We investigated the hyperlipidemic effect of different doses of lotus seed resistant starch (low-, medium and high-dose LRS, named as LLRS, MLRS and HLRS, respectively) in hyperlipidemic mice using gut microbiota-metabolic axis compared to high-fat diet mice (model control group, MC). Allobaculum was significantly decreased in LRS groups compared to MC group, while MLRS promoted the abundance of norank_f_Muribaculaceae and norank_f_Erysipelotrichaceae. Moreover, supplementation of LRS promoted cholic acid (CA) production and inhibited deoxycholic acid compared to MC group. Among, LLRS promoted formic acid, MLRS inhibited 20-Carboxy-leukotriene B4, while HLRS promoted 3, 4-Methyleneazelaic acid and inhibited Oleic acid and Malic acid. Finally, MLRS regulate microbiota composition, and this promoted cholesterol catabolism to form CA, which inhibited serum lipid index by gut microbiota-metabolic axis. In conclusion, MLRS can promote CA and inhibit medium chain fatty acids, so as to play the best role in lowering blood lipids in hyperlipidemia mice.
Keywords: Gut microbiota-metabolic axis; Hyperlipidemic mice; Lotus seed resistant starch; Serum lipid index; Untargeted metabolites.
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