Intestinal flora and serum cholesterol
Assimilation of cholesterol by Lactobacillus acidophilus. 1985
Considerable variation was found among strains of Lactobacillus acidophilus isolated from the fecal flora of pigs with regard to the ability to grow well in the presence of bile and to assimilate cholesterol from a laboratory growth medium. The uptake of cholesterol occurred only when the culture(s) was growing in the presence of bile under anaerobic conditions. Consumption of L. acidophilus RP32, which was selected for its ability to grow well in the presence of bile and to assimilate cholesterol from the laboratory medium, significantly inhibited increases in serum cholesterol levels of pigs (P less than 0.05) fed a high-cholesterol diet. Consumption of L. acidophilus P47, which was selected for its ability to grow in the presence of bile and lack of ability to remove cholesterol from the growth medium, failed to have a similar effect. This indicates that certain strains of L. acidophilus act directly on cholesterol in the gastrointestinal tract, and thus may be beneficial in reducing serum cholesterol levels.
Relationship among bile tolerance, bile salt deconjugation, and assimilation of cholesterol by Lactobacillus acidophilus, 1993
Factors to consider when selecting a culture of Lactobacillus acidophilus as a dietary adjunct to produce a hypocholesterolemic effect in humans. 1990
Anticarcinogenic, hypocholesterolemic, and antagonistic activities of Lactobacillus acidophilus. 1995
Serum cholesterol and bowel flora in the newborn. 1975
Bottle-fed infants have a total serum cholesterol of 147 mg/100 ml on the fifth day of life and their stools contain more Escherichia coli than Lactobacilli organisms. The ratio of these bacteria can be reversed by adding bicarbonate or Lactobacilli to feeds. This change is associated with a decrease in total cholesterol to a mean 119 mg/100 ml over the next 3 days. Lactobacilli organisms predominate in the stools when serum cholesterol is low and may play a role in the metabolism of cholesterol.
[Microbial ecology in man and animals and cholesterol metabolism. 2. Hypocholesterolemic effect of microorganisms]. 1992
Colonic bacterial flora and serum cholesterol: alterations induced by dietary citrus pectin. 1985
Development of a gut microbe–targeted nonlethal therapeutic to inhibit thrombosis potential | Nature Medicine 2018
Trimethylamine N-oxide (TMAO) is a gut microbiota–derived metabolite that enhances both platelet responsiveness and in vivo thrombosis potential in animal models, and TMAO plasma levels predict incident atherothrombotic event risks in human clinical studies. TMAO is formed by gut microbe–dependent metabolism of trimethylamine (TMA) moiety-containing nutrients, which are abundant in a Western diet. Here, using a mechanism-based inhibitor approach targeting a major microbial TMA-generating enzyme pair, CutC and CutD (CutC/D), we developed inhibitors that are potent, time-dependent, and irreversible and that do not affect commensal viability. In animal models, a single oral dose of a CutC/D inhibitor significantly reduced plasma TMAO levels for up to 3 d and rescued diet-induced enhanced platelet responsiveness and thrombus formation, without observable toxicity or increased bleeding risk. The inhibitor selectively accumulated within intestinal microbes to millimolar levels, a concentration over 1-million-fold higher than needed for a therapeutic effect. These studies reveal that mechanism-based inhibition of gut microbial TMA and TMAO production reduces thrombosis potential, a critical adverse complication in heart disease. They also offer a generalizable approach for the selective nonlethal targeting of gut microbial enzymes linked to host disease limiting systemic exposure of the inhibitor in the host.
Bacteria supplementation
- Pollagen
Integratore alimentare simbiotico a base di Lactobacillus acidophilus NCFM®, Bifidobacterium lactis BL-04 e frutto-oligosaccaridi (FOS) che favorisce l’equilibrio della flora intestinale.
Ingredienti
per dose (1 bustina da 3 g)
frutto- oligosaccaridi (FOS) 1 g
Lactobacillus acidophilus NCFM® ≥ 1 miliardo UFC*
Bifidobacterium lactis BL-04 ≥ 3 miliardo UFC*
