Journal of Practical Hepatology ›› 2025, Vol. 28 ›› Issue (4): 485-488.doi: 10.3969/j.issn.1672-5069.2025.04.002
Previous Articles Next Articles
Hou Yu, Zou Guangxu, Zhao Yingpeng
Received:
2024-11-13
Online:
2025-07-10
Published:
2025-07-14
Hou Yu, Zou Guangxu, Zhao Yingpeng. A metabolomics perspective: unveiling two types of fatty liver diseases[J]. Journal of Practical Hepatology, 2025, 28(4): 485-488.
[1] Wong V W, Ekstedt M, Wong G L, et al. Changing epidemiology, global trends and implications for outcomes of NAFLD. J Hepatol, 2023, 79(3): 842-852. [2] Younossi Z M, Golabi P, Paik J M, et al. The global epidemiology of nonalcoholic fatty liver disease (NAFLD) and nonalcoholic steatohepatitis (NASH): A systematic review. Hepatology, 2023, 77(4): 1335-1347. [3] Sandlers Y. The future perspective: Metabolomics in laboratory medicine for inborn errors of metabolism. Transl Res, 2017, 189: 65-75. [4] 王慧星, 盛佳洁, 李萌. 代谢组学技术在心肌梗死生物标志物筛选中的研究进展. 心脑血管病防治, 2024, 24(4): 45-48. [5] Wang J H, Byun J, Pennathur S. Analytical approaches to metabolomics and applications to systems biology. Semin Nephrol, 2010, 30(5): 500-511. [6] Christofk H, Metallo C, Liu G, et al. Metabolic heterogeneity in humans. Cell, 2024, 187(15): 3821-3823. [7] Loomba R, Friedman S L, Shulman G I. Mechanisms and disease consequences of nonalcoholic fatty liver disease. Cell, 2021, 184(10): 2537-2564. [8] Friedman S L, Neuschwander-Tetri B A, Rinella M, et al. Mechanisms of NAFLD development and therapeutic strategies. Nat Med, 2018, 24(7): 908-922. [9] Powell E E, Wong V W, Rinella M. Non-alcoholic fatty liver disease. Lancet, 2021, 397(10290): 2212-2224. [10] Alves-Bezerra M, Cohen D E. Triglyceride metabolism in the liver. Compr Physiol, 2017, 8(1): 1-8. [11] Holeek M. The role of skeletal muscle in the pathogenesis of altered concentrations of branched-chain amino acids (valine, leucine, and isoleucine) in liver cirrhosis, diabetes, and other diseases. Physiol Res, 2021, 70(3): 293-305. [12] Newgard C B, An J, Bain J R, et al. A branched-chain amino acid-related metabolic signature that differentiates obese and leanhumans and contributes to insulin resistance. Cell Metab, 2009, 9(4): 311-326. [13] Lo E K K, Felicianna, Xu J H, et al. The emerging role of branched-chain amino acids in liver diseases. Biomedicines, 2022, 10(6): 1444. [14] Grzych G, Vonghia L, Bout M A, et al. Plasma bcaa changes in patients with NAFLD are sex dependent. J Clin Endocrinol Metab, 2020, 105(7): 175. [15] Lee M S, Han H J, Han S Y, et al. Loss of the e3 ubiquitin ligase mkrn1 represses diet-induced metabolic syndrome through ampk activation. Nat Commun, 2018, 9(1): 3404. [16] Zhang Y, Zhan L, Zhang L, et al. Branched-chain amino acids in liver diseases: Complexity and controversy. Nutrients, 2024, 16(12): 1875. [17] Feldman A, Eder S K, Felder T K, et al. Clinical and metabolic characterization of obese subjects without non-alcoholic fatty liver: A targeted metabolomics approach. Diabetes Metab, 2019, 45(2): 132-139. [18] de Mello V D, Sehgal R, Männistö V, et al. Serum aromatic and branched-chain amino acids associated with NASH demonstrate divergent associations with serum lipids. Liver Int, 2021, 41(4): 754-763. [19] Sehgal R, Ilha M, Vaittinen M, et al. Indole-3-propionic acid, a gut-derived tryptophan metabolite, associates with hepatic fibrosis. Nutrients, 2021, 13(10): 3509. [20] Hu C, Wang T, Zhuang X, et al. Metabolic analysis of early nonalcoholic fatty liver disease in humans using liquid chromatography-mass spectrometry. J Transl Med, 2021, 19(1): 152. [21] Dong S, Zhan Z Y, Cao H Y, et al. Urinary metabolomics analysis identifies key biomarkers of different stages of nonalcoholic fatty liver disease. World J Gastroenterol, 2017, 23(15): 2771-2784. [22] Mowry C J, Alonso C, Iruarrizaga-Lejarreta M, et al. Utility of metabolomic biomarkers to identify nonalcoholic fatty liver disease in liver transplant recipients. Transplant Direct, 2021, 7(12): e784. [23] Masarone M, Troisi J, Aglitti A, et al. Untargeted metabolomics as a diagnostic tool in NAFLD: Discrimination of steatosis, steatohepatitis and cirrhosis. Metabolomics, 2021, 17(2): 12. [24] Cabré N, Luciano-Mateo F, Baiges-Gayà G, et al. Plasma metabolic alterations in patients with severe obesity and non-alcoholic steatohepatitis. Aliment Pharmacol Ther, 2020, 51(3): 374-387. [25] Paul B, Lewinska M, Andersen J B. Lipid alterations in chronic liver disease and liver cancer. JHEP Rep, 2022, 4(6): 100479. [26] Gao S S, Shen Y L, Chen Y W, et al. Liver metabolomics analysis revealing key metabolites associated with different stages of nonalcoholic fatty liver disease in hamsters. Comb Chem High Throughput Screen, 2024, 27(9): 1303-1317. [27] Xie S, Yuan L, Sui Y, et al. Nme4 mediates metabolic reprogramming and promotes nonalcoholic fatty liver disease progression. EMBO Rep, 2024, 25(1): 378-403. [28] Tian Y, Jellinek M J, Mehta K, et al. Membrane phospholipid remodeling modulates nonalcoholic steatohepatitis progression by regulating mitochondrial homeostasis. Hepatology, 2024, 79(4): 882-897. [29] 赵驿歌, 赵一颖, 丰晨然, 等. 高脂饮食诱导的非酒精性脂肪肝大鼠模型的代谢组学研究. 中南药学, 2023, 21(11): 2920-2925. [30] McGlinchey A J, Govaere O, Geng D, et al. Metabolic signatures across the full spectrum of non-alcoholic fatty liver disease. JHEP Rep, 2022, 4(5): 100477. [31] Mogna-Peláez P, Romo-Hualde A, Riezu-Boj J I, et al. Isoliquiritigenin in combination with visceral adipose tissue and related markers as a predictive tool for nonalcoholic fatty liver disease. J Physiol Biochem, 2024, 80(3): 639-653. [32] Noureddin M, Truong E, Mayo R, et al. Serum identification of at-risk mash: The metabolomics-advanced steatohepatitis fibrosis score (masef). Hepatology, 2024, 79(1): 135-148. [33] Rinella M E, Lazarus J V, Ratziu V, et al. A multisociety Delphi consensus statement on new fatty liver disease nomenclature. Hepatology, 2023, 78(6): 1966-1986. [34] Ma X, Chen A, Melo L, et al. Loss of hepatic drp1 exacerbates alcoholic hepatitis by inducing megamitochondria and mitochondrial maladaptation. Hepatology, 2023, 77(1): 159-175. [35] Paquot N. [the metabolism of alcohol]. Rev Med Liege, 2019, 74(5-6): 265-267. [36] Cederbaum A I. Alcohol metabolism. Clin Liver Dis, 2012, 16(4): 667-685. [37] Lu Y, Cederbaum A I. Cyp2e1 and oxidative liver injury by alcohol. Free Radic Biol Med, 2008, 44(5): 723-738. [38] Zakhari S. Overview: How is alcohol metabolized by the body? Alcohol Res Health, 2006, 29(4): 245-254. [39] Shi C, Wang L, Zhou K, et al. Targeted metabolomics identifies differential serum and liver amino acids biomarkers in rats with alcoholic liver disease. J Nutr Sci Vitaminol (Tokyo), 2020, 66(6): 536-544. [40] Kumar U, Sharma S, Durgappa M, et al. Serum metabolic disturbances associated with acute-on-chronic liver failure in patients with underlying alcoholic liver diseases: An elaborative nmr-based metabolomics study. J Pharm Bioallied Sci, 2021, 13(2): 276-282. [41] Huang Y, Niu M, Jing J, et al. Metabolomic analysis uncovers energy supply disturbance as an underlying mechanism of the development of alcohol-associated liver cirrhosis. Hepatol Commun, 2021, 5(6): 961-975. [42] Xu R, Vatsalya V, He L, et al. Altered urinary tryptophan metabolites in alcohol-associated liver disease. Alcohol Clin Exp Res (Hoboken), 2023, 47(9): 1665-1676. [43] Xu R, He L, Vatsalya V, et al. Metabolomics analysis of urine from patients with alcohol-associated liver disease reveals dysregulated caffeine metabolism. Am J Physiol Gastrointest Liver Physiol, 2023, 324(2): G142-g154. [44] Calzadilla N, Zilberstein N, Hanscom M, et al. Serum metabolomic analysis in cirrhotic alcohol-associated liver disease patients identified differentially altered microbial metabolites and novel potential biomarkers for disease severity. Dig Liver Dis, 2024, 56(6): 923-931. [45] Fitzinger J, Rodriguez-Blanco G, Herrmann M, et al. Gender-specific bile acid profiles in non-alcoholic fatty liver disease. Nutrients, 2024, 16(2): 250. [46] Wang Y, Zou Z, Wang S, et al. Golden bile powder prevents drunkenness and alcohol-induced liver injury in mice via the gut microbiota and metabolic modulation. Chin Med, 2024, 19(1): 39. [47] Sun Y Y, Wu D Q, Yin N N, et al. Arrb2 causes hepatic lipid metabolism disorder via ampk pathway based on metabolomics in alcoholic fatty liver. Clin Sci (Lond), 2021, 135(10): 1213-1232. [48] Dong T, Hu G, Fan Z, et al. Activation of gpr3-β-arrestin2-pkm2 pathway in kupffer cells stimulates glycolysis and inhibits obesity and liver pathogenesis. Nat Commun, 2024, 15(1): 807. [49] Thiele M, Suvitaival T, Trošt K, et al. Sphingolipids are depleted in alcohol-related liver fibrosis. Gastroenterology, 2023, 164(7): 1248-1260. |
Viewed | ||||||
Full text |
|
|||||
Abstract |
|
|||||