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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.
Cardiovascular Risk Factors
Published in Nicole M. Farmer, Andres Victor Ardisson Korat, Cooking for Health and Disease Prevention, 2022
Relevant to CVD risk factor reduction, soluble fibers can lower cholesterol through binding of bile acids. The available bile acid pool is related to levels of cholesterol as a function of the enterohepatic system, which regulates the production of cholesterol in relation to absorption of intestinal bile acids. When the available bile acid pool is decreased, then cholesterol production is decreased. Medications that bind intestinal bile acids deplete the endogenous bile acid pool by approximately 40%. This binding can increase bile acid synthesis from cholesterol, thus reducing low-lipoprotein cholesterol (LDL-C) by 15%–26% (Insull, 2006).
Bile Acid Interactions with Cholangiocytes
Published in Gianfranco Alpini, Domenico Alvaro, Marco Marzioni, Gene LeSage, Nicholas LaRusso, The Pathophysiology of Biliary Epithelia, 2020
Gianfranco Alpini, Shannon Glaser, Heather Francis, Marco Marzioni, Julie Venter, Jo Lynne Phinizy, Gene LeSage
Bile acids, phospholipids and cholesterol are synthesized in a cholangiocarcinoma cell line.80 Cholangiocytes have also been shown to conjugate bile acids.80 The contribution of cholangiocyte bile acid synthesis and conjugation to the over all bile acid pool seems minimal since less that 3 percent of the total liver mass is composed of cholangiocytes.81 The mechanisms for regulation of bile acid synthesis in cholangiocytes have not been determined.
In-silico, in-vitro and ex-vivo evidence of combining silymarin phytopharmaceutical with piperine, and fulvic acid for enhancing its solubility and permeability
Published in Pharmaceutical Development and Technology, 2023
Tanya Ralli, Zoya Saifi, Amita Kumari, Vidhu Aeri, Kanchan Kohli
Herbal drugs can act as a suitable treatment option for this disease due to the presence of multiple active ingredients in a single extract that modify various pathways. A recent detailed review by Yu Xu et al. have highlighted the mechanisms by which herbal drugs act for the treatment of NAFLD. They act by multiple pathways, a) improving the metabolism of lipids in the liver cells, b) modulating lipogenesis and beta oxidation in liver cells by acting through AMPK pathways, c) decreasing inflammation in the liver cells by acting through NF-κB signaling, d) inhibiting the apoptotic pathways in liver cells, e) promoting bile acid synthesis which in turns help in metabolizing the lipids, f) acts as anti-oxidant in the liver cells, g) inhibiting the production of reactive oxygen species by improving the mitochondrial function, h) for removing the degraded products, they also help in inducing autophagy and many more (Zhang et al. 2018; Xu et al. 2020). Thus, these benefits highlighted the importance of herbal drugs in treating NAFLD.
Kuhuang injection exerts a protective effect by activating PPAR-γ in an in vitro model of chlorpromazine-induced cholestatic liver injury constructed by tissue engineering
Published in Pharmaceutical Biology, 2022
Qiao Wu, Zhongping Duan, Long Huang, Zhijie Li
At the end of culture, the TBA level in the CPZ group was 18.90 ± 0.65 μmol/L, and Kuhuang reduced this level to 11.72 ± 1.31 μmol/L (p < 0.05, Figure 2(A)). The classic pathway of bile acid synthesis involves the action of CYP7A1, CYP8B1, and other enzymes. To clarify the molecular mechanisms by which Kuhuang regulates hepatic bile acids accumulation under CPZ treatment, CYP7A1 and CYP8B1 were measured by PCR and WB analysis (Figure 2(B–D)). The results showed that the expression of CYP7A1 and CYP8B1 increased significantly (p < 0.01) when CPZ was administered and that Kuhuang reduced the accumulation of bile acids in liver cells by inhibiting the expression of these two rate-limiting enzymes (CYP7A1, p < 0.05; CYP8B1, p < 0.01) compared to the CPZ group.
Effect of Acacia senegal on TGF-β1 and vascular mediators in a rat model of diabetic nephropathy
Published in Archives of Physiology and Biochemistry, 2022
Muataz E. Mohammed, Amr M. Abbas, Rehab M. Badi, Salah Omer Bashir, Osama M. Osman, Mohamed D. Morsy, Amal M. Saeed
Various mechanisms were suggested to explain the lipid-lowering effect of GA. Some studies explained that the viscosity of fermentable dietary fibres contributes substantially to the lipid-lowering effects in animals and humans (Gallaher et al.1993, Moundras et al.1994). Other study suggested that the mechanism is related to GA induced increase in faecal bile acid and neutral sterol excretion or modification of lipid digestion and absorption (Moundras et al.1994). GA is believed to either bind or sequester bile acids, diminishing their active reabsorption in the ileum and leading to their excretion in the faeces. This consequently results in promoting the diversion of cholesterol to bile acid synthesis; in addition to inducing increased numbers of lipoprotein receptors in the liver (Truswell and Beynen 1992). GA has a high cation-binding capacity, particularly for Ca2+. Degradation of GA in the caecum releases the sequestered bile acids. The bound calcium is also released and forms insoluble complexes with bile acids, thereby promoting their excretion in faeces (Moundras et al.1994).