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Evidence-Based Supplement Research
Evidence-Based Supplement Research

An exopolysaccharide-rich fraction from Bifidobacterium animalis subsp. lactis MG741 ameliorates high-fat diet-induced MASLD by enhancing intestinal barrier function.

  • 2026-04
  • International journal of biological macromolecules 359
    • Hee-Jin Kim
    • Hee-Kyoung Son
    • Yu Ra Lee
    • Yejin Ahn
    • Hye-Bin Lee
    • Ji-Yeon Lee
    • Miri Park
    • Jae-Ho Park
    • Ho-Young Park

Study Design

Population
high-fat diet (HFD)-induced MASLD mouse model
Methods
EPS-rich fraction from Bifidobacterium animalis subsp. lactis MG741 (EPS-BL) was prepared by ethanol precipitation and dialysis, characterized, and evaluated for prebiotic and barrier-supporting activities in vitro and in a high-fat diet (HFD)-induced MASLD mouse model; oral administration of EPS-BL (5 or 20 mg/kg, 8 weeks)
Exopolysaccharides (EPSs) produced by microorganisms have attracted interest as bioactive biopolymers, yet their roles in metabolic dysfunction-associated steatotic liver disease (MASLD) remain incompletely understood. Here, we prepared an EPS-rich fraction from Bifidobacterium animalis subsp. lactis MG741 (EPS-BL) by ethanol precipitation and dialysis, characterized its major molecular features, and evaluated its prebiotic and barrier-supporting activities in vitro and in a high-fat diet (HFD)-induced MASLD mouse model. EPS-BL was a mannose-dominant carbohydrate-rich preparation (219.38 mg/g mannose; weight-average molecular weight, 58.3 kDa) that also contained substantial protein, and should therefore be interpreted as a minimally processed EPS-rich material rather than a fully purified polysaccharide. In vitro, EPS-BL promoted the growth of L. plantarum and L. rhamnosus and upregulated mucin-related genes (MUC2 and MUC5AC) in LS174T goblet cells. In vivo, oral administration of EPS-BL (5 or 20 mg/kg, 8 weeks) reduced weight gain and fat mass, improved glucose-related indices, lowered circulating endotoxin, and ameliorated colonic and hepatic abnormalities in HFD-fed mice. EPS-BL also attenuated hepatic triglyceride accumulation, accompanied by suppression of lipogenesis-related proteins. Targeted metabolomics revealed coordinated shifts in serum and fecal metabolites associated with metabolic dysfunction biomarkers. Overall, EPS-BL mitigates HFD-induced MASLD in association with reinforcement of the gut barrier and modulation of the gut-liver metabolic axis, supporting its potential as a functional prebiotic ingredient.

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