Maternal obesity, diet, and the gut microbiome: implications for offspring cardiometabolic programming

Maternal obesity is associated with adverse pregnancy and long-term offspring outcomes. The maternal gut microbiome may contribute through altered microbial functions, barrier integrity, immune signaling, and metabolite production. Pregnancy itself entails microbial and metabolic remodeling, but obesity and obesogenic dietary patterns may modify these adaptations. Evidence from human cohorts and animal models links maternal obesity with context-dependent differences in microbial composition and function, reduced butyrate-producing capacity, altered bile acid and short-chain fatty acid profiles, and heightened inflammation. These changes may influence placental function and early-life microbial assembly through delivery-related exposures, breastfeeding, human milk oligosaccharides, and shared environmental and dietary factors. Maternal diets high in saturated fat and refined carbohydrate tend to be associated with less favorable microbial and cardiometabolic profiles, whereas fiber-rich, plant-diverse dietary patterns may support short-chain fatty acid production and metabolic resilience. However, causal inference is limited by heterogeneity, confounding, and inconsistent findings. Probiotic, prebiotic, and synbiotic interventions show potential, but clinical results-particularly for gestational diabetes prevention-remain mixed. This narrative review integrates evidence on diet-microbiome interactions in maternal obesity, microbial metabolites and immune pathways, early-life colonization, and implications for offspring obesity and cardiometabolic risk. Overall, the maternal microbiome is a plausible but incompletely validated target; well-powered longitudinal studies and pregnancy-specific randomized trials are needed before precision microbiome strategies can be incorporated into routine care.