This study examined how maternal vitamin B12 deprivation during pregnancy and lactation affects offspring metabolic health, gut microbiota composition, and susceptibility to high-fat-diet-induced obesity in a rodent model, with a focus on the mechanistic role of *Bifidobacterium pseudolongum* and its metabolite acetate.
Maternal B12 deprivation reduced early-life *B. pseudolongum* colonization in offspring and worsened high-fat-diet-induced obesity and metabolic dysregulation; early-life restoration of *B. pseudolongum* or acetate ameliorated these effects via the Ffar2 receptor and upregulation of *Ehhadh* expression.
The study appears to be conducted in an animal (rodent) model, limiting direct translation to humans; the clinical relevance of the specific Ffar2/Ehhadh mechanism in human infants is unconfirmed; and the study does not establish the minimum or optimal level of B12 needed to preserve protective microbiota colonization in humans.
Adequate vitamin B12 intake during pregnancy and lactation may be critical not just for fetal development but for establishing protective gut microbiota in infants that reduce long-term obesity risk. Clinicians should counsel pregnant and breastfeeding patients — especially those at risk of B12 deficiency (e.g., vegans, vegetarians) — on the importance of B12 supplementation.
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