The role of exercise intensity in the regulation of the gut microbiota and liver function in metabolic dysfunction–associated steatotic liver disease

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Abstract

Metabolic dysfunction–associated steatotic liver disease is currently regarded as one of the most prevalent metabolic disorders, closely linked to obesity, insulin resistance, and disturbances of the gut microbiome. Physical exercise is a key nonpharmacological strategy capable of modulating energy and metabolic homeostasis through its effects on interorgan communication along the gut–liver axis. This review summarizes experimental and clinical evidence regarding the effects of different types of physical activity, such as moderate-intensity continuous training and high-intensity interval training, on intestinal barrier integrity, hepatic lipid metabolism, mitochondrial and endoplasmic reticulum homeostasis, and systemic inflammation. Preclinical studies demonstrate that both training modalities increase the expression of tight junction proteins (ZO-1, occludin, JAM-A), enhance gut microbiota diversity, reduce endotoxemia, and attenuate the severity of steatosis. High-intensity interval training was superior in stimulating mitochondrial biogenesis, β-oxidation, and irisin secretion, as well as in reducing endoplasmic reticulum stress and macrophage-mediated inflammation. Clinical data confirm that regular physical activity, regardless of intensity, decreases hepatic fat accumulation and improves insulin sensitivity and cardiovascular function. However, clinical evidence remains limited, underscoring the need for further investigation of the molecular regulation mechanisms of the gut–liver axis. Overall, physical activity, particularly high-intensity interval training, is an effective, safe, and affordable approach for the prevention and treatment of metabolic dysfunction–associated steatotic liver disease, contributing to the restoration of metabolic balance and hepatic homeostasis.

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About the authors

Anna S. Stepanova

Samara State Medical University

Author for correspondence.
Email: annast2003.06@yandex.ru
ORCID iD: 0009-0000-5849-8057
Russian Federation, Samara

Ilmir A. Shaidullin

I.N. Ulyanov Chuvash State University

Email: shaidullinilmir@gmail.com
ORCID iD: 0009-0006-0757-3006
Russian Federation, Cheboksary

Liliya R. Sharafutdinova

I.N. Ulyanov Chuvash State University

Email: remka.lil.shar@gmail.com
ORCID iD: 0009-0006-6566-8847
Russian Federation, Cheboksary

Evgeny G. Prokopyev

I.N. Ulyanov Chuvash State University

Email: rikudasanin01@mail.ru
ORCID iD: 0009-0002-8229-1915
Russian Federation, Cheboksary

Yulia R. Romanova

I.N. Ulyanov Chuvash State University

Email: julia-romanova06@mail.ru
ORCID iD: 0009-0008-5753-9556
Russian Federation, Cheboksary

Renata I. Murzakaeva

Bashkir State Medical University

Email: sasha.ponomarenko.17@mail.ru
ORCID iD: 0009-0004-4889-5912
Russian Federation, Ufa

Kseniya A. Gerasimova

Bashkir State Medical University

Email: Ke1dji@yandex.ru
ORCID iD: 0009-0008-8869-7928
Russian Federation, Ufa

Sofia A. Safina

Bashkir State Medical University

Email: s_safina@internet.ru
ORCID iD: 0009-0004-6834-6910
Russian Federation, Ufa

Elina R. Abdrakhmanova

Bashkir State Medical University

Email: elli2202@mail.ru
ORCID iD: 0009-0002-0815-5667
Russian Federation, Ufa

Yana M. Samatova

Ryazan State Medical University

Email: yana.yana-2003@mail.ru
ORCID iD: 0009-0005-3573-8878
Russian Federation, Ryazan

Ekaterina S. Bashlykova

Voronezh State Medical University named after N.N. Burdenko

Email: katya31072002@bk.ru
ORCID iD: 0009-0008-4113-0422
Russian Federation, Voronezh

Maria V. Naumova

Voronezh State Medical University named after N.N. Burdenko

Email: voropaeva.2002@inbox.ru
ORCID iD: 0000-0002-5420-635X
Russian Federation, Voronezh

References

  1. Bondareva EA, Troshina EA. Obesity. Reasons, features and prospects. Obesity and metabolism. 2024;21(2):174–187. doi: 10.14341/omet13055 EDN: BRPHRR
  2. GBD 2021 Diabetes Collaborators. Global, regional, and national burden of diabetes from 1990 to 2021, with projections of prevalence to 2050: a systematic analysis for the Global Burden of Disease Study 2021. Lancet. 2023;402(10397):203–234. doi: 10.1016/S0140-6736(23)01301-6
  3. World Obesity Atlas 2025. London: World Obesity Federation; 2025.
  4. Ye Q, Zou B, Yeo YH, et al. Global prevalence, incidence, and outcomes of non-obese or lean non-alcoholic fatty liver disease: a systematic review and meta-analysis. Lancet Gastroenterol Hepatol. 2020;5(8):739–752. doi: 10.1016/S2468-1253(20)30077-7
  5. Borodich TS. The modifiable risk factors for obesity and overweight in early childhood period, the analysis of cumulative effects and the potential for prevention. Obesity and metabolism. 2015;12(2):51. doi: 10.14341/OMET2015251 EDN: UHHUYL
  6. Schwab U, Lauritzen L, Tholstrup T, et al. Effect of the amount and type of dietary fat on cardiometabolic risk factors and risk of developing type 2 diabetes, cardiovascular diseases, and cancer: a systematic review. Food Nutr Res. 2014;58:25145. doi: 10.3402/fnr.v58.25145
  7. Raatz SK, Conrad Z, Johnson LK, et al. Relationship of the reported intakes of fat and fatty acids to body weight in US adults. Nutrients. 2017;9(5):438. doi: 10.3390/nu9050438
  8. Strain T, Wijndaele K, Garcia L, et al. National, regional, and global trends in insufficient physical activity among adults from 2000 to 2022: a pooled analysis of 507 population-based surveys with 5.7 million participants. Lancet Glob Health. 2024;12(8):e1232–e1243. doi: 10.1016/S2214-109X(24)00208-5
  9. Longo M, Zatterale F, Naderi J, et al. Adipose tissue dysfunction as determinant of obesity-associated metabolic complications. Int J Mol Sci. 2019;20(9):2358. doi: 10.3390/ijms20092358
  10. Gustafson B, Smith U. Regulation of white adipogenesis and its relation to ectopic fat accumulation and cardiovascular risk. Atherosclerosis. 2015;241(1):27–35. doi: 10.1016/j.atherosclerosis.2015.04.814
  11. Svegliati-Baroni G, Saccomanno S, Rychlicki C, et al. Gut–pancreas–liver axis as a target for treatment of NAFLD/NASH. Int J Mol Sci. 2020;21(16):5820. doi: 10.3390/ijms21165820
  12. Vasques-Monteiro IML, Oliveira RB, Da Silva VE, et al. A rise in proteobacteria is an indicator of gut–liver axis-mediated nonalcoholic fatty liver disease in high-fructose-fed adult mice. Nutr Res. 2021;91:26–35. doi: 10.1016/j.nutres.2021.05.003
  13. Santana-Oliveira DA, Mendes BF, Faria CC, et al. Exercise prevents obesity by reducing gut-derived inflammatory signals to brown adipocytes in mice. J Endocrinol. 2023;259(1):e230123. doi: 10.1530/JOE-23-0123
  14. Cani PD, Amar J, Iglesias MA, et al. Changes in gut microbiota control metabolic endotoxemia-induced inflammation in high-fat diet-induced obesity and diabetes in mice. Diabetes. 2008;57(6):1470–1481. doi: 10.2337/db07-1403
  15. Park BS, Lee JO. Recognition of lipopolysaccharide pattern by TLR4 complexes. Exp Mol Med. 2013;45:e66. doi: 10.1038/emm.2013.97
  16. Gorman A, Golovanov AP. Lipopolysaccharide structure and the phenomenon of low endotoxin recovery. Eur J Pharm Biopharm. 2022;180:289–307. doi: 10.1016/j.ejpb.2022.06.008
  17. Buzzetti E, Pinzani M, Tsochatzis EA. The multiple-hit pathogenesis of non-alcoholic fatty liver disease (NAFLD). Metabolism. 2016;65(8):1038–1048. doi: 10.1016/j.metabol.2015.12.012
  18. Younossi ZM, Koenig AB, Abdelatif D, et al. The global epidemiology of nonalcoholic fatty liver disease (NAFLD) and nonalcoholic steatohepatitis (NASH): a systematic review. Hepatology. 2023;77(4):1335–1347. doi: 10.1002/hep.32762
  19. Silva-Veiga FM, Santos AC, Fernandes AC, et al. GW0742 (PPAR-beta agonist) attenuates hepatic endoplasmic reticulum stress by improving hepatic energy metabolism in high-fat diet fed mice. Mol Cell Endocrinol. 2018;474:227–237. doi: 10.1016/j.mce.2018.03.013
  20. Silva-Veiga FMS, Fernandes AC, Souza-Monteiro JR, et al. Anti-obesogenic effects of WY14643 (PPAR-alpha agonist): hepatic mitochondrial enhancement and suppressed lipogenic pathway in diet-induced obese mice. Biochimie. 2017;140:106–116. doi: 10.1016/j.biochi.2017.06.003
  21. Silva-Veiga FM, Souza-Monteiro JR, Fernandes AC, et al. Gut–liver axis modulation in fructose-fed mice: a role for PPAR-alpha and linagliptin. J Endocrinol. 2020;247(1):11–24. doi: 10.1530/JOE-19-0384
  22. Silva-Veiga FM, Fernandes AC, Souza-Monteiro JR, et al. Peroxisome proliferator-activated receptor-alpha activation and dipeptidyl peptidase-4 inhibition target dysbiosis to treat fatty liver in obese mice. World J Gastroenterol. 2022;28(17):1814–1829. doi: 10.3748/wjg.v28.i17.1814
  23. Liu S, Cui F, Liu C, et al. Role of irisin in physiology and pathology. Front Endocrinol (Lausanne). 2022;13:962968. doi: 10.3389/fendo.2022.962968
  24. Qian L, Fang J, Li Y, et al. Peroxisome proliferator-activated receptor gamma coactivator-1 (PGC-1) family in physiological and pathophysiological process and diseases. Signal Transduct Target Ther. 2024;9(1):50. doi: 10.1038/s41392-024-01672-2
  25. Park MJ, Kim DI, Choi JH, et al. New role of irisin in hepatocytes: the protective effect of hepatic steatosis in vitro. Cell Signal. 2015;27(9):1831–1839. doi: 10.1016/j.cellsig.2015.05.018
  26. Axelrod CL, Dantas WS, Kirwan JP. Sarcopenic obesity: emerging mechanisms and therapeutic potential. Metabolism. 2023;146:155639. doi: 10.1016/j.metabol.2023.155639
  27. Guo A, Li K, Xiao L, et al. FGF19 protects skeletal muscle against obesity-induced muscle atrophy, metabolic derangement and abnormal irisin levels via the AMPK/SIRT-1/PGC-alpha pathway. J Cell Mol Med. 2021;25(7):3585–3600. doi: 10.1111/jcmm.16400
  28. Xiao M, Zhang Y, Xu X. Calorie restriction combined with high-intensity interval training promotes browning of white adipose tissue by activating the PPARγ/PGC-1α/UCP1 pathway. Altern Ther Health Med. 2023;29(3):134–139.
  29. Abete I, Astrup A, Martínez JA, et al. Obesity and the metabolic syndrome: role of different dietary macronutrient distribution patterns and specific nutritional components on weight loss and maintenance. Nutr Rev. 2010;68(4):214–231. doi: 10.1111/j.1753-4887.2010.00280.x
  30. Atakan MM, Koşar ŞN, Güzel Y, et al. The role of exercise, diet, and cytokines in preventing obesity and improving adipose tissue. Nutrients. 2021;13(5):1459. doi: 10.3390/nu13051459
  31. Souza-Tavares H, Costa R, Mendes BF, et al. Exercise enhances hepatic mitochondrial structure and function while preventing endoplasmic reticulum stress and metabolic dysfunction-associated steatotic liver disease in mice fed a high-fat diet. Nutr Res. 2024;126:180–192. doi: 10.1016/j.nutres.2024.01.007
  32. Yudina YuV, Korsunsky AA, Aminova AI, et al. Gut microbiota as a separate body system. Russian Journal of Evidence-Based Gastroenterology. 2019;8(4):36–43. doi: 10.17116/dokgastro2019804-05136 EDN: VXOAUR
  33. Dicheva DT, Andreev DN. Pathogenetic and clinical significance of the gut-liver microbiota axis. Medical Council. 2022;(7):69–75. doi: 10.21518/2079-701X-2022-16-7-69-75 EDN: ZWZGUU
  34. Gruner N, Mattner J. Bile acids and microbiota: multifaceted and versatile regulators of the liver–gut axis. Int J Mol Sci. 2021;22(3):1397. doi: 10.3390/ijms22031397
  35. Simbrunner B, Trauner M, Reiberger T. Therapeutic aspects of bile acid signalling in the gut–liver axis. Aliment Pharmacol Ther. 2021;54(10):1243–1262. doi: 10.1111/apt.16615
  36. Kiriyama Y, Nochi H. Physiological role of bile acids modified by the gut microbiome. Microorganisms. 2021;10(1):68. doi: 10.3390/microorganisms10010068
  37. Qiu Y, Ding X, Sun J, et al. Exercise sustains the hallmarks of health. J Sport Health Sci. 2023;12(1):8–35. doi: 10.1016/j.jshs.2022.09.005
  38. Perez-Terzic CM. Exercise in cardiovascular diseases. PM R. 2012;4(11):867–873. doi: 10.1016/j.pmrj.2012.09.582
  39. Garber CE, Blissmer B, Deschenes MR, et al. American College of Sports Medicine position stand. Quantity and quality of exercise for developing and maintaining cardiorespiratory, musculoskeletal, and neuromotor fitness in apparently healthy adults: guidance for prescribing exercise. Med Sci Sports Exerc. 2011;43(7):1334–1359. doi: 10.1249/MSS.0b013e318213fefb
  40. Haskell WL, Lee I-M, Pate RR, et al. Physical activity and public health: updated recommendation for adults from the American College of Sports Medicine and the American Heart Association. Med Sci Sports Exerc. 2007;39(8):1423–1434. doi: 10.1249/mss.0b013e3180616b27
  41. Kesaniemi YK, Danforth E Jr, Jensen MD, et al. Dose-response issues concerning physical activity and health: an evidence-based symposium. Med Sci Sports Exerc. 2001;33(6 Suppl):S351–S358. doi: 10.1097/00005768-200106001-00027
  42. Howley ET. Type of activity: resistance, aerobic, and leisure versus occupational physical activity. Med Sci Sports Exerc. 2001;33(6 Suppl):S364–S369. doi: 10.1097/00005768-200106001-00029
  43. Dorelli B, Marchi L, Balia C, et al. Can physical activity influence human gut microbiota composition independently of diet? A systematic review. Nutrients. 2021;13(6):1890. doi: 10.3390/nu13061890
  44. Ahmad AM. Moderate-intensity continuous training: is it as good as high-intensity interval training for glycemic control in type 2 diabetes? J Exerc Rehabil. 2019;15(2):327–333. doi: 10.12965/jer.1938148.074
  45. de Oliveira Sa G, da Silva Alves F, de Castro AL, et al. High-intensity interval training has beneficial effects on cardiac remodeling through local renin-angiotensin system modulation in mice fed high-fat or high-fructose diets. Life Sci. 2017;189:8–17. doi: 10.1016/j.lfs.2017.08.018
  46. Gonzalez K, Fuentes J, Marquez JL. Physical inactivity, sedentary behavior and chronic diseases. Korean J Fam Med. 2017;38(3):111–115. doi: 10.4082/kjfm.2017.38.3.111
  47. Wang L, Li F, Guo Y, et al. High-intensity interval training and moderate-intensity continuous training attenuate oxidative damage and promote myokine response in the skeletal muscle of ApoE KO mice on a high-fat diet. Antioxidants (Basel). 2021;10(7):992. doi: 10.3390/antiox10070992
  48. Americo ALV, Oliveira C, Cordeiro T, et al. Aerobic exercise training prevents obesity and insulin resistance independent of the renin-angiotensin system modulation in the subcutaneous white adipose tissue. PLoS One. 2019;14(4):e0215896. doi: 10.1371/journal.pone.0215896
  49. Laskowski ER. The role of exercise in the treatment of obesity. PM R. 2012;4(11):840–844. doi: 10.1016/j.pmrj.2012.09.576
  50. Rahim HA, Damirchi A, Babaei P. Comparison of HIIT and НТСИ and further detraining on metabolic syndrome and asprosin signaling pathway in metabolic syndrome model of rats. Sci Rep. 2024;14(1):11313. doi: 10.1038/s41598-024-58154-7
  51. Motiani KK, Collado MC, Eskelinen JJ, et al. Exercise training modulates gut microbiota profile and improves endotoxemia. Med Sci Sports Exerc. 2020;52(1):94–104. doi: 10.1249/MSS.0000000000002103
  52. Abenavoli L, Scarpellini E, Colica C, et al. Gut microbiota and obesity: a role for probiotics. Nutrients. 2019;11(11):2690. doi: 10.3390/nu11112690
  53. Chae YR, Lee JY, Kim EY, et al. Diet-induced gut dysbiosis and leaky gut syndrome. J Microbiol Biotechnol. 2024;34(4):747–756. doi: 10.4014/jmb.2403.03001
  54. Li Y, Zhang Y, Xu J, et al. Updated mechanisms of MASLD pathogenesis. Lipids Health Dis. 2024;23(1):117. doi: 10.1186/s12944-024-02062-w
  55. Han Y, Zhang W, Zhang L, et al. Moderate-intensity continuous training and high-intensity interval training alleviate glycolipid metabolism through modulation of gut microbiota and their metabolite SCFAs in diabetic rats. Biochem Biophys Res Commun. 2024;735:150831. doi: 10.1016/j.bbrc.2024.150831
  56. Peng M, Zhang W, Zhao J, et al. High-intensity interval training and medium-intensity continuous training may affect cognitive function through regulation of intestinal microbial composition and its metabolite LPS by the gut-brain axis. Life Sci. 2024;352:122871. doi: 10.1016/j.lfs.2024.122871
  57. Sepulveda-Fragoso V, Gomez-Cabrera MC, Rojas-Garcia AE, et al. Comparison between aerobic exercise training and enalapril treatment as tools to improve diet-induced metabolic-associated fatty liver disease: effects on endoplasmic reticulum stress markers. Life Sci. 2022;311(Pt A):121136. doi: 10.1016/j.lfs.2022.121136
  58. Li X, Zhang H, Wu J, et al. Mitochondria-associated membranes contribution to exercise-mediated alleviation of hepatic insulin resistance: contrasting high-intensity interval training with moderate-intensity continuous training in a high-fat diet mouse model. J Diabetes. 2024;16(4):e13540. doi: 10.1111/1753-0407.13540
  59. Maillard F, Pereira B, Boisseau N. Effect of high-intensity interval training on total, abdominal and visceral fat mass: a meta-analysis. Sports Med. 2018;48(2):269–288. doi: 10.1007/s40279-017-0807-y
  60. Gibala MJ, Little JP, MacDonald MJ, et al. Physiological adaptations to low-volume, high-intensity interval training in health and disease. J Physiol. 2012;590(5):1077–1084. doi: 10.1113/jphysiol.2011.224725
  61. Motta VF, Crespilho AM, Rodrigues B, et al. Treating fructose-induced metabolic changes in mice with high-intensity interval training: insights in the liver, white adipose tissue, and skeletal muscle. J Appl Physiol (1985). 2017;123(4):699–709. doi: 10.1152/japplphysiol.00276.2017
  62. Duval C, Daval M, Mogilenko DA, et al. High-intensity exercise: can it protect you from a fast food diet? Nutrients. 2017;9(9):943. doi: 10.3390/nu9090943
  63. Wang N, Ding Y, Liu Y, et al. High-intensity interval versus moderate-intensity continuous training: superior metabolic benefits in diet-induced obesity mice. Life Sci. 2017;191:122–131. doi: 10.1016/j.lfs.2017.08.013
  64. Souza-Tavares H, Costa R, Mendes BF, et al. Exercise enhances hepatic mitochondrial structure and function while preventing endoplasmic reticulum stress and MASLD in high-fat-fed mice. Nutr Res. 2024;126:180–192. doi: 10.1016/j.nutres.2024.01.007
  65. Motta VF, Silva TP, Campos JC, et al. Browning is activated in the subcutaneous white adipose tissue of mice metabolically challenged with a high-fructose diet submitted to high-intensity interval training. J Nutr Biochem. 2019;70:164–173. doi: 10.1016/j.jnutbio.2019.05.006
  66. Jiménez-Maldonado A, Hernández-Torres RP, García-Suárez PC, et al. Impact of high-intensity interval training and sprint interval training on peripheral markers of glycemic control in metabolic syndrome and type 2 diabetes. Biochim Biophys Acta Mol Basis Dis. 2020;1866(8):165820. doi: 10.1016/j.bbadis.2020.165820
  67. Stevanovic J, Beleznai T, Berenyi B, et al. Physical exercise and liver “fitness”: role of mitochondrial function and epigenetics-related mechanisms in non-alcoholic fatty liver disease. Mol Metab. 2020;32:1–14. doi: 10.1016/j.molmet.2019.11.016
  68. da Silva Rosa SC, Martens MD, Milne KJ. Mechanisms of muscle insulin resistance and the cross-talk with liver and adipose tissue. Physiol Rep. 2020;8(19):e14607. doi: 10.14814/phy2.14607
  69. Liu Y, Zhao W, Chen Y, et al. Post-exercise effects and long-term training adaptations of hormone-sensitive lipase lipolysis induced by high-intensity interval training in adipose tissue of mice. Front Physiol. 2020;11:535722. doi: 10.3389/fphys.2020.535722
  70. Denou E, Marcinko K, Surette MG, et al. High-intensity exercise training increases the diversity and metabolic capacity of the mouse distal gut microbiota during diet-induced obesity. Am J Physiol Endocrinol Metab. 2016;310(11):E982–E993. doi: 10.1152/ajpendo.00537.2015
  71. Pushpanathan P, Srikanth P, Seshadri KG. Gut microbiota and its mysteries. Indian J Med Microbiol. 2019;37(2):268–277. doi: 10.4103/ijmm.IJMM_19_19
  72. Maillard F, Rousset S, Pereira B, et al. High-intensity interval training promotes total and visceral fat mass loss in obese Zucker rats without modulating gut microbiota. PLoS One. 2019;14(4):e0214660. doi: 10.1371/journal.pone.0214660
  73. Wang G, Zhao Y, Huang W, et al. Effects of high-intensity interval training on gut microbiota profiles in 12-month-old ICR mice. J Physiol Biochem. 2020;76(4):539–548. doi: 10.1007/s13105-020-00756-7
  74. Plissonneau C, Rousset S, Pereira B, et al. High-intensity interval training and alpha-linolenic acid supplementation improve DHA conversion and increase the abundance of gut mucosa-associated Oscillospira bacteria. Nutrients. 2021;13(3):788. doi: 10.3390/nu13030788
  75. Dupuit M, Pereira B, Maillard F, et al. The TOTUM-63 supplement and high-intensity interval training combination limits weight gain, improves glycemic control, and influences the composition of gut mucosa-associated bacteria in rats on a high-fat diet. Nutrients. 2021;13(5):1569. doi: 10.3390/nu13051569.
  76. Batacan RB Jr, Fenning AS, Dalbo VJ, et al. A gut reaction: the combined influence of exercise and diet on gastrointestinal microbiota in rats. J Appl Microbiol. 2017;122(6):1627–1638. doi: 10.1111/jam.13456
  77. Solouki S, Darbandi M, Hosseini A, et al. Efficacy of high-intensity interval and continuous endurance trainings on cecal microbiota metabolites and inflammatory factors in diabetic rats induced by high-fat diet. PLoS One. 2024;19(4):e0301532. doi: 10.1371/journal.pone.0301532
  78. Yu C, Zhang L, Zhao J, et al. Exercise ameliorates osteopenia in mice via intestinal microbial-mediated bile acid metabolism pathway. Theranostics. 2025;15(5):1741–1759. doi: 10.7150/thno.88686
  79. Cullen JMA, Shahzad S, Dhillon J. A systematic review on the effects of exercise on gut microbial diversity, taxonomic composition, and microbial metabolites: identifying research gaps and future directions. Front Physiol. 2023;14:1292673. doi: 10.3389/fphys.2023.1292673
  80. Yang W, Zhang L, Li C, et al. Moderate-intensity physical exercise affects the exercise performance and gut microbiota of mice. Front Cell Infect Microbiol. 2021;11:712381. doi: 10.3389/fcimb.2021.712381
  81. Handu D, Stote K, Piemonte T. Evaluating bioactive-substance-based interventions for adults with MASLD: results from a systematic scoping review. Nutrients. 2025;17(3):453. doi: 10.3390/nu17030453
  82. Paoli A. The influence of physical exercise, ketogenic diet, and time-restricted eating on de novo lipogenesis: a narrative review. Nutrients. 2025;17(4):663. doi: 10.3390/nu17040663
  83. Hao X, Wang L, Zhang Y, et al. Prophylactic effects of nutrition, dietary strategies, exercise, lifestyle and environment on nonalcoholic fatty liver disease. Ann Med. 2025;57(1):2464223. doi: 10.1080/07853890.2024.2464223
  84. Mambrini SP, Agostini D, Baldassarre M, et al. Diet and physical exercise as key players to tackle MASLD through improvement of insulin resistance and metabolic flexibility. Front Nutr. 2024;11:1426551. doi: 10.3389/fnut.2024.1426551
  85. Keating SE, Parker HM, George J, et al. Exercise in the management of metabolic-associated fatty liver disease (MAFLD) in adults: a position statement from Exercise and Sport Science Australia. Sports Med. 2023;53(12):2347–2371. doi: 10.1007/s40279-023-01845-5
  86. Fernández T, Pizarro M, Loaiza P, et al. Lifestyle changes in patients with non-alcoholic fatty liver disease: a systematic review and meta-analysis. PLoS One. 2022;17(2):e0263931. doi: 10.1371/journal.pone.0263931
  87. Zhang HJ, He J, Pan LL, et al. Effects of moderate and vigorous exercise on nonalcoholic fatty liver disease: a randomized clinical trial. JAMA Intern Med. 2016;176(8):1074–1082. doi: 10.1001/jamainternmed.2016.3202
  88. Sabag A, Way KL, Keating SE, et al. The effect of high-intensity interval training vs moderate-intensity continuous training on liver fat: a systematic review and meta-analysis. J Clin Endocrinol Metab. 2022;107(3):862–881. doi: 10.1210/clinem/dgab865
  89. Sargeant JA, Gray LJ, Bodicoat DH, et al. The effect of exercise training on intrahepatic triglyceride and hepatic insulin sensitivity: a systematic review and meta-analysis. Obes Rev. 2018;19(10):1446–1459. doi: 10.1111/obr.12717
  90. Xue Y, Zhang S, Zhang Q, et al. Effect of different exercise modalities on nonalcoholic fatty liver disease: a systematic review and network meta-analysis. Sci Rep. 2024;14(1):6212. doi: 10.1038/s41598-024-60578-5

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