Lotus Seed Resistant Starch and Sodium Lactate Regulate Colon Microflora and Improve Metabolic Disorders in Hyperlipidemic Rats

Type 3 resistant starch (RS3) regulates diet-related metabolic diseases by promoting short-chain fatty acids (SCFAs) and lactate production in the intestine. Additionally, RS3 facilitates microbial fermentation of lactate into butyrate in the gut. 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. The findings indicated that the administration of LRS3 resulted in an enhanced diversity of colonic microorganisms, leading to a composition more closely resembling the intestinal microecology 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 and down-regulating androsterone and 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.