al.

npj gut and liver., Journal Year: 2025, Volume and Issue: 2(1)

Published: Jan. 22, 2025

Language: Английский

Citations

1
Inflammatory Indices and MAFLD Prevalence in Hypertensive Patients: A Large-Scale Cross-Sectional Analysis from China DOI Creative Commons
Di Shen, Xintian Cai,

Junli Hu

et al.

Journal of Inflammation Research, Journal Year: 2025, Volume and Issue: Volume 18, P. 1623 - 1638

Published: Feb. 1, 2025

Objective: Hypertension development and progression are largely influenced by inflammation, which plays a critical role activating the immune system causing damage to vascular endothelium. Metabolic dysfunction-associated fatty liver disease (MAFLD) is also associated with chronic low-grade drives via metabolic imbalances adipose tissue dysfunction. This study investigates relationship between inflammatory indices MAFLD in hypertensive patients assesses predictive accuracy of these for MAFLD. Methods: We performed cross-sectional analysis involving 34,303 from Chinese hospital-based registry. The diagnosis was established using dysfunction criteria alongside evidence hepatic steatosis confirmed through imaging. Complete blood counts were used calculate indices, including monocyte-to-lymphocyte ratio (MLR), neutrophil-to-lymphocyte (NLR), platelet-to-lymphocyte (PLR), systemic response index (SIRI), immune-inflammation (SII), aggregate inflammation (AISI). To assess MAFLD, multivariable logistic regression adjustments potential confounders. diagnostic performance analyzed receiver operating characteristic (ROC) curves area under curve (AUC) calculations. Results: Patients exhibited significantly elevated levels all compared those without. After adjustment, each standard deviation increase AISI, SIRI, SII 74%, 62%, 58% increased odds respectively. AUC AISI 0.659, indicating moderate accuracy. AUCs SIRI 0.626 0.619, respectively, while NLR, PLR, MLR had lower 0.593, 0.558, 0.589, Conclusion: In patients, especially show strong association their utility risk stratification within clinical settings. Further research needed evaluate effectiveness markers management Keywords: metabolic-dysfunction-associated disease, hypertension,

Language: Английский

Citations

1