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Статті в журналах з теми "Biliary secretion"

Автор: Grafiati

Опубліковано: 20 квітня 2024

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1

Blot-Chabaud, M., M. Dumont, M. Corbic, and S. Erlinger. "Effect of acid-base balance on biliary bicarbonate secretion in the isolated perfused guinea pig liver." American Journal of Physiology-Gastrointestinal and Liver Physiology 258, no. 6 (1990): G863—G872. http://dx.doi.org/10.1152/ajpgi.1990.258.6.g863.

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Secretin-induced choleresis is of ductal origin and involves bicarbonate transport. Its mechanism is unknown. To determine the relative effects of systemic pH, PCO2, and bicarbonate concentration on secretin-stimulated bicarbonate transport, states of acute metabolic and respiratory acidosis or alkalosis were created in isolated perfused guinea pig livers with or without secretin infusion. During spontaneous secretion conditions, biliary bicarbonate secretion was not correlated with perfusate pH (7.19-7.62) or perfusate PCO2 (23.9-59.7) but was significantly correlated with perfusate bicarbona

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2

Uc, Aliye, Radhamma Giriyappa, David K. Meyerholz, et al. "Pancreatic and biliary secretion are both altered in cystic fibrosis pigs." American Journal of Physiology-Gastrointestinal and Liver Physiology 303, no. 8 (2012): G961—G968. http://dx.doi.org/10.1152/ajpgi.00030.2012.

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The pancreas, liver, and gallbladder are commonly involved in cystic fibrosis (CF), and acidic, dehydrated, and protein-rich secretions are characteristic findings. Pancreatic function studies in humans have been done by sampling the jejunal fluid. However, it has been difficult to separately study the function of pancreatic and biliary systems in humans with CF, because jejunal fluid contains a mixture of bile and pancreatic fluids. In contrast, pancreatic and biliary ducts open separately into the porcine intestine; therefore, biliary and pancreatic fluid can be individually analyzed in CF p

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3

Sætre, S. S., N. J. Andersen, T. Houe, et al. "Regulation of porcine biliary secretion by secretin." Acta Physiologica Scandinavica 163, no. 1 (1998): 113–19. http://dx.doi.org/10.1046/j.1365-201x.1998.00349.x.

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4

Alpini, G., R. Lenzi, W. R. Zhai, et al. "Bile secretory function of intrahepatic biliary epithelium in the rat." American Journal of Physiology-Gastrointestinal and Liver Physiology 257, no. 1 (1989): G124—G133. http://dx.doi.org/10.1152/ajpgi.1989.257.1.g124.

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To shed light on ductular fluid secretion, hepatic histology and ultrastructure, cell proliferation and phenotypes, and several aspects of biliary physiology were studied in rats with ductular cell hyperplasia induced by either biliary obstruction (0-14 days) or 1-naphthylisothiocyanate (ANIT) feeding (0-28 days). In both groups of experimental animals, bile duct hyperplasia and spontaneous bile flow and secretin-induced choleresis increased with time of treatment in a linear fashion. Measurements of [14C]mannitol biliary entry and of biliary tree volume showed that the increase in both sponta

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5

Zeniya, M., and A. Reuben. "Triton WR-1339-induced changes in serum lipids and biliary lipid secretion." American Journal of Physiology-Gastrointestinal and Liver Physiology 254, no. 3 (1988): G346—G354. http://dx.doi.org/10.1152/ajpgi.1988.254.3.g346.

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Biliary lipid secretion rates were measured in fed rats after an intravenous injection of Triton WR-1339 (TWR, 60 mg/100 g body wt), an agent that inhibits lipoprotein removal from the circulation. Serum triglyceride, phospholipid (PL), and cholesterol (CH) concentrations rose within 3 h of TWR to 45, 6.6, and 10 times control values, respectively, at 24-36 h. Serum lipids fell rapidly at 48 h and were normal by 72-96 h after TWR. TWR did not alter bile flow, hepatic bile acid transport, or biliary bile acid output. Within 0.5 h of TWR, biliary PL and CH outputs fell greater than 70%, and taur

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6

Hofmann, Alan F. "Biliary Secretion: Future Perspectives." Digestion 58, no. 1 (1997): 24–28. http://dx.doi.org/10.1159/000201519.

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7

Reuben, A., P. N. Maton, G. M. Murphy, and R. H. Dowling. "Bile Lipid Secretion in Obese and Non-Obese Individuals with and without Gallstones." Clinical Science 69, no. 1 (1985): 71–79. http://dx.doi.org/10.1042/cs0690071.

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1. Biliary lipid secretion rates were measured in non-obese and obese individuals with and without cholesterol gallstones, using a steady-state, amino acid duodenal perfusion method. In addition, biliary lipid secretion rates were measured in five obese gallstone patients receiving high-dose chenodeoxycholic acid therapy (16-22 mg day−1 kg−1). 2. Bile acid secretion rates in the non-obese patients with cholesterol gallstones (563+sem 70 μmol/h, n = 6) were significantly lower than in the non-obese controls (1078 + 210 μmol/h, n = 10, P < 0.05), whereas cholesterol secretion rates were simil

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8

Chanussot, F., H. Lafont, J. Hauton, B. Tuchweber, and I. Yousef. "Studies on the origin of biliary phospholipid. Effect of dehydrocholic acid and cholic acid infusions on hepatic and biliary phospholipids." Biochemical Journal 270, no. 3 (1990): 691–95. http://dx.doi.org/10.1042/bj2700691.

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The correlation between the secretion of biliary phospholipid (PL) and bile acid suggests a regulatory effect of bile acid on PL secretion. Bile acids may influence PL synthesis and/or the mobilization of a preformed PL pool. The objective of this study was to determine the contribution of these two sources to biliary PL, by using an experimental protocol in which dehydrocholic acid (DHCA) and cholic acid (CA) were infused to manipulate biliary PL secretion. In control rats, there was a steady state in bile flow. PL secretion and the biliary secretion of newly synthesized phosphatidylcholine (

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9

Han, Yuyan, Paolo Onori, Fanyin Meng, et al. "Prolonged exposure of cholestatic rats to complete dark inhibits biliary hyperplasia and liver fibrosis." American Journal of Physiology-Gastrointestinal and Liver Physiology 307, no. 9 (2014): G894—G904. http://dx.doi.org/10.1152/ajpgi.00288.2014.

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Biliary hyperplasia and liver fibrosis are common features in cholestatic liver disease. Melatonin is synthesized by the pineal gland as well as the liver. Melatonin inhibits biliary hyperplasia of bile duct-ligated (BDL) rats. Since melatonin synthesis (by the enzyme serotonin N-acetyltransferase, AANAT) from the pineal gland increases after dark exposure, we hypothesized that biliary hyperplasia and liver fibrosis are diminished by continuous darkness via increased melatonin synthesis from the pineal gland. Normal or BDL rats (immediately after surgery) were housed with light-dark cycles or

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10

Verkade, H. J., R. Havinga, A. Gerding, R. J. Vonk, and F. Kuipers. "Mechanism of bile acid-induced biliary lipid secretion in the rat: effect of conjugated bilirubin." American Journal of Physiology-Gastrointestinal and Liver Physiology 264, no. 3 (1993): G462—G469. http://dx.doi.org/10.1152/ajpgi.1993.264.3.g462.

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We have compared the effects of bilirubin and bilirubin ditaurate (BDT) on biliary phospholipid and cholesterol secretion in unanesthetized normal Wistar (NW) and Groningen Yellow (GY) Wistar rats under various experimental conditions. GY rats express a genetic defect in biliary secretion, but not in hepatic uptake, of various organic anions. Under physiological conditions, NW and GY rats showed similar biliary secretion rates of bile acids and of bilirubin, despite the fact that bilirubin concentrations in GY plasma were 25 times as high and in GY livers three times as high as in NW plasma an

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11

Gooijert, K. E. R., R. Havinga, H. Wolters, et al. "The mechanism of increased biliary lipid secretion in mice with genetic inactivation of bile salt export pump." American Journal of Physiology-Gastrointestinal and Liver Physiology 308, no. 5 (2015): G450—G457. http://dx.doi.org/10.1152/ajpgi.00391.2014.

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Human bile salt export pump ( BSEP) mutations underlie progressive familial intrahepatic cholestasis type 2 (PFIC2). In the PFIC2 animal model, Bsep−/−mice, biliary secretion of bile salts (BS) is decreased, but that of phospholipids (PL) and cholesterol (CH) is increased. Under physiological conditions, the biliary secretion of PL and CH is positively related (“coupled”) to that of BS. We aimed to elucidate the mechanism of increased biliary lipid secretion in Bsep−/−mice. The secretion of the BS tauro-β-muricholic acid (TβMCA) is relatively preserved in Bsep−/−mice. We infused Bsep−/−and Bse

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12

RAHMAN, KHALID, PHILIP J. LOWE, and ROGER COLEMAN. "Control of biliary phospholipid secretion." Biochemical Society Transactions 14, no. 4 (1986): 714. http://dx.doi.org/10.1042/bst0140714.

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13

LANZINI, A., and T. C. NORTHFIELD. "Biliary lipid secretion in man." European Journal of Clinical Investigation 21, no. 3 (1991): 259–72. http://dx.doi.org/10.1111/j.1365-2362.1991.tb01369.x.

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14

Takada, Tappei, Yoshihide Yamanashi, and Hiroshi Suzuki. "Transportsome in biliary cholesterol secretion." Folia Pharmacologica Japonica 139, no. 2 (2012): 56–60. http://dx.doi.org/10.1254/fpj.139.56.

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15

Speroni, E., E. Cavicchini, and S. Ferri. "Dynorphin a affects biliary secretion." Pharmacological Research Communications 20 (September 1988): 370. http://dx.doi.org/10.1016/s0031-6989(88)80500-9.

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16

Garone, Michael A., and Hans Fromm. "Determinants of biliary cholesterol secretion." Gastroenterology 91, no. 1 (1986): 252–53. http://dx.doi.org/10.1016/0016-5085(86)90469-5.

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17

Xia, Yun, Karel J. Lambert, Claudio D. Schteingart, Jing-Jing Gu, and Alan F. Hofmann. "Concentrative biliary secretion of ceftriaxone." Gastroenterology 99, no. 2 (1990): 454–65. http://dx.doi.org/10.1016/0016-5085(90)91029-6.

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18

Hofmann, Alan F. "Current concepts of biliary secretion." Digestive Diseases and Sciences 34, S12 (1989): S16—S20. http://dx.doi.org/10.1007/bf01536657.

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19

Apstein, Michael D., and Andrea R. Russo. "Ampicillin inhibits biliary cholesterol secretion." Digestive Diseases and Sciences 30, no. 3 (1985): 253–56. http://dx.doi.org/10.1007/bf01347893.

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20

Monte, M. J., R. A. Parslow, and R. Coleman. "Inhibitory action of cyclobutyrol on the secretion of biliary cholesterol and phospholipids." Biochemical Journal 266, no. 1 (1990): 165–71. http://dx.doi.org/10.1042/bj2660165.

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Анотація:

A number of organic anions are known to decrease biliary secretion of cholesterol and phospholipid without affecting bile acid secretion. Cyclobutyrol (CB) is a choleretic agent which also inhibits biliary lipid secretion. Using isolated perfused rat liver we have studied this inhibition in relation to possible mechanisms suggested for other anions. Shortly after its administration to the isolated perfused liver, CB decreases biliary outputs of cholesterol and phospholipid, without changes in bile acid secretion, at low (450 nmol/min), high (1350 nmol/min) and nil taurocholate infusion rates.

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21

McGill, James M., Margaret S. Yen, Oscar W. Cummings, et al. "Interleukin-5 inhibition of biliary cell chloride currents and bile flow." American Journal of Physiology-Gastrointestinal and Liver Physiology 280, no. 4 (2001): G738—G745. http://dx.doi.org/10.1152/ajpgi.2001.280.4.g738.

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Recent studies have detected significant elevations of interleukin (IL)-5 mRNA in the liver parenchyma of patients with both primary biliary cirrhosis and acute rejection after liver transplantation. In both of these disorders, intrahepatic biliary epithelial cells (BECs) are the targets of injury. We hypothesized that BECs may themselves express IL-5 receptors that may modulate key biliary functions. RNAs coding for IL-5α and -β receptors were amplified by RT/PCR from a biliary cell line derived from a human cholangiocarcinoma (Mz-ChA-1) and verified by DNA sequencing. IL-5 receptor distribut

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22

Lam, W. F., E. S. M. Muller, J. H. M. Souverijn, C. B. H. W. Lamers, and A. A. M. Masclee. "Effect of Acute Hyperglycaemia on Basal and Fat-Induced Exocrine Pancreatic Secretion in Humans." Clinical Science 93, no. 6 (1997): 573–80. http://dx.doi.org/10.1042/cs0930573.

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1. We have investigated the effect of acute hyperglycaemia on pancreatico-biliary secretion in healthy subjects. Duodenal outputs of trypsin, lipase, amylase, bicarbonate and bilirubin were measured for 90 min under basal conditions and for 90 min in response to intrajejunal fat administration (1 g/h) on 2 separate days: during normoglycaemia (blood glucose 5 mmol/l) and during acute hyperglycaemia aimed at 15 mmol/l. Plasma cholecystokinin levels, as the major hormonal stimulus of pancreatic and biliary secretion, and plasma pancreatic polypeptide levels, as an indirect measure of vagal-choli

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23

Deng, Xiaoying, Dulce R. Guarita, Martha R. A. Pedroso, et al. "PYY inhibits CCK-stimulated pancreatic secretion through the area postrema in unanesthetized rats." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 281, no. 2 (2001): R645—R653. http://dx.doi.org/10.1152/ajpregu.2001.281.2.r645.

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Peptide YY (PYY) inhibits CCK-8-secretin-stimulated pancreatic secretion in vivo. To investigate whether CCK-8-secretin-stimulated pancreatic secretion is mediated through a vago-vagal pathway and whether PYY inhibits this pathway through the area postrema (AP), chronic pancreatic, biliary, and duodenal catheters were implanted in AP-lesioned (APX) or sham-operated rats. The effects of APX on pancreatic secretion stimulated by bethanechol, pancreatic juice diversion (PJD), or CCK-8-secretin, were tested, with and without background PYY infusion, in unanesthetized rats. APX reduced basal pancre

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24

Miura, H., S. Tazuma, and G. Kajiyama. "Partial characterization of regulation of biliary lecithin hydrophobicity: association with organic anion-induced solute cholestasis in rats." Biochemical Journal 312, no. 3 (1995): 795–97. http://dx.doi.org/10.1042/bj3120795.

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We examined the effects of the depletion of bile salts and of the intravenous infusion of sodium taurocholate (STC) with or without bromosulphophthalein (BSP) in rats on the biliary secretion of lipids to clarify the regulatory mechanism(s). Each rat was equipped with a bile-duct cannula to collect bile. After the endogenous bile salt pool was depleted, STC was infused at a constant rate (160 nmol/min per 100 g body wt.) with or without BSP (50, 100, or 150 nmol/min per 100 g body wt.). BSP reduced the biliary secretion of cholesterol and phospholipids dose-dependently without affecting the se

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25

Li, Jianing, Sonja S. Pijut, Yuhuan Wang, et al. "Simultaneous Determination of Biliary and Intestinal Cholesterol Secretion Reveals That CETP (Cholesteryl Ester Transfer Protein) Alters Elimination Route in Mice." Arteriosclerosis, Thrombosis, and Vascular Biology 39, no. 10 (2019): 1986–95. http://dx.doi.org/10.1161/atvbaha.119.312952.

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Objective: Determine the impact of CETP (cholesteryl ester transfer protein) on the route of cholesterol elimination in mice. Approach and Results: We adapted our protocol for biliary cholesterol secretion with published methods for measuring transintestinal cholesterol elimination. Bile was diverted and biliary lipid secretion maintained by infusion of bile acid. The proximal small bowel was perfused with bile acid micelles. In high-fat, high-cholesterol–fed mice, the presence of a CETP transgene increased biliary cholesterol secretion at the expense of transintestinal cholesterol elimination

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26

Monte, M. J., F. Cava, A. Esteller, and R. Jimenez. "Inhibition of biliary cholesterol and phospholipid secretion during cyclobutyrol-induced hydrocholeresis." Biochemical Journal 263, no. 2 (1989): 513–18. http://dx.doi.org/10.1042/bj2630513.

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The effects of sodium cyclobutyrate, a synthetic hydrocholeretic drug, on biliary lipid secretion and on the biliary outputs of several plasma-membrane enzymes were investigated in anaesthetized rats. Administration of a single oral dose of cyclobutyrol (0.72 mmol/kg body wt.) reduced biliary concentration and output of cholesterol and phospholipid. However, bile acid secretion was not significantly modified. This uncoupling effect of lipid secretion remained even when the choleretic response to the drug had ceased. It additionally led to a statistically significant decrease in the cholesterol

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27

Werner, Anniek, Deanna M. Minich, Rick Havinga, et al. "Fat malabsorption in essential fatty acid-deficient mice is not due to impaired bile formation." American Journal of Physiology-Gastrointestinal and Liver Physiology 283, no. 4 (2002): G900—G908. http://dx.doi.org/10.1152/ajpgi.00094.2002.

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Essential fatty acid (EFA) deficiency induces fat malabsorption, but the pathophysiological mechanism is unknown. Bile salts (BS) and EFA-rich biliary phospholipids affect dietary fat solubilization and chylomicron formation, respectively. We investigated whether altered biliary BS and/or phospholipid secretion mediate EFA deficiency-induced fat malabsorption in mice. Free virus breed (FVB) mice received EFA-containing (EFA+) or EFA-deficient (EFA−) chow for 8 wk. Subsequently, fat absorption, bile flow, and bile composition were determined. Identical dietary experiments were performed in mult

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28

Yamashita, G., S. Tazuma, K. Horikawa, et al. "Partial characterization of mechanism(s) by which sulphobromophthalein reduces biliary lipid secretion." Biochemical Journal 291, no. 1 (1993): 173–77. http://dx.doi.org/10.1042/bj2910173.

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This study was performed to explore the mechanisms by which sulphobromophthalein (BSP) reduces the secretion of biliary lipid using Sprague-Dawley rats (SDR) and mutant rats with congenital conjugated hyperbilirubinaemia bred from SDR (EHBR). We infused the bile-salt-pool-depleted rats with sodium taurocholate at a constant rate of 160 nmol/min per 100 g body wt. with BSP (12.5, 25 and 50 nmol/min per 100 g body wt.) or BSP-GSH (12.5, 25 and 50 nmol/min per 100 g body wt.). The biliary secretion of BSP and BSP-GSH was markedly impaired in EHBR as compared with that in SDR. BSP reduced the bili

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29

Martin, Gregory G., Barbara P. Atshaves, Kerstin K. Landrock, et al. "Ablating L-FABP in SCP-2/SCP-x null mice impairs bile acid metabolism and biliary HDL-cholesterol secretion." American Journal of Physiology-Gastrointestinal and Liver Physiology 307, no. 11 (2014): G1130—G1143. http://dx.doi.org/10.1152/ajpgi.00209.2014.

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On the basis of their abilities to bind bile acids and/or cholesterol, the physiological role(s) of liver fatty acid-binding protein (L-FABP) and sterol carrier protein (SCP) 2/SCP-x (SCP-2/SCP-x) gene products in biliary bile acid and cholesterol formation was examined in gene-ablated male mice. L-FABP (LKO) or L-FABP/SCP-2/SCP-x [triple-knockout (TKO)] ablation markedly decreased hepatic bile acid concentration, while SCP-2/SCP-x [double-knockout (DKO)] ablation alone had no effect. In contrast, LKO increased biliary bile acid, while DKO and TKO had no effect on biliary bile acid levels. LKO

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30

Tavoloni, Nicola. "Biliary excretion of inorganic electrolytes: its role in hepatic bile formation." Canadian Journal of Physiology and Pharmacology 63, no. 10 (1985): 1245–51. http://dx.doi.org/10.1139/y85-206.

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To define the role of inorganic electrolyte secretion in hepatic bile formation, the effects of secretin, glucagon, and differently structured bile acids on bile flow and composition were studied in the dog, guinea pig, and rat. In the dog and guinea pig, secretin (2.5–10 clinical units∙kg−1∙30 min−1) increased bile flow and bicarbonate concentration in bile, a finding consistent with the hypothesis that the hormone stimulates a bicarbonate-dependent secretion possibly at the level of the bile ductule–duct. In the rat, secretin (5–15 CU∙kg−1∙30 min−1) failed to increase bile secretion. Glucago

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31

Yamashita, G., S. Tazuma, and G. Kajiyama. "Effects of organic anions on biliary lipid secretion in rats. Importance of association with biliary lipid structures." Biochemical Journal 286, no. 1 (1992): 193–96. http://dx.doi.org/10.1042/bj2860193.

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Анотація:

This study was performed to determine the effects of various organic anions on biliary lipid secretion in rats. We infused bile-salt-pool-depleted rats with sodium taurocholate at a constant rate, with or without various organic anions: Indocyanine Green (ICG), bromosulphophthalein (BSP), BSP-glutathione and Phenol Red (PR). BSP decreased biliary secretion of cholesterol and phospholipids in a dose-dependent manner without affecting bile salt secretion (uncoupling), and this change was fully reversible. In contrast, ICG, BSP-glutathione and PR did not cause such an uncoupling of biliary lipids

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32

VERKADE, Henkjan J., Marjan A. C. de BRUIJN, Menno A. BRINK, et al. "Interactions between organic anions, micelles and vesicles in model bile systems." Biochemical Journal 320, no. 3 (1996): 917–23. http://dx.doi.org/10.1042/bj3200917.

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Анотація:

Biliary lipid secretion probably involves both ‘micellization’ and ‘vesiculization’ of bile-canalicular membrane lipids. Several hydrophilic organic anions inhibit the secretion of lipids into the bile without altering bile salt secretion [Verkade, Vonk and Kuipers (1995) Hepatology 21, 1174–1189]. Hydrophobic organic anions do not interfere with biliary lipid secretion. We investigated whether the organic-anion-induced inhibition of biliary lipid secretion in vivo could be attributed to inhibition of micellization, by the application of in vitro models of micellization. Carboxyfluorescein was

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33

Rahman, K., T. G. Hammond, P. J. Lowe, S. G. Barnwell, B. Clark, and R. Coleman. "Control of biliary phospholipid secretion. Effect of continuous and discontinuous infusion of taurocholate on biliary phospholipid secretion." Biochemical Journal 234, no. 2 (1986): 421–27. http://dx.doi.org/10.1042/bj2340421.

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Анотація:

A major determinant of biliary lipid secretion is bile-salt secretion. Taurocholate (TC), a micelle-forming bile salt, was infused continuously at different rates in both isolated perfused livers and biliary-fistula rats. In both of these systems, infusion of TC brought about an elevated secretion of phosphatidylcholine for the duration of the TC infusion period. Initial phospholipid/bile-salt ratios in the bile were higher in the whole-animal model than in isolated livers, but at the higher infusion rates both secreted approx. 6 mol of phospholipid for every 100 mol of bile salt. The secretio

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34

Alpini, G., S. Glaser, W. Robertson, et al. "Large but not small intrahepatic bile ducts are involved in secretin-regulated ductal bile secretion." American Journal of Physiology-Gastrointestinal and Liver Physiology 272, no. 5 (1997): G1064—G1074. http://dx.doi.org/10.1152/ajpgi.1997.272.5.g1064.

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Анотація:

We have shown that agonist-regulated ductal secretion is limited to large cholangiocytes. To directly study cholangiocyte heterogeneity along the length of the normal biliary tree, we defined the genetic and functional expression of agonist-induced ductal secretion in intrahepatic bile duct units (IBDU) of different sizes. Small IBDU (< 15-microns diam) were separated from large IBDU (> or = 15-microns diam), and then ducts of different sizes were characterized by morphometric analysis, gene expression, secretin-induced adenosine 3',5'-cyclic monophosphate (cAMP) synthesis, and secretion

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35

Cava, F., J. Gonzalez, J. M. Gonzalez-Buitrago, C. Muriel, and R. Jimenez. "Inhibition of biliary cholesterol and phospholipid secretion by cefmetazole. The role of vesicular transport and of canalicular events." Biochemical Journal 275, no. 3 (1991): 591–95. http://dx.doi.org/10.1042/bj2750591.

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Анотація:

A number of organic anions selectively inhibit the biliary secretion of cholesterol and phospholipids without affecting bile acid secretion. We studied the effect of cefmetazole, a third-generation cephalosporin, on biliary lipid secretion in the rat. Injection of cefmetazole at a dose of 200 mumol/kg body wt. induced a choleretic effect and a significant decrease in the biliary output of cholesterol and phospholipid, without changes in bile acid secretion. The decrease was more marked for cholesterol than for phospholipid secretion, with a significant decrease in their molar ratio in bile. Th

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36

Yamada, T., M. Hoshino, T. Hayakawa, et al. "Dietary diosgenin attenuates subacute intestinal inflammation associated with indomethacin in rats." American Journal of Physiology-Gastrointestinal and Liver Physiology 273, no. 2 (1997): G355—G364. http://dx.doi.org/10.1152/ajpgi.1997.273.2.g355.

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We investigated the effects of dietary diosgenin (Dio), a plant-derived sapogenin, on indomethacin (Indo)-induced intestinal inflammation and alterations in bile secretion in rats. In anesthetized rats, bile secretion, intestinal inflammation, and blood chemistry were assessed 3 days after two subcutaneous injections of Indo given 24 h apart. Dio (> 80 mg.kg-1.day-1) pretreatment significantly inhibited weight and food intake decreases and intestinal inflammation. This protective effect was confirmed by examination of gross and histological findings and intestinal myeloperoxidase activity.

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37

Perez-Barriocanal, F., J. G. Redondo-Torres, G. R. Villanueva, E. Arteche, M. M. Berenson, and J. J. G. Marin. "Protoporphyrin IX-Induced Impairment of Biliary Lipid Secretion in the Rat." Clinical Science 77, no. 5 (1989): 473–78. http://dx.doi.org/10.1042/cs0770473.

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Анотація:

1. In order to gain information on the effect of protoporphyrin IX on changes in the properties of the canalicular plasma membrane, we studied the release of canalicular membrane constituents, namely phospholipids, cholesterol and 5′-nucleotidase, into bile in anaesthetized rats receiving saline or taurocholate (0.5 μmol min−1 100 g−1 body weight) with or without protoporphyrin IX infusion (10 or 20 μg min−1 100 g−1 body weight). 2. Protoporphyrin IX induced an impairment of spontaneous bile flow and of biliary secretion of cholesterol, phospholipids and bile acids. The taurocholate-induced in

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38

Lowe, P. J., K. S. Kan, S. G. Barnwell, R. K. Sharma, and R. Coleman. "Transcytosis and paracellular movements of horseradish peroxidase across liver parenchymal tissue from blood to bile. Effects of alpha-naphthylisothiocyanate and colchicine." Biochemical Journal 229, no. 2 (1985): 529–37. http://dx.doi.org/10.1042/bj2290529.

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The pathways for the entry of horseradish peroxidase (HRP) into bile have been investigated using the isolated perfused rat liver operating under one-pass conditions. Following a 1 min one-pass infusion of HRP, two peaks of HRP activity were noted in the bile. The first, at 5-7 min post-infusion, correlated with the biliary secretion of the [3H]methoxyinulin which was infused simultaneously with the HRP. The second peak of HRP activity occurred at 20-25 min, and correlated with the biliary secretion of 125I-IgA, which was also infused simultaneously with the HRP. If the isolated livers were pe

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39

Elferink, Ronald Oude. "Elucidation of the biliary secretion machinery." Current Gastroenterology Reports 5, no. 6 (2003): 439–40. http://dx.doi.org/10.1007/s11894-003-0029-3.

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40

Groen, Albert K., Ronald P. J. Oude Elferink, and Joseph M. Tager. "Control Analysis of Biliary Lipid Secretion." Journal of Theoretical Biology 182, no. 3 (1996): 427–36. http://dx.doi.org/10.1006/jtbi.1996.0183.

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41

Anagnostides, A. A., V. S. Chadwick, A. C. Selden, J. Barr, and P. N. Maton. "Human pancreatic and biliary responses to physiological concentrations of cholecystokinin octapeptide." Clinical Science 69, no. 3 (1985): 259–63. http://dx.doi.org/10.1042/cs0690259.

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1. To determine the functional significance of physiological plasma concentrations of cholecystokinin, five volunteers each received graded doses of intravenous infusions of cholecystokinin octapeptide (CCK-8). At each dose plasma concentrations of CCK-8 were determined and pancreatic and biliary outputs were measured. 2. Threshold plasma concentrations of CCK-8 for augmenting pancreatic trypsin secretion were undetectable (< 3 pmol/l), and maximal trypsin output of 21.9 ± 1.95 k-i.u./30 min was produced by 17.1 ± 6.4 pmol of CCK-8/1. Calculated half-maximal output was produced by 4.7 pmol

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42

Yamada, T., M. Hoshino, T. Hayakawa, et al. "Bile secretion in rats with indomethacin-induced intestinal inflammation." American Journal of Physiology-Gastrointestinal and Liver Physiology 270, no. 5 (1996): G804—G812. http://dx.doi.org/10.1152/ajpgi.1996.270.5.g804.

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The objective of this study was to characterize the bile secretion, including the composition of biliary bile acids, bile salt pool size, and transcytotic vesicle transport, in a rat model of subacute intestinal inflammation induced by indomethacin. Indomethacin treatment significantly decreased bile acid-independent bile flow and biliary secretion of bile acid and cholesterol, while increasing biliary phospholipid output in vivo. Although indomethacin treatment did not change the bile salt pool size in vivo, alpha- and beta-muricholic acids were significantly deceased and hyodeoxycholic and d

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43

Coleman, R., K. Rahman, K. S. Kan, and R. A. Parslow. "Retrograde intrabiliary injection of amphipathic materials causes phospholipid secretion into bile. Taurocholate causes phosphatidylcholine secretion, 3-[(3-cholamidopropyl)dimethylammonio]-propane-1-sulphonate (CHAPS) causes mixed phospholipid secretion." Biochemical Journal 258, no. 1 (1989): 17–22. http://dx.doi.org/10.1042/bj2580017.

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Анотація:

The control of biliary phospholipid and cholesterol secretions by bile acid was studied by using the technique of retrograde intrabiliary injection. Taurocholate (TC), a moderately hydrophobic bile acid, taurodehydrocholate (TDHC), a hydrophilic non-micelle-forming bile acid, and 3-[(3-cholamidopropyl)-dimethylammonio]propane-1-sulphonate (CHAPS), a detergent, were individually administered by retrograde intrabiliary injection (RII) into the biliary tree, and bile acids, phospholipids and cholesterol subsequently appearing in the bile were measured. TC (1.3 mumol; 45 microliters) injected retr

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Zhang, Linda S., Hirokazu Sato, Qing Yang, et al. "Apolipoprotein A-V is present in bile and its secretion increases with lipid absorption in Sprague-Dawley rats." American Journal of Physiology-Gastrointestinal and Liver Physiology 309, no. 11 (2015): G918—G925. http://dx.doi.org/10.1152/ajpgi.00227.2015.

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Apolipoprotein (apo) A-V is a protein synthesized only in the liver that dramatically modulates plasma triglyceride levels. Recent studies suggest a novel role for hepatic apoA-V in regulating the absorption of dietary triglycerides, but its mode of action on the gut remains unknown. The aim of this study was to test for apoA-V in bile and to determine whether its secretion is regulated by dietary lipids. After an overnight recovery, adult male Sprague-Dawley bile fistula rats indeed secreted apoA-V into bile at a constant rate under fasting conditions. An intraduodenal bolus of intralipid ( n

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45

Ballatori, N., and T. W. Clarkson. "Sulfobromophthalein inhibition of glutathione and methylmercury secretion into bile." American Journal of Physiology-Gastrointestinal and Liver Physiology 248, no. 2 (1985): G238—G245. http://dx.doi.org/10.1152/ajpgi.1985.248.2.g238.

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The mechanism through which sulfobromophthalein (BSP) inhibits the biliary secretion of glutathione (GSH) and methylmercury was examined in male rats anesthetized with pentobarbital sodium. The biliary secretion rates of GSH and methylmercury were measured following the bolus intravenous administration of various doses of BSP, the GSH conjugate of BSP (BSP-SG), and phenol-3,6-dibromphthalein disulfonate (DBSP, a nonmetabolizable analogue of BSP). The effects of BSP on GSH secretion were dose dependent; at a dose of 120 mumol/kg the rate of GSH secretion fell close to zero. DBSP also inhibited

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46

Lu, S. C., J. Kuhlenkamp, H. Wu, W. M. Sun, L. Stone, and N. Kaplowitz. "Progressive defect in biliary GSH secretion in streptozotocin-induced diabetic rats." American Journal of Physiology-Gastrointestinal and Liver Physiology 272, no. 2 (1997): G374—G382. http://dx.doi.org/10.1152/ajpgi.1997.272.2.g374.

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This study examined the effect of streptozotocin-induced diabetes on biliary reduced glutathione (GSH) efflux. Biliary GSH efflux was measured before and after acivicin, an irreversible inhibitor of gamma-glutamyl transpeptidase (GGT). One week after streptozotocin treatment, liver GGT activity doubled in diabetic rats but was inhibited by approximately 90% after acivicin to levels comparable to controls. Despite maximal GGT inhibition, biliary GSH efflux in untreated diabetic rats decreased progressively to approximately 10% of control levels by week 4 and was partially restored by insulin. T

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47

Coy, Donna J., Clavia R. Wooton-Kee, Baoxiang Yan, et al. "ABCG5/ABCG8-independent biliary cholesterol excretion in lactating rats." American Journal of Physiology-Gastrointestinal and Liver Physiology 299, no. 1 (2010): G228—G235. http://dx.doi.org/10.1152/ajpgi.00502.2009.

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Lactation is associated with increased expression of bile acid transporters and an increased size and hydrophobicity of the bile acid pool in rats. ATP-binding cassette (ABC) transporters multidrug resistance protein 2 (Mdr2), Abcb11 [bile salt export pump (Bsep)], and Abcg5/Abcg8 heterodimers are essential for the biliary secretion of phospholipids, bile acids, and cholesterol, respectively. We investigated the expression of these transporters and secretion of their substrates in female control and lactating Sprague Dawley rats and C57BL/6 mice. Expression of Abcg5/Abcg8 mRNA was decreased by

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48

Portal, I., T. Clerc, V. Sbarra, et al. "Importance of high-density lipoprotein-phosphatidylcholine in secretion of phospholipid and cholesterol in bile." American Journal of Physiology-Gastrointestinal and Liver Physiology 264, no. 6 (1993): G1052—G1056. http://dx.doi.org/10.1152/ajpgi.1993.264.6.g1052.

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The purpose of this work was to evaluate biliary phosphatidylcholine (PC) secretion after intravenous infusion of high density lipoprotein (HDL)-[3H]phosphatidylcholine (HDL-[3H]PC) in rats and to study the effect of infusion of dehydrocholic and cholic acids, which, respectively, inhibit and stimulate biliary secretion of PC. The data obtained in this study showed that, in the basal state, HDL-PC accounted for 38% of biliary PC. Dehydrocholic acid infusion caused only a "residual" secretion of HDL-PC in the bile; however, cholic acid infusion stimulated the secretion of HDL-PC as well as PC f

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49

Hillebrant, C. G., B. Nyberg, K. Einarsson, and M. Eriksson. "The effect of plasma low density lipoprotein apheresis on the hepatic secretion of biliary lipids in humans." Gut 41, no. 5 (1997): 700–704. http://dx.doi.org/10.1136/gut.41.5.700.

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Анотація:

Background—The liver is a key organ in the metabolism of cholesterol in humans. It is the only organ by which substantial amounts of cholesterol are excreted from the body, either directly as free cholesterol into the bile or after conversion to bile acids. The major part of cholesterol synthesis in the body occurs in the liver. Cholesterol is also taken up by the liver from plasma lipoproteins. The relative contributions of newly synthesised cholesterol and plasma lipoprotein cholesterol to bile acid synthesis and biliary cholesterol secretion, respectively, are not known in detail.Aims—To de

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50

Dutta, Amal K., Kristy Boggs, Al-karim Khimji, et al. "Signaling through the interleukin-4 and interleukin-13 receptor complexes regulates cholangiocyte TMEM16A expression and biliary secretion." American Journal of Physiology-Gastrointestinal and Liver Physiology 318, no. 4 (2020): G763—G771. http://dx.doi.org/10.1152/ajpgi.00219.2019.

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TMEM16A is a Ca2+-activated Cl− channel in the apical membrane of biliary epithelial cells, known as cholangiocytes, which contributes importantly to ductular bile formation. Whereas cholangiocyte TMEM16A activity is regulated by extracellular ATP-binding membrane purinergic receptors, channel expression is regulated by interleukin-4 (IL-4) through an unknown mechanism. Therefore, the aim of the present study was to identify the signaling pathways involved in TMEM16A expression and cholangiocyte secretion. Studies were performed in polarized normal rat cholangiocyte monolayers, human Mz-Cha-1

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