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Here, DPS was evaluated in mice with Type 2 diabetes mellitus induced by a high\u2010fat diet and streptozotocin. Low\u2010 and high\u2010dose DPS interventions were assessed through serum biochemistry, liver histology, inflammatory cytokine measurements, intestinal barrier evaluation, hepatic molecular analysis, 16S rRNA gene sequencing, targeted quantification of tryptophan metabolites, and untargeted serum metabolomics. Relative to untreated diabetic mice, DPS\u2010treated animals showed improved serum lipid profiles, lower ALT and AST activities, reduced circulating inflammatory cytokines, and less hepatic lipid deposition. DPS treatment was also accompanied by improved intestinal morphology, increased ZO\u20101 and Occludin expression, and lower circulating lipopolysaccharide concentrations. In the high\u2010dose group, gut microbial community composition differed from that of untreated diabetic mice, with relative increases in Akkermansia and Lactobacillus. In parallel, DPS treatment was associated with increased serum tryptophan and indole\u20103\u2010propionic acid concentrations, lower kynurenine concentrations and Kyn\/Trp ratios, reduced hepatic TDO2 expression, increased AhR expression, and lower NF\u2010\u03baB p65 phosphorylation. Overall, DPS improved metabolic and liver\u2010related abnormalities in diabetic mice and was accompanied by coordinated changes in intestinal barrier\u2010related indices, gut microbial composition, tryptophan metabolites, and hepatic AhR\/NF\u2010\u03baB\u2010related markers. As microbiota\u2010directed and AhR\u2010targeted intervention experiments were not conducted, these observations remain associative and do not demonstrate a causal gut microbiota\u2013tryptophan\u2013AhR mechanism. Moreover, as these observations were obtained in a single HFD\/STZ\u2010induced mouse model, their relevance to the heterogeneity and natural course of human T2DM\u2010associated MASLD requires confirmation in additional preclinical models and clinical studies.<\/jats:p>","DOI":"10.1002\/fsn3.72455","type":"journal-article","created":{"date-parts":[[2026,10,9]],"date-time":"2026-10-09T04:51:03Z","timestamp":1791521463000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":0,"title":["D\u2010Psicose Attenuates Hepatic Steatosis and Inflammatory Injury in\n                    <scp>HFD<\/scp>\n                    \/\n                    <scp>STZ<\/scp>\n                    \u2010Induced\n                    <scp>T2DM<\/scp>\n                    Mice and Is Associated With Alterations in Gut Microbiota, Tryptophan Metabolism, and Hepatic\n                    <scp>AhR<\/scp>\n                    \u2010Related Signaling"],"prefix":"10.1002","volume":"14","author":[{"ORCID":"https:\/\/orcid.org\/0000-0002-8241-2433","authenticated-orcid":false,"given":"Liang","family":"Wu","sequence":"first","affiliation":[{"name":"Department of Laboratory Medicine, School of Medicine Jiangsu University  Zhenjiang China"},{"name":"Molecular Medical Research Center Yancheng Clinical Medical College of Jiangsu University (The First People's Hospital of Yancheng)  Yancheng China"},{"name":"Jiangsu Key Laboratory of Medical Science and Laboratory Medicine, School of Medicine Jiangsu University  Zhenjiang Jiangsu China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0009-0003-2724-9033","authenticated-orcid":false,"given":"Xueyun","family":"Dong","sequence":"additional","affiliation":[{"name":"Department of Laboratory Medicine, School of Medicine Jiangsu University  Zhenjiang 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