Legume intake on gut microbiome and glycemia in type 2 diabetes management: narrative review
Open Access
- 1 April 2026
- journal article
- Published by Frontiers Media SA in Frontiers in Nutrition
- Vol. 13
Abstract
Legumes are rich in dietary fiber, plant proteins, micronutrients, and bioactive compounds, offering a sustainable and affordable addition to the diet. However, the extent to which legume-induced modulation of the gut microbiota contributes to glycemic regulation in type 2 diabetes (T2D), relative to microbiota-independent physiological mechanisms, remains insufficiently defined. This narrative review synthesizes current evidence on legume-based interventions and their effects on gut microbiota composition and function in relation to glycemic control. Relevant studies were identified through structured searches of MEDLINE and the Cochrane Central Register of Controlled Trials via Ovid, complemented by manual screening of reference lists. Seventeen studies (three human and 14 animal trials) were considered in this review. Human studies report that consuming legumes is associated with improved glucose tolerance and blood glucose levels, although effects on microbiota composition are variable and modest. Conversely, animal studies demonstrate improvements in insulin sensitivity, glucose tolerance, and microbial diversity with higher dose legume interventions. Legume consumption has been associated with enrichment of beneficial microbial taxa, such as Bifidobacterium , Akkermansia , Ruminococcus , and Bacteroides , as well as increased concentrations of microbial metabolites such as short-chain fatty acids (SCFAs). These microbial features are implicated in metabolic pathways relevant to insulin signaling and glycemic regulation; however, current human evidence does not establish that microbiota alterations causally mediate glycemic improvements. Well-designed, adequately powered clinical studies incorporating functional microbiome analyses and formal mediation approaches are required to clarify microbiota-dependent and microbiota-independent mechanisms.Keywords
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