China
Africa
Explore chapters and articles related to this topic
Gut Microbiota—Specific Food Design
Published in Megh R. Goyal, Preeti Birwal, Santosh K. Mishra, Phytochemicals and Medicinal Plants in Food Design, 2022
Aparna V. Sudhakaran, Himanshi Solanki
Bile acids in the small intestine largely influence the digestion and absorption of dietary lipids. Chemically, the synthesis of primary bile acids takes place in the liver and secondary bile acids take place in the large intestine. Majority of primary bile acids (cholic acid and chenodeoxychlic acid) will be absorbed from Ileum for recycling in the liver. The remaining bile acids (1%–5%) reaching the colon will be modulated by the gut microbiota. The gut microflora regulates the bile acid synthesis as well as the conjugation of secondary bile acids (biotransformation). The secondary bile acids like deoxycholic acid have greater detergent properties thereby controlling the bacterial populations. The gut microbes have bile salt hydrolase (BSH) enzymes, which mediates the biotransformation of bile by hydrolyzing the glycol and tauro conjugates. Some of the genera reported to produce BSH are the Bacteroides, Bifidobacterium, Clostridium, Lactobacillus, and Listeria.
Bile Acids in the Pathogenesis of Necrotizing Enterocolitis
Published in David J. Hackam, Necrotizing Enterocolitis, 2021
In addition to recirculation of BAs from the small intestine back to the liver, some BAs pass into the colon. There, anaerobic bacteria in the Clostridium and Eubacterium genera promote 7α-dehydroxylation of CA and CDCA to form secondary bile acids—deoxycholic acid (DCA) and lithocholic acid (LCA)—followed by transport of BAs back to the liver (Figure 35.2). Hydrophobic BAs—LCA, DCA, and CDCA—are more cytotoxic than the hydrophilic CA and ursodeoxycholic acid (UDCA), which is the 7β-OH epimer of CDCA (21–26). While the majority of conjugated CA and CDCA entering the small intestine are absorbed intact, approximately 15% are deconjugated by species of Bacteroides, Bifidobacterium, Clostridium, and Lactobacillus capable of producing bile salt hydrolase (BSH) (27). Thus, the intestinal microbiome of the premature infant, which can be influenced by birth route (28, 29), diet (30), treatments (31, 32), and the neonatal intensive care unit (NICU) environment itself (28, 33), can have a profound effect on the composition of intestinal BAs, some of which can be highly cytotoxic (34).
Effect of Short-Chain Fatty Acids Produced by Probiotics
Published in Marcela Albuquerque Cavalcanti de Albuquerque, Alejandra de Moreno de LeBlanc, Jean Guy LeBlanc, Raquel Bedani, Lactic Acid Bacteria, 2020
Milena Fernandes da Silva, Meire dos Santos Falcão de Lima, Attilio Converti
Previous studies with axenic cultures of probiotics belonging mainly to Lactobacillus and Bifidobacterium genera have demonstrated the ability of probiotic therapy to decrease body weight and to mitigate insulin resistance, chronic systemic inflammation and hepatic steatosis in experimental obesity models (Nova et al. 2016). Fifteen Lactobacillus and 3 Bifidobacterium strains have been tested by Cani and Van Hul (2015) in order to check their efficacy as obesity treatments; only 10 reduced total body and/or visceral adipose tissue weight, while 12 mitigated liver and/or fat tissue inflammation, with strain-specific variations attributable to different action mechanisms. The same authors mentioned the following mechanisms underlying the therapeutic action of probiotic strains: (a) regulation of absorption and excretion of fat; (b) increase in primary cholic acids due to the action of bile salt hydrolase (Renga et al. 2010); (c) increase in the level of glucagon-like peptides, resulting in alleviation of hunger, decreased energy consumption, and improved sensitivity to insulin and β-cell function; (d) regulation of gene expression to decrease de novo lipogenesis and accelerate β-oxidation; (e) regulation of the expression of proteins (ZO-1 and ZO-2) responsible for restoration/maintenance of gut barrier function as well as reduction of lipopolysaccharide absorption and metabolic endotoxemia; (f) increase in the intestinal levels of SCFAs, mostly butyrate, with consequent mitigation of chronic systemic inflammation, release of anti-inflammatory cytokines by fat tissue, reduction of insulin resistance, enhancement of β-cell differentiation, proliferation and development (Koblyliak et al. 2018).
Effects of intestinal flora on pharmacokinetics and pharmacodynamics of drugs
Published in Drug Metabolism Reviews, 2023
Amina Džidić-Krivić, Jasna Kusturica, Emina Karahmet Sher, Nejra Selak, Nejra Osmančević, Esma Karahmet Farhat, Farooq Sher
Generally, in healthy organism and physiological conditions, the gut microbiota could modulate the proteome as well as the set of RNA transcripts. Transcriptome and collection of metabolites called metabolome in the liver mainly by down-regulating CYP-mediated xenobiotic metabolism and changing the hepatic expression of genes. After the secretion of bile acids from the liver to the bile, their enterohepatic cycle starts. The bile acids are reabsorbed in the ileum, where they interact with the farnesoid X receptor (FXR). FXR is placed in the gut and could detect an increased concentration of bile acids intracellularly. This onsets the production of different growth factors, such as fibroblast growth factor 19 that enters the portal blood circulation and interacts with fibroblast growth factor 4 (Dempsey and Cui 2019). Consequently, downregulation of CYP7A1 and a decrease in the production of new primary bile acids could be noted as shown in Figure 2. Interestingly, it was shown that the expression of FXR is effected by changes in microbiota composition. The lower levels of Lactobacillus genera lead to a lower production of an enzyme called bile salt hydrolase (BHS). This increased the levels of tauro-β-muricholic acid (MCA) that is the potent antagonist of FXR, consequently leading to the development of insulin resistance, obesity and fatty liver disease. Therefore, the FXR has a protective role in the organism and it is possible to enhance its effects by altering the gut microbiota and bacterial genera that are included in its expression (Dempsey and Cui 2019).
Vancomycin prevents fermentable fiber-induced liver cancer in mice with dysbiotic gut microbiota
Published in Gut Microbes, 2020
Vishal Singh, Beng San Yeoh, Ahmed A. Abokor, Rachel M. Golonka, Yuan Tian, Andrew D. Patterson, Bina Joe, Mathias Heikenwalder, Matam Vijay-Kumar
In summary, the present study sheds light on the contributory role of Gram-positive bacteria, specifically secondary bile acid producers, in promoting ICD-induced HCC in T5KO mice (Figure 6). Notwithstanding the efficacy of vancomycin against Gram-positive bacteria including those with multi-drug resistance, vancomycin use in clinical settings is not recommended due to potential side effects and the risk of engendering vancomycin-resistant bacteria. Such concerns certainly limit the prospect of employing vancomycin-based interventions for treating human HCC. One thought is that instead of a simple generic depletion of gut bacteria using antibiotics, it is perhaps more ideal to inhibit their bile acid catabolism in the GI tract. This could be achieved by administering difructose anhydride III that is shown to decrease secondary bile acid generation, purportedly via inhibiting bacterial 7α-dehydroxylase.7,30 As an alternate means, bile salt hydrolase inhibitors could also be considered for restricting the generation of secondary bile acids.31 Another viable alternative is to employ β-acids from hops (Humulus lupulus), which we had previously shown to be effective in inhibiting gut fermentation and thus prevent fermenting bacteria from generating SCFAs.9 Collectively, our study suggests that selective targeting of certain bacterial species or their metabolism, rather than indiscriminately eradicating the entire microbiota with broad spectrum antibiotics, may be a fruitful approach to limit the generation of hepatotoxic metabolites in the gut.
Role of the microbiota in circadian rhythms of the host
Published in Chronobiology International, 2020
The enterohepatic circulation, in which the liver secretes bile into the intestine and reabsorbs them in the distal ileum, follows a daily rhythm (Govindarajan et al. 2016; Parkar et al. 2019). However, some of these liver-derived conjugated bile acids flow into the colon and are deconjugated by gut bacteria possessing the enzyme bile salt hydrolase. The emerging unconjugated bile acids are subject to further microbial modifications via bile acid-inducible enzymes, which create secondary bile acids like deoxycholic acid (DCA) and lithocholic acid (Govindarajan et al. 2016; Parkar et al. 2019). If mice are given the microbiota-derived unconjugated bile acids DCA and chenodeoxycholic acid orally, the expression of clock genes and clock-controlled genes is altered in the ileum, colon, and liver (Govindarajan et al. 2016). The effects of unconjugated bile acids on circadian clock genes are not achieved by the equimolar administration of conjugated bile acids. Only the gut bacteria can produce unconjugated and secondary bile acids and, therefore, indirectly influence host circadian rhythms (Govindarajan et al. 2016). Lastly, orally administered bile acids alter the microbial composition and are also subject to the enterohepatic circulation of the host (Govindarajan et al. 2016).