Effect of lotus seed resistant starch on the bioconversion pathway of taurocholic acid by regulating the intestinal microbiota.

Taurocholic acid (TCA) is abundant in the rat intestine and has multiple health benefits. In the gut, intestinal microbiota can transform TCA into different bile acid (BA) derivatives, with the composition of microbiota playing a crucial role in the transformation process. This study aims to investigate how lotus seed resistant starch (LRS) can regulate microbiota to influence BA transformation. A fecal fermentation study was conducted in vitro, using either LRS, high-amylose maize starch (HAMS), or glucose (GLU) to analyze microbiota composition, BA content, and metabolic enzyme activities over different fermentation times. Bioinformatics analysis found that LRS increased the relative abundance of Enterococcus, Bacillus, and Lactobacillus, and decreased Escherichia-Shigella, compared with HAMS and GLU. LRS also reduced total BA content and accelerated the conversion of TCA to cholic acid, deoxycholic acid, and other derivatives. These results reveal that LRS and GLU tend to mediate the dehydroxy pathway, whereas HAMS tends to secrete metabolic enzymes in the epimerization pathway. Therefore, the evidence that LRS may regulate TCA bioconversion may benefit human colon health research and provide an important theoretical basis, as well as offer new concepts for the development of functional foods.

Bile acid and its bidirectional interactions with gut microbiota: a review.

Bile acids (BAs) are an important metabolite produced by cholesterol catabolism. It serves important roles in glucose and lipid metabolism and host-microbe interaction. Recent research has shown that different gut-microbiota can secrete different metabolic-enzymes to mediate the deconjugation, dehydroxylation and epimerization of BAs. In addition, microbes mediate BAs transformation and exert physiological functions in metabolic diseases may have a potentially close relationship with diet. Therefore, elaborating the pathways by which gut microbes mediate the transformation of BAs through enzymatic reactions involved are principal to understand the mechanism of effects between dietary patterns, gut microbes and BAs, and to provide theoretical knowledge for the development of functional foods to regulate metabolic diseases. In the present review, we summarized works on the physiological function of BAs, as well as the classification and composition of BAs in different animal models and its organs. In addition, we mainly focus on the bidirectional interactions of gut microbes with BAs transformation, and discuss the effects of diet on microbial transformation of BAs. Finally, we raised the question of further in-depth investigation of the food-gut microbial-BAs relationship, which might contribute to the improvement of metabolic diseases through dietary interventions in the future.

Gut microbiota-metabolic axis insight into the hyperlipidemic effect of lotus seed resistant starch in hyperlipidemic mice.

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.