Summary
This experimental study in rats demonstrates that maternal obesity induces sex-specific alterations in offspring gut microbiota at weaning, with male offspring showing increased Blautia and decreased Mucispirillum abundance compared to controls. Microbial changes correlated inversely with fecal endocannabinoid levels (PEA and OEA), which themselves showed negative correlation with early-life obesity. The findings suggest a molecular mechanism linking maternal obesity, gut dysbiosis, reduced endocannabinoid signalling, and metabolic dysfunction in the next generation.
Regional applicability
This is a rat model study conducted in Brazil; direct applicability to United Kingdom human populations is limited. However, the mechanistic insights regarding maternal obesity-induced dysbiosis and endocannabinoid signalling may inform understanding of developmental programming in human infants and could support future dietary or probiotic intervention research in UK maternal and child health contexts.
Key measures
Gut microbiota composition (16S rRNA sequencing); fecal PEA and OEA levels; offspring body weight and adiposity; Blautia and Mucispirillum abundance
Outcomes reported
The study examined sex-specific changes in offspring gut microbiota composition and fecal endocannabinoid levels (PEA and OEA) at weaning following maternal obesity exposure. Correlations between microbial taxa, endocannabinoid levels, and offspring adiposity were measured.
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