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Fatty liver hemorrhagic syndrome (FLHS) is a major nutritional and metabolic disorder in high-producing laying hens, characterized by excessive hepatic lipid deposition, steatosis, hemorrhagic injury, impaired laying performance, and increased mortality. Growing evidence indicates that disruption of the gut microbiota-gut-liver axis is associated with FLHS through changes in intestinal barrier integrity, portal endotoxin exposure, and microbiota-related metabolites, including short-chain fatty acids, bile acids, tryptophan metabolites, and choline-derived metabolites. Plant-derived bioactive compounds are promising nutritional interventions because they combine antioxidant, anti-inflammatory, barrier-protective, lipid-regulating, and microbiota-modulating activities. This review synthesizes evidence for polyphenols, flavonoids, alkaloids, polysaccharides, glycosides, saponins, and plant-derived feed materials, while distinguishing associative observations from mechanistically supportive and microbiota-dependent evidence. Fecal microbiota transplantation provides the strongest evidence for partial microbiota dependence of the hepatoprotective effects of Ginkgo biloba extract, magnolol, and Hericium erinaceus polysaccharides. Across interventions, the major proposed mechanisms involve modulation of microbial metabolites, maintenance of intestinal barrier integrity, regulation of hepatic lipid metabolism, and attenuation of inflammatory signaling. However, much of the current evidence remains based on associative microbiome analyses rather than direct experimental demonstration of microbiota-mediated causality. Integrating metagenomics, targeted metabolomics, and functional microbial manipulation will be essential for translating plant bioactives into reproducible strategies for FLHS prevention. Future studies should define effective doses, bioavailability, commercial efficacy, toxicity, and long-term safety.
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Huang et al. (2026) studied this question.
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