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Role of Plant-Based Medicines for Gallstones
Published in Megh R. Goyal, Preeti Birwal, Durgesh Nandini Chauhan, Herbs, Spices, and Medicinal Plants for Human Gastrointestinal Disorders, 2023
Vivek Kumar, Anju Dhiman, Pooja Chawla, Viney Chawla
The cholelithiasis results from the disturbance in cholesterol metabolism. Cholesterol is virtually water insoluble and forms a micellar solution with bile acids, phospholipids by the action of bile acids. Phospholipids and bile salts are key members that are responsible for the dissolution of cholesterol in bile. It involves metabolic disturbance that causes an increase in the amount of cholesterol with respect to bile acids and phospholipids and form unsteady vesicles of cholesterol, which in turn join to form large multilayered vesicles leading to crystals of cholesterol precipitation. Mainly three types of disturbances are considered to be responsible for cholelithiasis occurrence: The first disturbance includes the supersaturation of bile with cholesterol. It is the main and essential requirement for cholelithiasis and might be helped by two additional metabolic disturbances, such as reduction of the bile acid pool, and enhancement in the conversion of cholic acid to deoxycholic acid. Bile acid pool reduction is caused by snappy depletion of bile acid from the small intestinal tract into the colon. The enhancement in deoxycholic acid results due to the dehydroxylation of cholic acid and expanded absorption of recently made deoxycholic acid. The cholesterol hypersecretion is caused by the updated level of deoxycholate and hence causing the supersaturation of bile with cholesterol.
Intrahepatic Cholestasis of Pregnancy
Published in Vincenzo Berghella, Maternal-Fetal Evidence Based Guidelines, 2022
Mechanism of action for ursodiol, which is a hydrophilic bile acid that inhibits intestinal absorption of other bile acids, enhances excretory hepatocyte function and choleretic activity, stabilizes hepatocyte cell membranes and dilutes toxic bile acids in the enterohepatic circulation [13]. Ursodiol may also allow for transport of bile acids out of fetal compartment. After treatment, ursodeoxycholic acid (UDCA) becomes the main component of the total bile acid measurement, thus reducing the proportion of cholic acid, that has been repeatedly implicated in the pathogenesis of fetal complications [21].
Functions of the Liver
Published in Peter Kam, Ian Power, Michael J. Cousins, Philip J. Siddal, Principles of Physiology for the Anaesthetist, 2020
Peter Kam, Ian Power, Michael J. Cousins, Philip J. Siddal
The liver produces about 1 L of bile per day, and this passes into the gall bladder where it is concentrated to about one-fifth of its volume. Bile consists of electrolytes, protein, bilirubin, bile salts and lipids. Bile acids (cholic acid and chenodeoxycholic acid) are produced in the liver from cholesterol. In the gut, bacterial action on cholic and chenodeoxycholic acids produces secondary bile acids such as deoxycholic acid and lithocholic acid. The bile acids conjugate with glycine or taurine to form bile salts (Figure 37.5). Bile salts are more water soluble and less lipid soluble, which limits the passive absorption in the small intestine so that the bile salts remain within the gut. The main function of bile salts is the emulsification of dietary fat, which is essential for fat absorption. In addition, bile salts are also important for the absorption of fat-soluble vitamins, especially vitamins A, D, E and K. At the terminal ileum, bile salts are reabsorbed by the apical sodium-dependent bile transporter. The reabsorbed bile salts are carried to the liver in the portal circulation, mostly bound to plasma proteins. The recirculation of bile salts is referred to as enterohepatic circulation.
mPEG-Cholic acid/TPGS mixed micelles for combined delivery of paclitaxel and bufalin to treat hepatocellular carcinoma
Published in Pharmaceutical Development and Technology, 2022
Yujia Liu, Xiaoyu Lu, Zhenhai Zhang, Shulong Jiang, Huixia Lv
In this study, mPEG-CA was successfully synthesized and PTX and BF were loaded respectively to prepare mPEG-CA/TPGS polymer micelles for combined administration to treat HCC. Cholic acid groups could achieve liver targeting function and PEG could prolong circulation time, while the combination of the two drugs achieved a synergistic therapeutic effect. In vitro cell tests confirmed that PB/PCTm exhibited superior synergistic anti-tumor and targeted effect on HCC. In vivo studies conducted on bioluminescence orthotopic hepatocellular carcinoma bearing mice model demonstrated that PB/PCTm possessed a tumor inhibition rate up to 82.29%. Therefore, PB/PCTm as an effective drug delivery system could be used to enhance the combined therapeutic effect of PTX and BF and achieve the purpose of synergistic and attenuation for hepatocellular carcinoma treatment.
Liver metabolomic characterization of Sophora flavescens alcohol extract-induced hepatotoxicity in rats through UPLC/LTQ-Orbitrap mass spectrometry
Published in Xenobiotica, 2020
Peng Jiang, Yancai Sun, Nengneng Cheng
Bile acids synthesized from cholesterol in the liver pass into the intestinal tract and can be reabsorbed by liver for reuse. The efficient utilization of bile acids has been regarded as a pathway for the elimination of cholesterol. Cholic acid, TUDCA, TCA, GCA and GUDCA were generally decreased after SFAE treatment was administered. Conversely, taurine was increased. Cholic acid was the primary bile acid. The prevention of bile acid synthesis can result in accumulation of cholesterol and hepatic dysfunction. Sphingosin-1-phosphate receptor 2 (S1P2) is expressed in hepatocytes. Conjugated bile acids, TUDCA, TCA and GCA can activate S1P2 signaling, which is mainly attributed to the activation of ERK1/2 and AKT signaling in rat hepatocytes (Wang et al., 2017). The perturbation of bile acid pool is an early pathological finding of DILI in rodent model (Yamazaki et al., 2013). A small panel of bile acids, such as taurocholate, glycocholate and urinary cholate combination, was considered to be early preclinical indicators for DILI in rats.
Ileostomy diarrhea: Pathophysiology and management
Published in Baylor University Medical Center Proceedings, 2020
Kyle M. Rowe, Lawrence R. Schiller
Traditional bile acid diarrhea resulting from bile acid malabsorption is not possible in the colectomized patient, as the secretory mechanism resides in the colon. Thus, bile acid binders such as cholestyramine may only serve to worsen fat malabsorption and steatorrhea and should not be prescribed in patients with end ileostomies. In those with larger ileal resections, usually >100 cm, bile acid loss may outpace hepatic production, and steatorrhea due to bile acid deficiency may result. In these cases supplementary bile acid should be considered.19,83 The only bile acid supplement approved by the US Food and Drug Administration (FDA) is cholic acid (Cholbam); however, this drug is approved only for bile acid synthesis disorders and would require off-label use, which would be cost-prohibitive at the current price point. Ox bile supplements can be purchased but are not approved or regulated by the FDA. A reasonable dose would be 1 to 2 g daily taken in divided dose with meals.