{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,28]],"date-time":"2026-09-28T07:57:57Z","timestamp":1790582277633,"version":"4.1.0"},"reference-count":166,"publisher":"Frontiers Media SA","license":[{"start":{"date-parts":[[2026,9,28]],"date-time":"2026-09-28T00:00:00Z","timestamp":1790553600000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/creativecommons.org\/licenses\/by\/4.0\/"}],"content-domain":{"domain":["frontiersin.org"],"crossmark-restriction":true},"short-container-title":["Front. Med."],"abstract":"<jats:p>Metabolic dysfunction-associated steatotic liver disease (MASLD) exhibits substantial phenotypic heterogeneity, yet pathways centered on body mass index (BMI) and liver non-invasive tests (NITs) do not adequately identify reduced metabolic reserve, functional vulnerability, or the risk of treatment-related muscle loss. This review aims to delineate the conceptual boundaries among sarcopenic obesity (SO), non-obese sarcopenia, and myosteatosis; evaluate their mechanistic, histological, and prognostic relationships with MASLD; compare body-composition assessment tools; and propose a body composition risk characterization framework for future validation. A formal diagnosis of SO should not be based on a mechanical combination of BMI and a single muscle mass threshold, but should concurrently establish excess adiposity, impaired muscle function, and reduced skeletal muscle mass\/quantity confirmed by body-composition assessment. Current evidence indicates that low muscle mass, low muscle strength, and myosteatosis are associated with metabolic dysfunction-associated steatohepatitis (MASH), liver fibrosis, and adverse outcomes, although observational associations remain influenced by reverse causation, physical activity, visceral adiposity, and disease stage. Compartment-specific apolipoprotein J (ApoJ\/clusterin) signaling illustrates liver-to-muscle endocrine communication and context-dependent intrahepatic or remote-organ effects. We propose four muscle phenotypes: phenotype A, preserved muscle function\/quantity without myosteatosis; phenotype B, isolated myosteatosis; phenotype C, abnormal muscle function and\/or quantity without myosteatosis; and phenotype D, coexisting abnormalities in muscle function\/quantity and myosteatosis. Excess adiposity is treated as an independent modifying axis, and phenotypes C or D are considered SO-related only when excess adiposity is independently confirmed and formal SO criteria are fulfilled, thereby avoiding the misclassification of non-obese sarcopenia as SO. The model is intended for validation in a multicenter prospective biopsy cohort using centrally reviewed, blinded liver histology as the reference for MASH and fibrosis, with its incremental value assessed beyond the fibrosis-4 index (FIB-4), vibration-controlled transient elastography (VCTE), the enhanced liver fibrosis (ELF) test, or magnetic resonance elastography (MRE). Body-composition assessment should complement rather than replace liver NITs, and the four-phenotype classification, selective clinical pathway, and dual liver\u2013muscle endpoint framework remain conceptual, hypothesis-generating tools that require histological, longitudinal-outcome, and clinical-utility validation.<\/jats:p>","DOI":"10.3389\/fmed.2026.1954630","type":"journal-article","created":{"date-parts":[[2026,9,28]],"date-time":"2026-09-28T07:39:55Z","timestamp":1790581195000},"update-policy":"https:\/\/doi.org\/10.3389\/crossmark-policy","source":"Crossref","is-referenced-by-count":0,"title":["The liver\u2013muscle axis in metabolic dysfunction-associated steatotic liver disease: a narrative review and conceptual framework for body-composition phenotyping"],"prefix":"10.3389","volume":"13","author":[{"given":"Zhendong","family":"Ma","sequence":"first","affiliation":[{"name":"College of Traditional Chinese Medicine, Changchun University of Traditional Chinese Medicine","place":["Changchun, Jilin, China"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Xinri","family":"Zhang","sequence":"additional","affiliation":[{"name":"College of Traditional Chinese Medicine, Changchun University of Traditional Chinese Medicine","place":["Changchun, Jilin, China"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Yan","family":"Leng","sequence":"additional","affiliation":[{"name":"Department of Liver, Spleen and Gastroenterology, Affiliated Hospital of Changchun University of Traditional Chinese Medicine","place":["Changchun, Jilin, China"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Xingyu","family":"Chen","sequence":"additional","affiliation":[{"name":"Department of Liver, Spleen and Gastroenterology, Affiliated Hospital of Changchun University of Traditional Chinese Medicine","place":["Changchun, Jilin, China"]}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"1965","published-online":{"date-parts":[[2026,9,28]]},"reference":[{"key":"B1","doi-asserted-by":"publisher","first-page":"S32","DOI":"10.3350\/cmh.2024.0431","article-title":"Epidemiology of metabolic dysfunction-associated steatotic liver disease","volume":"31","author":"Younossi","year":"2025","journal-title":"Clin Mol Hepatol"},{"key":"B2","doi-asserted-by":"publisher","first-page":"155246","DOI":"10.1016\/j.metabol.2022.155246","article-title":"Time to transition from a negative nomenclature describing what NAFLD is not, to a novel, pathophysiology-based, umbrella classification of fatty liver disease (FLD)","volume":"134","author":"Valenzuela-Vallejo","year":"2022","journal-title":"Metab Clin Exp"},{"key":"B3","doi-asserted-by":"publisher","first-page":"202","DOI":"10.1016\/j.jhep.2020.03.039","article-title":"A new definition for metabolic dysfunction-associated fatty liver disease: an international expert 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