Ganoderma applanatum Polysaccharides in Obesity-Associated Dysglycaemia and Liver Injury: Gut–Liver Mechanisms and Translational Gaps Ganoderma and Metabolic Liver Injury
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Keywords
mushroom polysaccharides, obesity, insulin resistance, metabolic-associated fatty liver disease, oxidative stress, gut-liver axis, MACAPOS-2, Ganoderma applanatum
Abstract
Obesity-associated dysglycaemia and metabolic dysfunction-associated steatotic liver disease (MASLD) arise from interacting inflammatory, oxidative, lipotoxic, and gut-liver mechanisms. Ganoderma applanatum polysaccharides are an under-characterized candidate adjunct, but their translational relevance remains uncertain. The study aims to narratively review mechanistic and preclinical evidence linking G. applanatum polysaccharides with obesity-associated dysglycaemia and liver injury and to identify key translational gaps. A structured narrative review of PubMed/MEDLINE and Google Scholar literature, complemented by backward citation screening, was undertaken. Evidence on preparation chemistry, structural features, metabolic and hepatic outcomes, gut-liver mechanisms, and clinical translation was synthesized qualitatively. Available evidence is limited and predominantly preclinical, with MACAPOS-2 obese rat studies providing the main G. applanatum data. Defined water-soluble preparations have been associated with improved glucose tolerance, insulin responsiveness, dyslipidaemia, oxidative stress markers, aminotransferases, and histologic liver injury. A biologically coherent explanation is gut-centered modulation involving microbiota remodelling, microbial metabolite signalling, barrier reinforcement, and downstream attenuation of endotoxemia-linked hepatic inflammatory and oxidative stress. However, the evidence base is constrained by preparation heterogeneity, incomplete structural characterization, modest sample sizes, limited direct measurement of gut-liver pathway engagement, and heavy reliance on a single research network. G. applanatum polysaccharides should currently be viewed as preparation-specific, biologically plausible immunometabolic modulators rather than clinically ready therapies. Progress requires structurally defined preparations, independent replication, mechanism-anchored biomarkers, and adequately powered human studies in carefully phenotyped populations.
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