Journal articles: 'Biliary secretion'

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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 (June 1, 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 bicarbonate concentration (17.5-37.9 mM). Under secretion infusion (25 mU/min), bile flow and biliary bicarbonate concentration increased significantly (109 and 51%, respectively). Biliary bicarbonate secretion was not correlated with perfusate pH (7.19-7.60) but was significantly correlated both with perfusate bicarbonate concentration (14.6-36.8 mM) and PCO2 (25.8-54.3 mmHg). Spontaneous and secretin-induced bile flow were correlated with biliary bicarbonate concentration. The correlation between biliary bicarbonate secretion and PCO2 during secretin-induced choleresis supports the hypothesis that secretin-induced biliary bicarbonate secretion could, at least in part, involve a transport of H+ (or OH-) rather than HCO3- itself and that intracellular pH could play a role in the regulation of this secretion. Amiloride (5 X 10(-4) M) did not influence secretin-induced biliary bicarbonate secretion. This result suggests that the Na(+)-H+ exchange is not involved in bicarbonate secretion by ductular cells.

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Uc, Aliye, Radhamma Giriyappa, David K. Meyerholz, Michelle Griffin, Lynda S. Ostedgaard, Xiao Xiao Tang, Marwa Abu-El-Haija, et al. "Pancreatic and biliary secretion are both altered in cystic fibrosis pigs." American Journal of Physiology-Gastrointestinal and Liver Physiology 303, no. 8 (October 15, 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 pigs. We studied newborn wild-type (WT) and CF pigs and found that CFTR was localized to the pancreatic ducts. We collected bile and pancreatic fluid and analyzed pancreatic enzymes with activity assays and immunoblot. Pancreatic enzyme expression was significantly decreased in CF compared with WT pigs. The volume and pH of pancreatic fluid were significantly lower and protein concentration was >5-fold higher in CF pigs. Secretin stimulation increased pancreatic fluid volume and pH in WT, but not CF, pigs. Baseline bile volume did not differ between WT and CF pigs, but volume did not increase in response to secretin in CF pigs. Bile pH was lower and protein concentration was twofold higher in CF pigs. These results indicate that pancreatic and biliary secretions are altered in CF pigs. Abnormal pancreatic and biliary secretion in CF may have important implications in disease pathogenesis.

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Sætre, S. S., N. J. Andersen, T. Houe, P. Svendsen, J. F. Rehfeld, O. Olsen, and O. B. Schaffalitzky de Muckadell. "Regulation of porcine biliary secretion by secretin." Acta Physiologica Scandinavica 163, no. 1 (May 1998): 113–19. http://dx.doi.org/10.1046/j.1365-201x.1998.00349.x.

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Alpini, G., R. Lenzi, W. R. Zhai, P. A. Slott, M. H. Liu, L. Sarkozi, and N. Tavoloni. "Bile secretory function of intrahepatic biliary epithelium in the rat." American Journal of Physiology-Gastrointestinal and Liver Physiology 257, no. 1 (July 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 spontaneous and secretin-stimulated bile flow originated at the proliferated biliary structures. Ultrastructural examination, [3H]thymidine incorporation, and histochemical and immunohistochemical staining for various markers demonstrated that in both hyperplastic reactions the proliferated cells were the progeny of preexisting biliary epithelial cells and retained their characteristics. These results indicate that the increased bile secretory activity associated with either biliary obstruction or ANIT intoxication reflects a quantitative change due to the proliferation of biliary epithelial cells. Thus both models of bile ductular cell hyperplasia lend themselves to assessment of the transport function of intrahepatic biliary epithelium and its contribution to normal bile formation. In the present studies, we have estimated that net ductular secretion in the normal rat accounts for 10-13% of spontaneously secreted hepatic bile.

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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 (March 1, 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 taurocholate-stimulated biliary PL secretion was markedly reduced. Biliary PL and CH secretion rates were approximately 30 and approximately 40% suppressed, respectively, 24 h after TWR, 160 and 330% elevated, respectively, at 48 h, and normally by 72 h, despite normal taurocholate-stimulated biliary PL secretion. Biliary beta-glucuronidase secretion (a lysosomal enzyme) was unchanged for 3 h after TWR but was increased at 24, 48, and 72 h, independent of biliary lipid secretion. Thus TWR acutely dissociates bile acid from lipid secretion without impairing bile acid transport or biliary lysosomal discharge. Late changes in biliary lipid secretion relate closely to TWR-induced change in serum lipid metabolism but not to stimulation of biliary lysosomal discharge.

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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 (July 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 similar in the non-obese individuals with and without gallstones (51+7 and 42+4 μmol/h respectively). 3. In the obese, both with and without gallstones, the major abnormality was hypersecretion of cholesterol (107+7 μmol/h, n = 7, and 81 + 15 μmol/h, n = 7, respectively). Both these values were significantly greater than those in the non-obese controls (P < 0.01-0.02). 4. Biliary cholesterol secretion rates correlated significantly with bile acid secretion rates but, for every mole of bile acid secreted, the obese secreted more cholesterol than the non-obese. 5. Chenodeoxycholic acid treatment lowered biliary cholesterol saturation in obese gallstone patients by reducing biliary cholesterol secretion. 6. These results suggest that there are two major types of defect in biliary lipid secretion in gallstone patients: reduced biliary bile acid secretion in non-obese gallstone patients and excessive biliary cholesterol secretion in the obese.

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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 (September 15, 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 (PC). The specific radioactivity of PC in bile was significantly higher than in plasma, microsomes and canalicular membranes. DHCA infusion decreased biliary PC secretion rate by 80%, and secretion returned to normal values at the transport maximum of CA. The specific radioactivity of biliary PC was decreased by 30% by DHCA infusion and reached normal values during CA infusion. There were no significant changes in the specific radioactivity of PC in plasma or cellular organelles during infusion of bile acids. These data indicate that: (1) newly synthesized PC contributes a small percentage to biliary PC; thus a preformed pool (microsomal and extrahepatic) is a major source of biliary PL; (2) the contribution of the extrahepatic pool to the biliary PL may be more important than the microsomal pool.

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9

Han, Yuyan, Paolo Onori, Fanyin Meng, Sharon DeMorrow, Julie Venter, Heather Francis, Antonio Franchitto, 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 (November 1, 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 complete dark for 1 wk before evaluation of 1) the expression of AANAT in the pineal gland and melatonin levels in pineal gland tissue supernatants and serum; 2) biliary proliferation and intrahepatic bile duct mass, liver histology, and serum chemistry; 3) secretin-stimulated ductal secretion (functional index of biliary growth); 4) collagen deposition, liver fibrosis markers in liver sections, total liver, and cholangiocytes; and 5) expression of clock genes in cholangiocytes. In BDL rats exposed to dark there was 1) enhanced AANAT expression/melatonin secretion in pineal gland and melatonin serum levels; 2) improved liver morphology, serum chemistry and decreased biliary proliferation and secretin-stimulated choleresis; and 4) decreased fibrosis and expression of fibrosis markers in liver sections, total liver and cholangiocytes and reduced biliary expression of the clock genes PER1, BMAL1, CLOCK, and Cry1. Thus prolonged dark exposure may be a beneficial noninvasive therapeutic approach for the management of biliary disorders.

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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 (March 1, 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 and livers, respectively. Secretion of cholesterol and phospholipids was not impaired in GY rats under these conditions. Biliary secretion of intravenously injected BDT (3 mumol/100 g body wt) was delayed in eight-day bile-diverted GY rats and showed lower peak values when compared with NW rats. The inhibitory effects of BDT on phospholipid and cholesterol secretion paralleled these differences, being delayed and much less pronounced in GY rats. No overshoot in phospholipid or cholesterol secretion was observed when bilirubin output returned to preinjection values. Stimulation of [14C]choline-labeled phospholipid secretion after a bolus injection of taurochenodeoxycholic acid (1 mumol/100 g body wt) closely followed biliary bile acid concentration. Similarly, inhibition of labeled phospholipid secretion by BDT closely paralleled the biliary bilirubin concentration. Gel filtration studies (Sepharose 4B-CL) under micelle-preserving conditions demonstrated a specific interaction of BDT with biliary bile acids. The presented data indicate that conjugated bilirubin does not inhibit biliary lipid secretion via interaction with bile acids inside the hepatocyte.(ABSTRACT TRUNCATED AT 250 WORDS)

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11

Gooijert, K. E. R., R. Havinga, H. Wolters, R. Wang, V. Ling, S. Tazuma, and H. J. Verkade. "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 (March 1, 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 Bsep+/+(control) mice with TβMCA in stepwise increasing dosages (150–600 nmol/min) and determined biliary bile flow, BS, PL, and CH secretion. mRNA and protein expression of relevant canalicular transporters was analyzed in livers from noninfused Bsep−/−and control mice. TβMCA infusion increased BS secretion in both Bsep−/−and control mice. The secreted PL or CH amount per BS, i.e., the “coupling,” was continuously two- to threefold higher in Bsep−/−mice ( P < 0.05). Hepatic mRNA expression of canalicular lipid transporters Mdr2, Abcg5, and Abcg8 was 45–55% higher in Bsep−/−mice (Abcg5; P < 0.05), as was canalicular Mdr2 and Abcg5 protein expression. Potential other explanations for the increased coupling of the biliary secretion of PL and CH to that of BS in Bsep−/−mice could be excluded. We conclude that the mechanism of increased biliary lipid secretion in Bsep−/−mice is based on increased expression of the responsible canalicular transporter proteins.

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12

RAHMAN, KHALID, PHILIP J. LOWE, and ROGER COLEMAN. "Control of biliary phospholipid secretion." Biochemical Society Transactions 14, no. 4 (August 1, 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 (June 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 (July 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 (August 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 (December 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 (March 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 (February 15, 1990): 165–71. http://dx.doi.org/10.1042/bj2660165.

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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. The absolute inhibition does not appear to be decreased by elevated bile acid secretion. There is a differential effect on secretion of cholesterol and phospholipid, more marked at low bile acid secretion rates. Biliary outputs of the canalicular membrane enzymes 5′-nucleotidase and alkaline phosphodiesterase I are also depressed by CB administration, but the anion does not affect the biliary output of bovine serum albumin or the output of rat serum albumin into the perfusion fluid. Since CB does not inhibit intracellular vesicular transport or apparently inhibit intracanalicular events, its effect is different from the effect of several other anions. From these studies it appears that the most likely effect of CB is exerted at the level of the canalicular membrane.

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21

McGill, James M., Margaret S. Yen, Oscar W. Cummings, Gianfranco Alpini, Gene LeSage, Karen E. Pollok, Barbara Miller, Steven K. Engle, and Ann P. Stansfield. "Interleukin-5 inhibition of biliary cell chloride currents and bile flow." American Journal of Physiology-Gastrointestinal and Liver Physiology 280, no. 4 (April 1, 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 distribution was detected immunocytochemically on Mz-ChA-1 cells, immortalized murine BEC, bile duct-ligated rat liver, and isolated cholangiocytes. Patch-clamp studies on Mz-ChA-1 cells showed that IL-5 inhibits 5′- N-ethylcarboxamidoadenosine-stimulated chloride currents. Additional functional studies showed that IL-5 inhibits secretin-induced bile flow. We conclude that BECs express IL-5 receptors and that IL-5 modulates BEC chloride currents and fluid secretion. Since IL-5 has previously been associated with cholestatic liver disease, we speculate that IL-5 may contribute to liver injury through its effects on biliary secretion.

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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 (December 1, 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-cholinergic tone, were determined at regular intervals. 2. In the basal period pancreatico-biliary secretion was significantly (P < 0.05) reduced during hyperglycaemia compared with normoglycaemia. During normoglycaemia and hyperglycaemia intrajejunal fat significantly (P < 0.05) stimulated pancreaticobiliary secretion. However, during hyperglycaemia, fat-stimulated 90 min pancreatico-biliary secretion was significantly (P < 0.05) reduced compared with normoglycaemia: trypsin (23 ± 7 units versus 66 ± 20 units), lipase (36 ± 8 k-units versus 74 ± 18 k-units), amylase (8 ± 2 k-units versus 18 ± 5 k-units) and bilirubin (32 ± 8 μmol versus 71 ± 14 μmol). Plasma cholecystokinin levels increased significantly (P < 0.05) during fat administration and were not different between the two experiments. Plasma pancreatic polypeptide levels were significantly (P < 0.05) reduced during hyperglycaemia both in the basal period and during intrajejunal fat administration. 3. It is concluded that basal and fat-stimulated pancreatico-biliary secretion are significantly reduced during acute hyperglycaemia. Acute hyperglycaemia does not affect intrajejunal fat-stimulated cholecystokinin secretion. Acute hyperglycaemia inhibits basal and stimulated pancreatic polypeptide secretion suggesting vagal-cholinergic inhibition of pancreatico-biliary secretion during hyperglycaemia.

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Deng, Xiaoying, Dulce R. Guarita, Martha R. A. Pedroso, Christianna Kreiss, Paul G. Wood, Alan F. Sved, and David C. Whitcomb. "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 (August 1, 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 pancreatic secretion by 15–20% ( P < 0.01). APX had no effect on bethanechol-stimulated secretion and potentiated protein secretion stimulated by PJD (396 vs. 284%) and exogenous CCK-8-secretin. In sham-operated rats, background PYY potently inhibited CCK-8-secretin-stimulated pancreatic fluid (1.8 vs. 48.2%) and protein secretion (3.7 vs. 45.8%) but potentiated fluid (52.9 vs. 43.1%) and protein (132.9 vs. 68.9%) secretion in APX rats. Our findings demonstrate that PYY inhibits CCK-8-secretin-stimulated pancreatic secretion through an AP-dependent mechanism in sham-operated rats. The AP also contributes to basal pancreatic secretion.

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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 (December 15, 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 secretion of bile salts (uncoupling phenomenon). Compared with the physiological and STC-infused condition, the biliary cholesterol/phospholipid ratio and saturated/unsaturated fatty acid ratio increased under the bile salts depletion and uncoupling phenomenon. Data indicate that the hydrophobicity of biliary lecithin increases with a decrease in the bile salt micelle capacity to induce biliary lipid secretion, resulting in a higher packing density of biliary vesicle. The cholesterol-holding capacity of the biliary vesicle is therefore enhanced during the depletion of bile salts and the uncoupling phenomenon.

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Li, Jianing, Sonja S. Pijut, Yuhuan Wang, Ailing Ji, Rupinder Kaur, Ryan E. Temel, Deneys R. van der Westhuyzen, and Gregory A. Graf. "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 (October 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. The increase in biliary cholesterol secretion was not associated with increases in hepatic SR-BI (scavenger receptor BI) or ABCG5 (ATP-binding cassette G5) ABCG8. The decline in intestinal cholesterol secretion was associated with an increase in intestinal Niemann-Pick disease, type C1, gene-like 1 mRNA. Finally, we followed the delivery of HDL (high-density lipoprotein) or LDL (low-density lipoprotein) cholesteryl esters (CE) from plasma to bile and intestinal perfusates. HDL-CE favored the biliary pathway. Following high-fat feeding, the presence of CETP directed HDL-CE away from the bile and towards the intestine. The presence of CETP increased LDL-CE delivery to bile, whereas the appearance of LDL-CE in intestinal perfusate was near the lower limit of detection. Conclusions: Biliary and intestinal cholesterol secretion can be simultaneously measured in mice and used as a model to examine factors that alter cholesterol elimination. Plasma factors, such as CETP, alter the route of cholesterol elimination from the body. Intestinal and biliary cholesterol secretion rates are independent of transhepatic or transintestinal delivery of HDL-CE, whereas LDL-CE was eliminated almost exclusively in the hepatobiliary pathway.

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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 (October 15, 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/bile acid and phospholipid/bile acid molar ratios and in the lithogenic index of the bile. The biliary outputs of the plasma-membrane enzymes alkaline phosphatase and gamma-glutamyltransferase were markedly reduced by the drug. When cyclobutyrol was administered to rats which had been previously fed with a high-cholesterol diet, the effects of cyclobutyrol persisted, but were less marked. Our results demonstrate that the bile acid-independent choleresis induced by cyclobutyrol (related to its pharmacokinetic effect) is accompanied by a pharmacodynamic action that selectively reduces the secretion of biliary lipids. This is due to an uncoupling of the secretion of cholesterol and phospholipids from that of bile acids. Possible explanations for the biliary response to cyclobutyrol are discussed.

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Werner, Anniek, Deanna M. Minich, Rick Havinga, Vincent Bloks, Harry Van Goor, Folkert Kuipers, and Henkjan J. Verkade. "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 (October 1, 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 multidrug resistance gene-2-deficient [ Mdr2(−/−)] mice, secreting phospholipid-free bile. After 8 wk, EFA−-fed wild-type [ Mdr2(+/+)] and Mdr2(−/−)mice were markedly EFA deficient [plasma triene (20:3n-9)-to-tetraene (20:4n-6) ratio >0.2]. Fat absorption decreased (70.1 ± 4.2 vs. 99.1 ± 0.3%, P < 0.001), but bile flow and biliary BS secretion increased in EFA−mice compared with EFA+controls (4.87 ± 0.36 vs. 2.87 ± 0.29 μl · min−1· 100 g body wt−1, P < 0.001, and 252 ± 30 vs. 145 ± 20 nmol · min−1· 100 g body wt−1, P < 0.001, respectively). BS composition was similar in EFA+- and EFA−-fed mice. Similar to EFA−Mdr2(+/+)mice, EFA−Mdr2(−/−)mice developed fat malabsorption associated with twofold increase in bile flow and BS secretion. Fat malabsorption in EFA−mice is not due to impaired biliary BS or phospholipid secretion. We hypothesize that EFA deficiency affects intracellular processing of dietary fat by enterocytes.

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Yamashita, G., S. Tazuma, K. Horikawa, N. Aihara, H. Ochi, K. Teramen, Y. Yamashita, M. Sasaki, T. Ohya, and G. Kajiyama. "Partial characterization of mechanism(s) by which sulphobromophthalein reduces biliary lipid secretion." Biochemical Journal 291, no. 1 (April 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 biliary secretion of cholesterol and phospholipids in a dose-dependent manner without affecting the secretion of bile salts and composition of fatty acids in phospholipids in SDR, but had no effect on lipid secretion in EHBR. In contrast, BSP-GSH had no such effect on biliary lipids, either in the SDR or EHBR. In addition, the amount of BSP in the liver of EHBR was in the same range as that of SDR. Therefore it is unlikely that an intracellular mechanism is involved in the phenomenon of uncoupling by BSP. We conclude that the uncoupling of biliary lipids from bile-salt secretion by BSP occurs at the level of the bile canaliculus following the secretion of unconjugated BSP.

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29

Martin, Gregory G., Barbara P. Atshaves, Kerstin K. Landrock, Danilo Landrock, Stephen M. Storey, Philip N. Howles, Ann B. Kier, and Friedhelm Schroeder. "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 (December 1, 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 and DKO also altered biliary bile acid composition to increase bile acid hydrophobicity. Furthermore, LKO and TKO decreased hepatic uptake and biliary secretion of high-density lipoprotein (HDL)-derived 22-( N-(7-nitrobenz-2-oxa-1,3-diazol-4-yl)amino)-23,24-bisnor-5-cholen-3β-ol (NBD-cholesterol), while DKO alone had no effect. Finally, LKO and, to a lesser extent, DKO decreased most indexes contributing to cholesterol solubility in biliary bile. These results suggest different, but complementary, roles for L-FABP and SCP-2/SCP-x in biliary bile acid and cholesterol formation. L-FABP appears to function more in hepatic retention of bile acids as well as hepatic uptake and biliary secretion of HDL-cholesterol. Conversely, SCP-2/SCP-x may function more in formation and biliary secretion of bile acid, with less impact on hepatic uptake or biliary secretion of HDL-cholesterol.

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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 (October 1, 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. Glucagon (1.25–300 μg∙kg−1∙30 min−1) increased bile flow in all the three species, and produced no changes in biliary bicarbonate concentrations in the dog and rat. In the guinea pig, however, glucagon choleresis was associated with an increase in bicarbonate concentration in bile, similar to that observed with secretin. The choleretic activities of various bile acids (taurocholate, chenodeoxycholate, glycochenodeoxycholate, tauroursodeoxycholate, and ursodeoxycholic acid, infused at 30–360 μmol∙kg−1∙30 min−1) were similar in the rat (6.9–7.2 μL/μmol), but different in the guinea pig (11–31 μL/μmol). In the latter species, the more hydrophobic the bile acid, the greater was its choleretic activity. In all instances, bile acid choleresis was associated with a decline in the biliary concentrations of chloride, but with no major change in bicarbonate levels. The prominent finding of these studies is that, regardless of whether bile flow was stimulated by hormones or different bile acids, bicarbonate concentrations in bile were always similar to or higher than those in plasma. This is construed to support the view that bicarbonate is transported into bile, possibly at multiple sites within the biliary tree. Its excretion most likely provides the driving force for hormone-induced choleresis, and may in part account for the flow of bile associated with bile acid secretion.

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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 (August 15, 1992): 193–96. http://dx.doi.org/10.1042/bj2860193.

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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. In addition, the distribution pattern of each organic anion to various lipid particles was determined by gel-permeation chromatography. BSP was predominantly associated with bile salt micelles, whereas vesicular association was dominant for ICG, and both BSP-glutathione and PR formed only self-aggregations. From these data, we concluded that the uncoupling of biliary lipids from bile salt secretion by BSP resulted from the interaction between BSP and bile salt micelles in the bile canaliculus, and that this interaction inhibited the capacity of bile salts to induce the secretion of phospholipids and cholesterol.

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32

VERKADE, Henkjan J., Marjan A. C. de BRUIJN, Menno A. BRINK, Herre TALSMA, Roel J. VONK, Folkert KUIPERS, and Albert K. GROEN. "Interactions between organic anions, micelles and vesicles in model bile systems." Biochemical Journal 320, no. 3 (December 15, 1996): 917–23. http://dx.doi.org/10.1042/bj3200917.

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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 entrapped in a self-quenching concentration in small unilamellar vesicles (SUV) composed of cholesterol/egg phosphatidylcholine (molar ratios 0, 0.2 and 0.5). Certain organic anions clearly affected the bile-salt-induced release of fluorescence from these SUV, reflecting interference with micellization. However, the effects of hydrophilic and hydrophobic organic anions did not correspond with their effects on biliary lipid secretion in vivo, irrespective of the bile salt species used (taurocholate, taurodeoxycholate or tauroursodeoxycholate) and of the lipid composition of the SUV. Ultracentrifugation and dynamic light-scattering studies indicated that organic anions do interact with bile salt/phosphatidylcholine/cholesterol mixed micelles, but that they do not inhibit micellization, for example by competing with phosphatidylcholine and/or cholesterol for incorporation into mixed micelles. In conclusion, the present in vitro data indicate that the in vivo mechanism of organic-anion-induced inhibition of biliary lipid secretion is not mediated by inhibition of micellization.

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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 (March 1, 1986): 421–27. http://dx.doi.org/10.1042/bj2340421.

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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 secretion of phospholipid, which was maintained even at high rates of bile-salt infusion, suggest a continuous and regulated phospholipid supply and secretion mechanism. In contrast, however, multiple short pulses of TC to the perfused liver, which brought about relatively equal biliary bile-salt output pulses, did not bring about equal phospholipid outputs, since the phospholipid peak size declined with each bile-salt pulse. These experiments taken together suggest either that a threshold (intracellular) bile-salt concentration may be required to ‘switch-on’ the phospholipid supply and that it may need to be maintained for continuous biliary phospholipid supply to the canalicular membrane.

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34

Alpini, G., S. Glaser, W. Robertson, R. E. Rodgers, J. L. Phinizy, J. Lasater, and G. D. LeSage. "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 (May 1, 1997): G1064—G1074. http://dx.doi.org/10.1152/ajpgi.1997.272.5.g1064.

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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 by change in luminal size in response to agonists. IBDU diameters ranged from 11 to 65 microns. Secretin increased ductal secretion solely in large IBDU. Forskolin induced a modest increase in ductal secretion in small IBDU but markedly increased ductal secretion in large IBDU. Secretion increased Cl-/HCO3- exchanger activity and cAMP levels in large but not small IBDU. Secretin receptor and Cl-/HCO3 exchanger mRNAs were detected only in large IBDU. We propose that agonist-induced ductal secretion occurs in large (> or = 15-microns diam) but not small (< 15-microns diam) intrahepatic ducts.

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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 (May 1, 1991): 591–95. http://dx.doi.org/10.1042/bj2750591.

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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. The effects were apparently unrelated to an inhibition of intracellular vesicular transport because, after injection of horseradish peroxidase, both the time course and total amount secreted of the protein did not significantly differ between control animals and those receiving cefmetazole. The secretory rate of the lysosomal marker acid phosphatase was not affected by cefmetazole administration. Biliary outputs of the plasma-membrane enzymes alkaline phosphatase and gamma-glutamyltransferase were significantly decreased by the antibiotic. These results point to an effect of cefmetazole at the level of the canalicular membrane.

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36

Yamada, T., M. Hoshino, T. Hayakawa, H. Ohhara, H. Yamada, T. Nakazawa, T. Inagaki, et al. "Dietary diosgenin attenuates subacute intestinal inflammation associated with indomethacin in rats." American Journal of Physiology-Gastrointestinal and Liver Physiology 273, no. 2 (August 1, 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. Dio significantly increased biliary cholesterol (Chol) output and prevented the decreases in bile flow, bile acid output, and biliary alpha-muricholic acid and the increases in biliary hyodeoxycholic acid, deoxycholic acid, and hydrophobicity index of bile. Significantly more biliary Chol and phospholipids were present in macromolecules separate from bile acids and Indo in Dio-treated rats. Dio significantly increased the elimination constant of Indo and reduced plasma Indo levels at 3 and 12 h but did not influence biliary secretion of Indo for 3.5 h after injection. Although Dio dose-dependently attenuated subacute intestinal inflammation and normalized bile secretion in this model, it may also compromise the anti-inflammatory action of indo.

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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 (November 1, 1989): 473–78. http://dx.doi.org/10.1042/cs0770473.

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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 increase in bile acid output was not significantly reduced by protoporphyrin IX at either of the doses used. However, when a cholestatic dose of protoporphyrin IX was infused, the taurocholate-induced bile flow and secretion of lecithin and cholesterol were significantly reduced. 3. Biliary output of phospholipid species other than lecithin did not counterbalance the protoporphyrin IX-induced reduction in biliary lecithin secretion. Biliary outputs of both total phospholipid and lecithin were inhibited by protoporphyrin IX to similar extents. 4. Protoporphyrin IX alone had no effect on the biliary release of 5′-nucleotidase, whereas when it was given with taurocholate, it increased the bile acid-induced biliary output of this enzyme markedly. 5. In summary, these results indicate that protoporphyrin IX impairs the biliary secretion of phospholipids and cholesterol but not that of bile acid. The release of canalicular membrane constituents other than lipids was also modified by protoporphyrin IX.

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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 (July 15, 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 perfused with a medium containing 2.5 microM-colchicine, the biliary secretion of IgA and the second secretion peak of HRP were inhibited by 60%. If rats were pretreated for 12h with alpha-naphthylisothiocyanate (25mg/100g body wt.) prior to liver isolation, the biliary secretion of [3H]methoxyinulin and the first secretion peak of HRP were increased. Taken together, these results suggest that HRP enters the bile via two routes. The faster route, which was increased by alpha-naphthylisothiocyanate and correlated with [3H]methoxyinulin entry into bile, was probably paracellular, involving diffusion across tight junctions. The slower route, which was inhibited by colchicine and correlated with the secretion of IgA, was probably due to transcytosis, possibly within IgA and other transport vesicles.

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Elferink, Ronald Oude. "Elucidation of the biliary secretion machinery." Current Gastroenterology Reports 5, no. 6 (December 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 (October 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 (September 1, 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 of CCK-8/1. 3. Maximal trypsin output during infusions of CCK-8 was significantly less than that after a combination of the CCK-like peptide, caerulein, and secretin (32.95 ± 2.16 k-i.u./30 min, P < 0.001). 4. Biliary bile acid and bilirubin outputs were significantly augmented only when plasma concentrations of CCK-8 were > 5 pmol/l. 5. Plasma concentrations of CCK-8 in the low picomolar range exert significant effects on pancreatic and biliary secretion. CCK-8 fulfills the criteria for a circulating hormone.

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Yamada, T., M. Hoshino, T. Hayakawa, Y. Kamiya, H. Ohhara, K. Mizuno, H. Yamada, et al. "Bile secretion in rats with indomethacin-induced intestinal inflammation." American Journal of Physiology-Gastrointestinal and Liver Physiology 270, no. 5 (May 1, 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 deoxycholic acids were increased in bile. Bile flow and the transport maximum of taurocholate did not decrease, and biliary horseradish peroxidase output was significantly enhanced in isolated perfused livers from indomethacin-treated rats. Endotoxin in the portal blood was significantly increased in rats treated with indomethacin. Clindamycin slightly reduced intestinal inflammation but significantly prevented decreases in bile flow, bile acid output, and transport maximum of taurocholate. We conclude that, although biliary secretory function was apparently decreased in vivo, that of hepatocyte function was maintained in this model.

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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 (February 15, 1989): 17–22. http://dx.doi.org/10.1042/bj2580017.

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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 retrogradely provoked a 3.5-fold increase in biliary phospholipid output for 40 min, as compared with the saline control. Injection of 2.7 mumol of TC (90 microliters) caused a 7.5-fold increase in phospholipid output, which reached a peak at 12 min after RII, and phospholipid output continued for 40 min. Cholesterol output was also elicited under these conditions, showing both dose-dependency and extended secretion. Injection of 1.8 mumol of TDHC caused very little increase in either biliary phospholipid or cholesterol. Injection of 0.9 mumol of CHAPS (45 microliters) provoked a single substantial peak of phospholipid output in the 3 min bile sample. T.l.c. analysis of the phospholipid extracts of the bile collected after each compound showed, for TC, a single compound which co-migrated with the phosphatidylcholine standard, whereas for CHAPS substantial amounts of other phospholipids were present.

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Zhang, Linda S., Hirokazu Sato, Qing Yang, Robert O. Ryan, David Q. H. Wang, Philip N. Howles, and Patrick Tso. "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 (December 1, 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 = 12) increased the biliary secretion of apoA-V but not of other apolipoproteins, such as A-I, A-IV, B, and E. The lipid-induced increase of biliary apoA-V was abolished under conditions of poor lymphatic lipid transport, suggesting that the stimulation is regulated by the magnitude of lipids associated with chylomicrons transported into lymph. We also studied the secretion of apoA-V into bile immediately following bile duct cannulation. Biliary apoA-V increased over time (∼6-fold increase at hour 16, n = 8) but the secretions of other apolipoproteins remained constant. Replenishing luminal phosphatidylcholine and taurocholate ( n = 9) only enhanced apoA-V secretion in bile, suggesting that the increase was not due to depletion of phospholipids or bile salts. This is the first study to demonstrate that apoA-V is secreted into bile, introducing a potential route of delivery of hepatic apoA-V to the gut lumen. Our study also reveals the uniqueness of apoA-V secretion into bile that is regulated by mechanisms different from other apolipoproteins.

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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 (February 1, 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 GSH secretion, although the inhibition was not as complete as observed after BSP administration; at a dose of 180 mumol/kg GSH secretion fell to 18% of control. BSP-SG, in contrast, had no effect on GSH secretion into bile when given at a dose of 120 mumol/kg. At doses of 240 and 360 mumol BSP-SG/kg, there were only minor changes in the rate of GSH secretion. The changes in GSH secretion induced by these dyes were accompanied by proportional changes in glutathione disulfide (GSSG) secretion into bile, so that the molar ratio of GSSG to GSH in bile remained within the range of 0.07–0.18. In all experiments the changes in methylmercury secretion were parallel to the changes in GSH secretion. The results suggest that the BSP-induced inhibition of GSH, GSSG, and methylmercury secretion into bile is due to the direct inhibition of the biliary GSH transport process.

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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 (February 1, 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. The mechanism for the decrease in biliary GSH efflux was not increased paracellular permeability. GSH transport kinetics, ATP-stimulated taurocholate, and oxidized glutathione (GSSG) transport in canalicular liver plasma membrane prepared from diabetic and control rats were similar. Inhibition of protein kinase C (PKC) with high-dose H-7 increased biliary GSH efflux in diabetic animals to near control basal levels. In conclusion, streptozotocin-induced diabetic rats exhibit a progressive impairment in biliary GSH transport. One of the responsible mechanisms is heightened PKC tone in diabetic animals.

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Coy, Donna J., Clavia R. Wooton-Kee, Baoxiang Yan, Nadezhda Sabeva, Kai Su, Gregory Graf, and Mary Vore. "ABCG5/ABCG8-independent biliary cholesterol excretion in lactating rats." American Journal of Physiology-Gastrointestinal and Liver Physiology 299, no. 1 (July 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 97 and 60% by midlactation in rats and mice, respectively; protein levels of Abcg8 were below detection limits in lactating rats. Mdr2 mRNA expression was decreased in lactating rats and mice by 47 and 59%, respectively. Despite these changes in transporter expression, basal concentrations of cholesterol and phospholipid in bile were unchanged in rats and mice, whereas increased Bsep mRNA expression in early lactation coincided with an increased basal biliary bile acid concentration in lactating mice. Following taurocholate infusion, coupling of phospholipid and taurocholate secretion in bile of lactating mice was significantly impaired relative to control mice, with no significant changes in maximal secretion of cholesterol or bile acids. In rats, taurocholate infusion revealed a significantly impaired coupling of cholesterol to taurocholate secretion in bile in lactating vs. control animals. These data reveal marked utilization of an Abcg5/Abcg8-independent mechanism for basal biliary cholesterol secretion in rats during lactation, but a dependence on Abcg5/g8 for maximal biliary cholesterol secretion.

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Portal, I., T. Clerc, V. Sbarra, H. Portugal, A. M. Pauli, H. Lafont, B. Tuchweber, I. Yousef, and F. Chanussot. "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 (June 1, 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 from intrahepatic microsomes. The low level of radioactivity of HDL-PC in intrahepatic compartments suggests that HDL-PC taken up by the liver is predestined for the bile secretion. The correlation between the kinetics of bile secretion of HDL-cholesterol and HDL-[3H]PC suggests the importance of HDL-PC in reverse transport of cholesterol to the liver and its transport to the bile. The differences between the effects of dehydrocholic acid and cholic acid infusions can be explained by the differences in bile salts binding to the surface of HDL.

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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 (November 1, 1997): 700–704. http://dx.doi.org/10.1136/gut.41.5.700.

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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 determine how a rapid lowering of plasma low density lipoprotein (LDL) and very low density lipoprotein (VLDL) cholesterol influences the biliary secretion rates of cholesterol and bile acids in patients with cholesterol gallstones and complete biliary drainage. In this model with a completely interrupted enterohepatic circulation, the secretion of bile acids equals the new synthesis of bile acids in the liver.Patients—Eight patients with common bile duct stones of cholesterol type undergoing conventional cholecystectomy and choledocholithotomy.Methods—At operation a balloon occludable Foley catheter attached to a T tube was inserted into the bile duct with the balloon placed just past the distal limb of the T tube. The T tube was allowed to drain the bile externally. One week after the operation the Foley catheter balloon was inflated, creating complete biliary drainage. Twelve hours following the inflation plasma LDL apheresis was carried out for two hours. Bile was collected for 15 minute periods starting one hour before the apheresis and ending two hours after its termination. During the collection of bile, plasma lipids were analysed on several occasions.Results—The plasma level of LDL cholesterol decreased by 26% from (mean (SEM)) 2.19 (0.29) to 1.63 (0.17) mmol/l during the LDL apheresis while high density lipoprotein (HDL) cholesterol in plasma was unaffected. During LDL apheresis apolipoprotein B containing lipoproteins bind to the column, causing a significant decrease of not only plasma LDL but also of VLDL cholesterol. The secretion rate of bile acids decreased significantly by 31% from 131 (38) to 90 (16) μmol/15 minutes (p=0.045). The output of phospholipids also decreased by 19%. The biliary secretion rate of cholesterol was not, however, affected by the plasma LDL apheresis.Conclusions—The results suggest that, in patients with cholesterol gallstones and complete biliary drainage, lowering of plasma LDL and VLDL cholesterol reduces the biliary secretion rate—synthesis—of bile acids without affecting the biliary secretion rate of cholesterol.

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Dutta, Amal K., Kristy Boggs, Al-karim Khimji, Yonas Getachew, Youxue Wang, Charles Kresge, Don C. Rockey, and Andrew P. Feranchak. "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 (April 1, 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 biliary cells, and cholangiocytes isolated from murine liver tissue. The results demonstrate that all the biliary models expressed the IL-4Rα/IL-13Rα1 receptor complex. Incubation of cholangiocytes with either IL-13 or IL-4 increased the expression of TMEM16A protein, which was associated with an increase in the magnitude of Ca2+-activated Cl− currents in response to ATP in single cells and the short-circuit current response in polarized monolayers. The IL-4- and IL-13-mediated increase in TMEM16A expression was also associated with an increase in STAT6 phosphorylation. Specific inhibition of JAK-3 inhibited the increase in TMEM16A expression and the IL-4-mediated increase in ATP-stimulated currents, whereas inhibition of STAT6 inhibited both IL-4- and IL-13-mediated increases in TMEM16A expression and ATP-stimulated secretion. These studies demonstrate that the cytokines IL-13 and IL-4 regulate the expression and function of biliary TMEM16A channels through a signaling pathway involving STAT6. Identification of this regulatory pathway provides new insight into biliary secretion and suggests new targets to enhance bile formation in the treatment of cholestatic liver disorders. NEW & NOTEWORTHY The Ca2+-activated Cl− channel transmembrane member 16A (TMEM16A) has emerged as an important regulator of biliary secretion and hence, ductular bile formation. The present studies represent the initial description of the regulation of TMEM16A expression in biliary epithelium. Identification of this regulatory pathway involving the IL-4 and IL-13 receptor complex and JAK-3 and STAT-6 signaling provides new insight into biliary secretion and suggests new therapeutic targets to enhance bile formation in the treatment of cholestatic liver disorders.

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Journal articles on the topic 'Biliary secretion'

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