中文|English
ISSN 1001-5256 (Print)
ISSN 2097-3497 (Online)
CN 22-1108/R
Volume 42 Issue 9
Sep.  2026
Turn off MathJax
Article Contents

Association of different blood lipid components with the severity of hepatic steatosis in metabolic dysfunction-associated fatty liver disease

DOI: 10.12449/JCH260910
Research funding:

Noncommunicable Chronic Diseases-National Science and Technology Major Project (2023ZD0508702);

Beijing Key Project of Major Disease by Chinese Medicine and Western Medicine (2023BJSZDYNJBXTGG-017);

Beijing High-Level Public Health Technical Personnel Construction Project (Discipline Backbone-03-40)

More Information
  • Corresponding author: You Hong, youhongliver@ccmu.edu.cn (ORCID: 0000-0001-9409-1158); Zhao Jingjie, zhaojj@ccmu.edu.cn (ORCID: 0000-0001-7763-1351)
  • Received Date: 2026-02-13
  • Accepted Date: 2026-03-20
  • Published Date: 2026-09-25
  •   Objective  To clarify the independent and synergistic effects of dyslipidemia in the progression of hepatic steatosis in metabolic dysfunction-associated fatty liver disease (MAFLD).  Methods  A total of 7 697 participants who underwent physical examination in Beijing Friendship Hospital, Capital Medical University, from January 2022 to December 2024 were enrolled, and finally 2 177 patients with MAFLD were enrolled as subjects. Transient elastography was used to quantify the severity of hepatic steatosis (grades S1-S3). The multivariable ordinal Logistic regression analysis was used to investigate the independent and synergistic associations of serum triglyceride (TG), high-density lipoprotein cholesterol (HDL-C), and low-density lipoprotein cholesterol (LDL-C) with the severity of hepatic steatosis, and their interactions and potential nonlinear relationships with metabolic factors were also examined. One-way analysis of variance or Kruskal-Wallis H test was used for comparison of continuous data between groups, and chi-square test was used for comparison of categorical data between groups.  Results  An increase in TG (odds ratio [OR]=1.77, 95% confidence interval [CI]: 1.48 — 2.10, P<0.001) and a reduction in HDL-C (OR=1.35, 95%CI: 1.11 — 1.65, P=0.003) were independently associated with a greater severity of hepatic steatosis, with the strongest association when both abnormalities coexisted (OR=2.40, 95%CI: 1.87 — 3.07, P<0.001). The dose-response relationship analysis further revealed a nonlinear threshold effect of TG on hepatic steatosis at the threshold of 1.51 mmol/L (Pnonlinearity=0.001), below which the severity of steatosis increased more rapidly with the increase in TG concentration (P=0.001). The subgroup analysis showed that the association between the reduction in HDL-C and the severity of steatosis was observed only in males, young adults (aged <45 years), and metabolically healthier subgroups (without diabetes, obesity, hyperuricemia or hypertension). Significant interactions were observed between the presence or absence of obesity and the abnormal levels of TG and HDL‑C (both Pinteraction<0.05). The association of the increase in LDL-C with steatosis was confined to specific subgroups (without obesity or hyperuricemia).  Conclusion  The increase in TG and the reduction in HDL-C are independently associated with the severity of hepatic steatosis in MAFLD. The synergistic effect of blood lipids and their interactions with metabolic factors may further refine risk stratification, so as to provide a basis for precise management of MAFLD.

     

  • loading
  • [1]
    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[J]. Hepatology, 2023, 77( 4): 1335- 1347. DOI: 10.1097/HEP.0000000000000004.
    [2]
    Huang D Q, Wong V W S, Rinella M E, et al. Metabolic dysfunction-associated steatotic liver disease in adults[J]. Nat Rev Dis Primers, 2025, 11: 14. DOI: 10.1038/s41572-025-00599-1.
    [3]
    Vilar-Gomez E, Vuppalanchi R, Gawrieh S, et al. CAP and LSM as determined by VCTE are independent predictors of all-cause mortality in the US adult population[J]. Hepatology, 2023, 77( 4): 1241- 1252. DOI: 10.1097/HEP.0000000000000023.
    [4]
    Semova I, Biddinger S B. Triglycerides in nonalcoholic fatty liver disease: Guilty until proven innocent[J]. Trends Pharmacol Sci, 2021, 42( 3): 183- 190. DOI: 10.1016/j.tips.2020.12.001.
    [5]
    García-Ruiz I, Solís-Muñoz P, Fernández-Moreira D, et al. NADPH oxidase is implicated in the pathogenesis of oxidative phosphorylation dysfunction in mice fed a high-fat diet[J]. Sci Rep, 2016, 6: 23664. DOI: 10.1038/srep23664.
    [6]
    Du T T, Sun X X, Yuan G, et al. Lipid phenotypes in patients with nonalcoholic fatty liver disease[J]. Metabolism, 2016, 65( 9): 1391- 1398. DOI: 10.1016/j.metabol.2016.06.006.
    [7]
    Tsutsumi T, Kawaguchi T, Fujii H, et al. Low HDL cholesterol levels in women and hypertriglyceridemia in men: Predictors of MASLD onset in individuals without steatosis[J]. J Gastroenterol, 2025, 60( 7): 891- 904. DOI: 10.1007/s00535-025-02242-y.
    [8]
    Yuan J, He X Q, Lu Y, et al. Triglycerides/high-density lipoprotein-cholesterol ratio outperforms traditional lipid indicators in predicting metabolic dysfunction-associated steatotic liver disease among U.S. adults[J]. Front Endocrinol, 2025, 16: 1591241. DOI: 10.3389/fendo.2025.1591241.
    [9]
    Li B Y, Liu Y W, Ma X R, et al. The association between non-high-density lipoprotein cholesterol to high-density lipoprotein cholesterol ratio and hepatic steatosis and liver fibrosis among US adults based on NHANES[J]. Sci Rep, 2025, 15( 1): 6527. DOI: 10.1038/s41598-025-90773-y.
    [10]
    Fan J G, Xu X Y, Yang R X, et al. Guideline for the prevention and treatment of metabolic dysfunction-associated fatty liver disease(version 2024)[J]. J Clin Transl Hepatol, 2024, 12( 11): 955- 974. DOI: 10.14218/JCTH.2024.00311.
    [11]
    Liu W Y, Huang S S, Ji H S, et al. From“burnt-out” to“burning-out”: Capturing liver fat loss in patients with advanced metabolic dysfunction–associated steatotic liver disease from a dynamic perspective[J]. Gastroenterology, 2025, 169( 2): 326- 336. DOI: 10.1053/j.gastro.2025.02.034.
    [12]
    Karlas T, Petroff D, Sasso M, et al. Individual patient data meta-analysis of controlled attenuation parameter(CAP) technology for assessing steatosis[J]. J Hepatol, 2017, 66( 5): 1022- 1030. DOI: 10.1016/j.jhep.2016.12.022.
    [13]
    Joint Committee on the Chinese Guidelines for Lipid Management. Chinese guidelines for lipid management(2023)[J]. Chin Circulation J, 2023, 38( 3): 237- 271. DOI: 10.3969/j.issn.1000-3614.2023.03.001.

    中国血脂管理指南修订联合专家委员会. 中国血脂管理指南(2023年)[J]. 中国循环杂志, 2023, 38( 3): 237- 271. DOI: 10.3969/j.issn.1000-3614.2023.03.001.
    [14]
    Donnelly K L, Smith C I, Schwarzenberg S J, et al. Sources of fatty acids stored in liver and secreted via lipoproteins in patients with nonalcoholic fatty liver disease[J]. J Clin Invest, 2005, 115( 5): 1343- 1351. DOI: 10.1172/JCI23621.
    [15]
    Lee E, Korf H, Vidal-Puig A. An adipocentric perspective on the development and progression of non-alcoholic fatty liver disease[J]. J Hepatol, 2023, 78( 5): 1048- 1062. DOI: 10.1016/j.jhep.2023.01.024.
    [16]
    Adiels M, Westerbacka J, Soro-Paavonen A, et al. Acute suppression of VLDL1 secretion rate by insulin is associated with hepatic fat content and insulin resistance[J]. Diabetologia, 2007, 50( 11): 2356- 2365. DOI: 10.1007/s00125-007-0790-1.
    [17]
    Scorletti E, Carr R M. A new perspective on NAFLD: Focusing on lipid droplets[J]. J Hepatol, 2022, 76( 4): 934- 945. DOI: 10.1016/j.jhep.2021.11.009.
    [18]
    Adiels M, Taskinen M R, Packard C, et al. Overproduction of large VLDL particles is driven by increased liver fat content in man[J]. Diabetologia, 2006, 49( 4): 755- 765. DOI: 10.1007/s00125-005-0125-z.
    [19]
    Fabbrini E, Mohammed B S, Magkos F, et al. Alterations in adipose tissue and hepatic lipid kinetics in obese men and women with nonalcoholic fatty liver disease[J]. Gastroenterology, 2008, 134( 2): 424- 431. DOI: 10.1053/j.gastro.2007.11.038.
    [20]
    Jakubowski H. The molecular bases of anti-oxidative and anti-inflammatory properties of paraoxonase 1[J]. Antioxidants, 2024, 13( 11): 1292. DOI: 10.3390/antiox13111292.
    [21]
    Petersen M C, Shulman G I. Roles of diacylglycerols and ceramides in hepatic insulin resistance[J]. Trends Pharmacol Sci, 2017, 38( 7): 649- 665. DOI: 10.1016/j.tips.2017.04.004.
    [22]
    Dongiovanni P, Stender S, Pietrelli A, et al. Causal relationship of hepatic fat with liver damage and insulin resistance in nonalcoholic fatty liver[J]. J Intern Med, 2018, 283( 4): 356- 370. DOI: 10.1111/joim.12719.
    [23]
    Vilar-Gomez E, Nephew L D, Vuppalanchi R, et al. High-quality diet, physical activity, and college education are associated with low risk of NAFLD among the US population[J]. Hepatology, 2022, 75( 6): 1491- 1506. DOI: 10.1002/hep.32207.
    [24]
    Vávrová L, Kodydková J, Zeman M, et al. Altered activities of antioxidant enzymes in patients with metabolic syndrome[J]. Obes Facts, 2013, 6( 1): 39- 47. DOI: 10.1159/000348569.
    [25]
    Barrera J, Chambliss K L, Ahmed M, et al. Bazedoxifene and conjugated estrogen prevent diet-induced obesity, hepatic steatosis, and type 2 diabetes in mice without impacting the reproductive tract[J]. Am J Physiol Endocrinol Metab, 2014, 307( 3): E345- E354. DOI: 10.1152/ajpendo.00653.2013.
    [26]
    Zhang Y J, Klein K, Sugathan A, et al. Transcriptional profiling of human liver identifies sex-biased genes associated with polygenic dyslipidemia and coronary artery disease[J]. PLoS One, 2011, 6( 8): e23506. DOI: 10.1371/journal.pone.0023506.
    [27]
    Palmisano B T, Zhu L, Stafford J M. Role of estrogens in the regulation of liver lipid metabolism[M]// Sex and Gender Factors Affecting Metabolic Homeostasis, Diabetes and Obesity. Cham: Springer International Publishing, 2017: 227- 256. DOI: 10.1007/978-3-319-70178-3_12.
    [28]
    Bhathena J, Kulamarva A, Martoni C, et al. Diet-induced metabolic Hamster model of nonalcoholic fatty liver disease[J]. Diabetes Metab Syndr Obes, 2011, 4: 195- 203. DOI: 10.2147/DMSO.S18435.
    [29]
    Côté I, Ngo Sock E T, Lévy É, et al. An atherogenic diet decreases liver FXR gene expression and causes severe hepatic steatosis and hepatic cholesterol accumulation: Effect of endurance training[J]. Eur J Nutr, 2013, 52( 5): 1523- 1532. DOI: 10.1007/s00394-012-0459-5.
  • 加载中

Catalog

    通讯作者: 陈斌, bchen63@163.com
    • 1. 

      沈阳化工大学材料科学与工程学院 沈阳 110142

    1. 本站搜索
    2. 百度学术搜索
    3. 万方数据库搜索
    4. CNKI搜索

    Figures(4)  / Tables(2)

    Article Metrics

    Article views (92) PDF downloads(20) Cited by()
    Proportional views
    Related

    /

    DownLoad:  Full-Size Img  PowerPoint
    Return
    Return