Gut microbiota and the early prevention window in type 1 diabetes and latent autoimmune diabetes in adults: a state-of-the-art narrative review on diet and metabolites.

Autoimmune type 1 diabetes (T1D) is typically the end point of a prolonged process involving genetic susceptibility, the emergence of islet autoimmunity, and progressive loss of pancreatic beta-cell reserve rather than the day hyperglycaemia is first diagnosed. In parallel, research on the gut microbiome has shifted from searching for single causal taxa to examining ecosystem-level functions, microbial metabolites, and host-pathway interactions. In this narrative review, we synthesise prospective, mechanistic, and translational evidence on the role of the gut microbiome in T1D and latent autoimmune diabetes in adults (LADA) using a stage-aware, function-first framework. Across the current literature, the most consistent signals concern impaired intestinal barrier homeostasis, reduced fermentation-related capacity, altered short-chain fatty acid signalling, perturbations in tryptophan-derived and bile acid-related pathways, and their downstream effects on immune regulation and inflammatory tone. In T1D, evidence from prospective early-life cohorts suggests that microbiome maturation, together with diet, infections, and antibiotic exposure, may influence the risk of islet autoimmunity and the tempo of progression toward clinical disease. In LADA, the available evidence is more limited and largely cross-sectional, but supports an immunometabolic interpretation that includes altered microbiome and metabolomic profiles. We propose that the main translational priority is not taxon-specific manipulation, but identification of stage- and age-specific windows of susceptibility across the life course and alignment of these windows with low-risk, mechanistically plausible dietary and microbiome-modulating strategies. This framework may help guide microbiome-informed counselling, study design, and research prioritisation in autoimmune diabetes.

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