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Biliary Atresia
Published in Gianfranco Alpini, Domenico Alvaro, Marco Marzioni, Gene LeSage, Nicholas LaRusso, The Pathophysiology of Biliary Epithelia, 2020
Several approaches have been used to attempt to enhance adequate bile drainage after the Kasai procedure including the use of choleretics, such as ursodeoxycholic acid and phenobarbital, bile aid binding resins, and anti-inflammatory drugs, even corticosteroids.47,48 In Japan, patients are treated post-operatively with a protocol that includes intravenous dehydrocholic acid, oral ursodeoxycholic acid and intravenous methylprednisolone. The patients are then treated with oral prednisone every other day for 2 months.49 Unfortunately, due to the limited nature with which these approaches have been studied, there is no evidence that they are successful. Many approaches have also been used to reduce the likelihood of cholangitis/sepsis after the hepatoportoenterostomy. Patients have been treated with postoperative intravenous antibiotics and others with long-term prophylactic oral antibiotics. The Roux-en-Y limb of the portoenterostomy has been lengthened, exteriorized or made into a valved conduit. None of these interventions has any substantive proven benefit. Ultimately only 10–20% of the patients who undergo the Kasai procedure will have sustained relief of biliary obstruction.43–45
Inhibiting Insulin Resistance and Accumulation of Triglycerides and Cholesterol in the Liver
Published in Christophe Wiart, Medicinal Plants in Asia for Metabolic Syndrome, 2017
Kirchhoff et al. provided evidence that an extract of Cynara scolymus L. (containing mainly 1,3-di-O-caffeoylquinic acid also known as cynarin) given orally at a single dose: 1.92 g to healthy volunteers increased bile secretion.401 Aqueous extract of leaves of Cynara scolymus L. given orally to Wistar rats at a dose of 400 mg/kg increased bile flow from 0.1 to 0.2 mL/100 g animal/h, and this effect was similar to positive standard: dehydrocholic acid at 20 mg/kg.402 The extract given for 7 days twice a day at a dose of 400 mg/kg increased bile flow from 0.1 to 0.2 mL/100 g animal/h (dehydrocholic acid at 20 mg/kg: 0.3 mL/100 g animal/h).402 Ethanol extract for flowering head of Cynara scolymus L. given orally at a dose of 1500 mg/kg to Wistar rats before food pellet consumption lowered 120 minutes peak glycaemia from 130 to about 110 mg/dL. The extract given to obese Zucker obese rats orally at a dose of 1500 mg/kg before food pellet consumption lowered 60 minutes peak glycaemia from 150 to about 130 mg/dL.403 Cynaropicrin, apigenin 7-O-glucoside, and cynarin at a concentration of 10 mg/mL increased the secretion of bile by perfused rat liver by 47%, 30%, and 5%, respectively.404 Apigenin 7-O-glucoside is probably metabolized by bacterial intestinal flora and first-pass metabolism and it seems improbable to obtain hepatic pharmacological concentrations of this flavonoid upon oral administration. Cynaropicrin inhibited at a single dose of 100 mg/kg triglyceride absorption in rodents on partial account of gastric emptying delay.405 The mode of action of cynaropicrin on bile secretion could be due to irritation of gut muscles. In a subsequent study, 200 mg of ethanol extract of flowering heads of Cynara scolymus L. given to overweight and obese volunteers with impaired fasting glycaemia (body mass index between 25 and 35 kg/m2, fasting glycaemia between 6.1 and 7 mmol/L) three times per day orally before meals for 8 weeks evoked a decrease in fasting blood glucose by 9.6%, insulin resistance and had no effect on insulinemia.406 This supplementation lowered plasma cholesterol by 6.3% and had no effect in triglycerides.406 Aqueous extract of leaves given to Wistar rats on cholesterol-enriched diet orally at a dose of 300 mg/kg/day (simvastatin 4 mg/kg/day) for 30 days lowered total cholesterol by 51.9% (simvastatin 4 mg/kg/day: 41.9%) and low-density lipoprotein–cholesterol by 54.8% (simvastatin 4 mg/kg/day: 46.7%).407 This extract had no effect on high-density lipoprotein–cholesterol and very low-density lipoprotein–cholesterol, lowered proinflammatory cytokines interleukin-1, interleukin-6, tumor necrosis factor-α, and INF-γ close to normal values.407 Intake of artichoke could be beneficial in metabolic syndrome.
Steroids interfere with human carbonic anhydrase activity by using alternative binding mechanisms
Published in Journal of Enzyme Inhibition and Medicinal Chemistry, 2018
Alessio Nocentini, Alessandro Bonardi, Paola Gratteri, Bruno Cerra, Antimo Gioiello, Claudiu T. Supuran
Chenodeoxycholic acid (1), ursodeoxycholic acid (5), hyodeoxycholic acid (8), hyocholic acid (9), coprostan-3-ol (12), trans-dehydroandrosterone (15), progesterone (17), 11α-hydroprogesterone (18), α-estradiol (19), and diosgenin (22) were purchased from Sigma-Aldrich. Cholic acid (2), lithocholic acid (3), deoxycholic acid (4), cholesterol (11), testosterone (13), and oestron (20) were purchased from Fluka. Dehydrocholic acid (10) and hydrocortisone (21) were purchased from Janssen Chimica and BDH Chemicals, respectively. Glyco (6) and tauroursodeoxycholic acid (7) were prepared as previously reported14,15. Purity of tested compounds 1–22 was >95%.
Gut microbiota remodeling reverses aging-associated inflammation and dysregulation of systemic bile acid homeostasis in mice sex-specifically
Published in Gut Microbes, 2020
Junli Ma, Ying Hong, Ningning Zheng, Guoxiang Xie, Yuanzhi Lyu, Yu Gu, Chuchu Xi, Linlin Chen, Gaosong Wu, Yue Li, Xin Tao, Jing Zhong, Zhenzhen Huang, Wenbin Wu, Lin Yuan, Min Lin, Xiong Lu, Weidong Zhang, Wei Jia, Lili Sheng, Houkai Li
All of the 39 bile acids standards including taurohyocholic acid (THCA), hyocholic acid (HCA), ω-muricholic acid (ωMCA), tauro-ω-muricholic acid (TωMCA), tauro-α muricholic acid (TαMCA), tauro-β-muricholic acid (TβMCA), tauroursodeoxycholic acid (TUDCA), glycoursodeoxycholic acid (GUDCA), glycohyodeoxycholic acid (GHDCA), taurohyodeoxycholi acid (THDCA), taurocholic acid (TCA), glycoursodeoxycholic acid (GCA), 12-dehydrocholic acid (12-DHCA), β-muricholic acid (βMCA), α-muricholic acid (αMCA), 7-dehydrocholic acid (7-DHCA), 3-dehydrocholic acid (3-DHCA), taurochenodeoxycholic acid (TCDCA), 3β-cholic acid (βCA), taurodeoxycholic acid (TDCA), glycochenodeoxycholic acid (GCDCA), glycol deoxycholic acid (GDCA), ursodeoxycholic acid (UDCA), hyodeoxycholic acid (HDCA), cholic acid (CA), ursocholic acid (UCA), 23-nordeoxycholic acid (NorDCA), norcholic acid (NorCA), allocholic acid (ACA), 3β-chenodeoxycholic acid (βCDCA), taurolithocholicacid (TLCA), 3β deoxycholic acid (βDCA), glycolithocholic acid (GLCA), chenodeoxycholic acid (CDCA), deoxycholic acid (DCA), 6-ketolithocholic acid (6-ketoLCA), 7-ketolithocholic acid (7-ketoLCA), 12-ketolithocholic acid (12-ketoLCA), lithocholic acid (LCA) were purchased from Steraloids Inc. (Newport, RI) and TRC Chemicals (Toronto, ON, Canada), and 9 stable isotope-labeled standards were obtained from C/D/N Isotopes Inc. (Quebec, Canada) and Steraloids Inc. (Newport, RI). The standards and stable isotope-labeled standards were accurately weighed and prepared in methanol at a concentration of 5.0 mM (stock solution). Further dilution was performed to obtain a series of calibration concentration of 2000, 400, 160, 32, 12.8, 2.5, or 1 nM with methanol/water (50/50, v/v). Internal Standard (IS) concentrations were kept constant at all the calibration points at 100 nM for GCA-d4, TCA-d4, TCDCA-d9, UDCA-d4, CA-d4, GCDCA-d4, GDCA-d4, DCA-d4, and 200 nM for LCA-d4.