Can Prebiotics Support Microbial Metabolic Function Following Low-FODMAP Restriction in Irritable Bowel Syndrome?

Irritable bowel syndrome (IBS) is one of the most common disorders of gut–brain interaction, and dietary interventions play a central role in symptom management. Among these, the low-fermentable oligosaccharides, disaccharides, monosaccharides, and polyols (low-FODMAP) diet has been shown to improve abdominal pain, bloating, and altered bowel habits in a substantial proportion of patients. However, restriction of fermentable carbohydrates may reduce the availability of substrates for the gut microbiota and has been associated with reductions in selected microbial taxa, including Bifidobacterium, raising questions about its effects on microbial ecology and metabolism. Dietary prebiotics selectively stimulate gut microorganisms and promote microbial fermentation and the production of metabolites, including short-chain fatty acids, that may contribute to intestinal homeostasis. However, many prebiotics are also highly fermentable substrates, and their gastrointestinal effects may vary substantially among individuals with IBS. This creates a challenge in balancing symptom control with continued exposure to substrates that may support microbial and metabolic functions. In this narrative review, we critically examine the metabolic and clinical implications of dietary prebiotics in IBS, with particular emphasis on their potential role following low-FODMAP restriction. We discuss their effects on gut microbiota composition and function, microbial metabolites, and clinically relevant outcomes, with particular attention to the relationship between microbial and symptomatic responses. We further consider the potential role of structured reintroduction and personalization of tolerated fermentable substrates in maintaining dietary variety and microbial substrate availability while minimizing gastrointestinal symptoms. Finally, we discuss interindividual variability in responses to fermentable substrates and factors that may contribute to differential responses, highlighting current limitations in linking microbiota composition, microbial function, metabolite production, and clinical outcomes in IBS, and identifying possible directions for future research.