Synergistic regulation of colon microflora and metabolic environment by resistant starch and sodium lactate in hyperlipidemic rats.

Type 3 resistant starch (RS3) regulates diet-related metabolic diseases by promoting intestinal short-chain fatty acids (SCFAs) and lactate production, and facilitating microbial lactate-to-butyrate fermentation. However, its precise in vivo mechanism remains unclear. Therefore, we studied the effects of type 3 lotus seed resistant starch (LRS3) and sodium lactate (SL) on colonic microbiota composition, metabolism, and lipid parameters. This study aimed to elucidate the mechanism by which LRS3 and SL modulate colonic microbiota and metabolism to mitigate hyperlipidemia in rats induced by a high-fat diet. Results showed LRS3 increased colonic microbial diversity, shifting the composition towards that of healthy rats. LRS3 intake reduced lactic acid-producing bacteria such as Allobaculum, Collinsella, and Blautia in the colon while promoting SCFAs-producing Ruminococcaceae. SL alone stimulated Lachnospiraceae growth. When both were administered, there was a significant increase in Treponema and Ruminococcaceae. The co-intervention of LRS3 and SL significantly affected lipid metabolism-related metabolites, up-regulating palmitic acid while down-regulating androsterone and phosphatidylcholine (PC) substances PC (14:0/20:4(8Z,11Z,14Z,17Z)), influencing unsaturated fatty acid biosynthesis pathways and inhibiting steroid hormone biosynthesis. Finally, via the microbial-metabolism-lipid correlation network, we identified that LRS3 and SL increased SCFAs production through Treponema and Ruminococcaceae metabolism, influencing organic acid and lipid composition in the colon. This indirectly reduced blood lipid levels in hyperlipidemic rats by modulating intestinal microecology.