The rapid digestion of starch is closely linked to an elevated risk of diet‑related chronic conditions. In recent years, blending starch with other food components has become a common strategy to slow its digestibility. Among various approaches, dietary fiber (DF) has drawn considerable interest owing to its marked inhibitory effects on starch digestion. Although numerous studies have reported these effects, systematic discussions of the underlying mechanisms remain scarce. In this review, we first classified the factors that influence the impact of DF on starch digestion and examined the interrelationships among them. We then systematically dissected the inhibitory mechanisms, which included direct interactions between DF and starch that altered starch physicochemical properties, suppression of digestive enzyme activity, increased viscosity or altered mass transfer, and modulation of gut microbiota and their metabolites. In addition, we surveyed the applications of DF‑mediated regulation of starch digestion in the food industry, where consumer demand and acceptance for such functional products were steadily growing. This review thus offers important insights for the development of slow‑digesting foods.

Type 2 diabetes mellitus (T2DM) is a chronic endocrine disorder characterized by metabolic disturbances. Currently, the treatment strategies for T2DM mainly focus on improving insulin sensitivity and regulating blood glucose homeostasis. However, due to the incomplete understanding of the interaction network mediating gene-metabolism-microbiota regulation, breakthroughs in targeted therapy have been limited. In this study, the hypoglycemic effects of Spirulina platensis polysaccharide (SPP) and its selenium-modified polysaccharide (SeSPP) on a high-fat diet/streptozotocin-induced T2DM mice model were thoroughly investigated, along with their underlying mechanisms. Transcriptomics and metabolomics analysis revealed that SPP and SeSPP exerted their hypoglycemic effects primarily by regulating lipid metabolism, carbohydrate metabolism, and cellular signaling pathways. They resulted in a reduction of Propionyl-CoA and Lyso-PI (0:0/18:1(9Z)) levels, while simultaneously increasing the level of 12,13-diHOME. Furthermore, they upregulated the expression of the Acot3 gene and downregulated the expression of the Acsm2 gene, thereby activating the fatty acid metabolic pathway. SPP and SeSPP significantly ameliorated the gut microbiota imbalance induced by T2DM by enhancing the abundance of Lactobacillus and Faecalibaculum, while simultaneously reducing the levels of Alloprevotella and Bacteroides. In conclusion, SPP and SeSPP have the potential to reshape the gut microbiota, thereby restoring microecological balance, including disorders in glucose and lipid metabolism, chronic low-grade inflammation, and oxidative stress.