{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,8,29]],"date-time":"2026-08-29T05:18:28Z","timestamp":1787980708781,"version":"build-2784847793"},"reference-count":57,"publisher":"MDPI AG","issue":"17","license":[{"start":{"date-parts":[[2026,8,27]],"date-time":"2026-08-27T00:00:00Z","timestamp":1787788800000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/creativecommons.org\/licenses\/by\/4.0\/"}],"funder":[{"DOI":"10.13039\/501100001807","name":"FAPESP","doi-asserted-by":"publisher","award":["2023\/06553-3"],"award-info":[{"award-number":["2023\/06553-3"]}],"id":[{"id":"10.13039\/501100001807","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/501100001807","name":"FAPESP","doi-asserted-by":"publisher","award":["2024\/03604-9"],"award-info":[{"award-number":["2024\/03604-9"]}],"id":[{"id":"10.13039\/501100001807","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/501100003593","name":"CNPq","doi-asserted-by":"publisher","award":["313752\/2023-0"],"award-info":[{"award-number":["313752\/2023-0"]}],"id":[{"id":"10.13039\/501100003593","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/501100002322","name":"CAPES","doi-asserted-by":"crossref","award":["PROEX 001"],"award-info":[{"award-number":["PROEX 001"]}],"id":[{"id":"10.13039\/501100002322","id-type":"DOI","asserted-by":"crossref"}]}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Cells"],"abstract":"<jats:p>Metabolic dysfunction-associated steatohepatitis (MASH) is characterized by hepatic steatosis, inflammation, fibrosis, and metabolic dysfunction, with limited therapeutic options currently available. This study investigated whether pharmacological inhibition of Galectin-3 (Gal-3), a \u03b2-galactoside-binding lectin implicated in inflammation and fibrosis, using modified citrus pectin (MCP), attenuates established MASH in ApoE-deficient mice. Mice were assigned to four groups: standard chow (CTL), standard chow plus MCP (CTL + MCP), Western diet with fructose-enriched drinking water (WD), and WD plus MCP (WD + MCP). MCP (1% in drinking water) was administered during the final four weeks of the 11-week experimental protocol, after the establishment of metabolic dysfunction and hepatic steatosis. Compared with untreated WD mice, WD + MCP mice exhibited improved glucose tolerance, as evidenced by a 22.9% reduction in glucose area under the curve (p = 0.01), and enhanced hepatic insulin signaling, reflected by a 254.1% increase in insulin-stimulated AKT2 phosphorylation (p = 0.0002). MCP treatment also reduced hepatic lipid accumulation (39.8%, p = 0.0055) and hepatic triglyceride content (26.1%, p = 0.0003), accompanied by reductions in circulating triglyceride and cholesterol concentrations. Furthermore, WD + MCP mice exhibited reduced hepatic Gal-3 expression (25.8%, p = 0.0199), decreased F4\/80 immunoreactivity (49.2%, p = 0.0061), attenuated JNK phosphorylation (46.6%, p = 0.0118), reduced collagen deposition (47.0%, p = 0.0002), and lower plasma ALT (52.9%, p = 0.0009) and AST (48.8%, p = 0.04) activities. Collectively, these findings demonstrate that MCP attenuates multiple metabolic, inflammatory, fibrotic, and hepatic injury features of established Western diet-induced MASH, supporting Gal-3 as a promising therapeutic target and MCP as a potential pharmacological strategy for MASH.<\/jats:p>","DOI":"10.3390\/cells15171544","type":"journal-article","created":{"date-parts":[[2026,8,27]],"date-time":"2026-08-27T08:02:27Z","timestamp":1787817747000},"page":"1544","update-policy":"https:\/\/doi.org\/10.3390\/mdpi_crossmark_policy","source":"Crossref","is-referenced-by-count":0,"title":["Modified Citrus Pectin-Mediated Gal-3 Reduction Attenuates Metabolic Dysfunction-Associated Steatohepatitis in an Experimental Model"],"prefix":"10.3390","volume":"15","author":[{"ORCID":"https:\/\/orcid.org\/0009-0007-8633-4595","authenticated-orcid":false,"given":"Anne R. 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M.","family":"Santos","sequence":"additional","affiliation":[{"name":"Department of Physiology, Ribeirao Preto School of Medicine, University of Sao Paulo, Ribeirao Preto 14049-900, Brazil"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0003-3205-3011","authenticated-orcid":false,"given":"Jorge F. A.","family":"Model","sequence":"additional","affiliation":[{"name":"Department of Physiology, Ribeirao Preto School of Medicine, University of Sao Paulo, Ribeirao Preto 14049-900, Brazil"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Jos\u00e9 F. 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