-
World Journal of Gastroenterology Apr 2017To evaluate the ability of HN001 and BB536 to colonize the intestinal environment of healthy subjects and modify the gut microbiota composition. (Clinical Trial)
Clinical Trial
AIM
To evaluate the ability of HN001 and BB536 to colonize the intestinal environment of healthy subjects and modify the gut microbiota composition.
METHODS
Twenty healthy Italian volunteers, eight males and twelve females, participated in the study. Ten subjects took a sachet containing 4 × 10 colony-forming units (CFU) of BB536 and 10 CFU of HN001, 30 min before breakfast (pre-prandial administration), while ten subjects took a sachet of probiotic product 30 min after breakfast (post-prandial administration). The ability of HN001 and BB536 to colonize human gut microbiota was assessed by means of quantitative real-time PCR, while changes in gut microbiota composition were detected by using Ion Torrent Personal Genome Machine.
RESULTS
Immediately after 1-mo of probiotic administration, BB536 and HN001 load was increased in the majority of subjects in both pre-prandial and post-prandial groups. This increase was found also 1 mo after the end of probiotic oral intake in both groups, if compared to samples collected before probiotic consumption. At phyla level a significant decrease in abundance was detected immediately after 1-mo of BB536 and HN001 oral intake. This reduction persisted up to 1 mo after the end of probiotic oral intake together with a significant decrease of abundance if compared to samples collected before probiotic administration. Whereas, at species level, a higher abundance of , and was observed, together with a reduction of , , and abundance. In addition, during follow-up period we observed a further reduction in and , together with a decrease in and abundance. Conversely, the abundance of was increased if compared to samples collected at the beginning of the experimental time course.
CONCLUSION
BB536 and HN001 showed the ability to modulate the gut microbiota composition, leading to a significant reduction of potentially harmful bacteria and an increase of beneficial ones. Further studies are needed to better understand the specific mechanisms involved in gut microbiota modulation.
Topics: Adult; Bifidobacterium longum; Female; Gastrointestinal Microbiome; Healthy Volunteers; Humans; Lacticaseibacillus rhamnosus; Male; Middle Aged; Probiotics
PubMed: 28487606
DOI: 10.3748/wjg.v23.i15.2696 -
Frontiers in Nutrition 2024To produce the health-associated metabolite propionate, gut microbes require vitamin B12 as a cofactor to convert succinate to propionate. B12 is sourced in the human...
To produce the health-associated metabolite propionate, gut microbes require vitamin B12 as a cofactor to convert succinate to propionate. B12 is sourced in the human gut from the unabsorbed dietary fraction and microbial production. However, experimental data for B12 production by gut microbes is scarce, especially on their produced B12-analogues. Further, the promotion of propionate production by microbially-produced and dietary B12 is not yet fully understood. Here, we demonstrated B12 production in 6 out of 8 predicted B12-producing bacteria from the human gut. Next, we showed that B12 produced by , and promoted succinate to propionate conversion of two prevalent B12-auxotrophic gut bacteria, and . Finally, we examined the propiogenic effect of commercially available B12-analogues present in the human diet (cyano-B12, adenosyl-B12 and hydroxy-B12) at two doses. The low dose resulted in partial conversion of succinate to propionate for when grown with adenosyl-B12 (14.6 ± 2.4 mM succinate and 18.7 ± 0.6 mM propionate) and hydroxy-B12 (13.0 ± 1.1 mM and 21.9 ± 1.2 mM), in comparison to cyano-B12 (0.7 ± 0.1 mM and 34.1 ± 0.1 mM). Higher doses of adenosyl-B12 and hydroxy-B12 resulted in significantly more conversion of succinate to propionate in both propionate-producing species, compared to the low dose. B12 analogues have different potential to impact the propionate metabolism of prevalent propionate producers in the gut. These results could contribute to strategies for managing gut disorders associated with decreased propionate production.
PubMed: 38389799
DOI: 10.3389/fnut.2024.1360199