ArticleFrontiers in nutrition2026
Perinatal phlorizin alleviates maternal high-fat diet-induced metabolic syndrome in female mouse offspring and is associated with modulation of the gut microbiota.
Article in Frontiers in nutrition, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Introduction: Maternal obesity induces transgenerational metabolic syndrome (MS). The role of phlorizin (PHZ) in improving MS has been confirmed; however, the transgenerational metabolic benefits of PHZ in female offspring remain unclear. This study aimed to investigate whether perinatal PHZ intake could mitigate the adverse metabolic effects of maternal high-fat diet (HFD) in female offspring and to elucidate the role of the gut microbiota in mediating these transgenerational effects. Methods: C57BL/6 mice with maternal HFD ± perinatal PHZ (0.8 g/kg diet) intervention were used. After weaning, Female offspring's glucolipid metabolism, gut barrier, gut microbiota, and SCFAs were analyzed. Obesogenic dietary challenge and fecal microbiota transplantation (FMT) were implemented to verify microbiota mediation. Results: Maternal HFD induces metabolic abnormalities in female offspring, characterized by disrupted glucolipid metabolism during weaning and mild obesity. In adulthood, although these offspring did not display overt obesity, they exhibited gut microbial dysbiosis (increase Conclusion: Our findings suggested that maternal PHZ alleviates maternal HFD-induced transgenerational metabolic dysfunction in female offspring and is associated with modulation of the gut microbiota, positioning PHZ as a promising functional food component with transgenerational metabolic protective potential.
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