Recently, we have demonstrated that green tea extract (GTE) decreases the intestinal absorption of benzo[a]pyrene (BAP), which is an extremely lipophilic food contaminant. The present study was conducted to examine if an enteral infusion of GTE would influence the biliary secretion of BAP and lipids in rats. Female rats were fed an AIN-93G diet with or without (control) GTE at 5 g/kg diet for 4 week. Following the 4-week dietary treatment, rats with bile duct cannula were infused continuously for 8 hr at 3.0 mL/hr via a duodenal catheter with a lipid emulsion containing $4.0\;{\mu}mol$ BAP labeled with $^{14}C$ ($^{14}C$-BAP), $20.7\;{\mu}mol$ cholesterol, $452\;{\mu}mol$ triolein, and $3.1\;{\mu}mol$${\alpha}$-tocopherol, and $396.0\;{\mu}mol$ Na-taurocholate with or without 76.1 mg GTE powder in PBS buffer (pH, 6.4). Bile was collected hourly via bile cannula for an 8 hr period. Our results showed that bile flow did not differ between groups. However, the biliary secretion of $^{14}C$-BAP was significantly enhanced by GTE infusion, compared with those infused with the lipid emulsion alone. However, GTE did not affect the biliary outputs of cholesterol, fat, phospholipid and ${\alpha}$-tocopherol. These findings indicate that GTE has a profound stimulatory effect on the biliary excretion of BAP in rats, without affecting other biliary lipids. The mechanism(s) by which GTE enhances the biliary secretion of BAP remains to be investigated.
Purpose: Many diagnostic modalities for neonatal cholestasis have shown features that are helpful, however until recently none of them are not pathognomonic of biliary atresia (BA). We carried out a prospective study of infants with cholestatic jaundice with the aim of establishing an efficient method of diagnosing BA. Methods: Twenty-seven consecutive infants with cholestatic jaundice were enrolled in this study and ranged from 7 to 152 days in age (mean; $51.2{\pm}34.2$ days). Gastroduodenoscopy was carried out using a fiberscope (Olympus N30). All the babies were fasted for at least 4 hours before the procedure and 20 ml of 10% dextrose solution was given at the time of endoscopy. The endoscopic examination focused on the 5 minutes observation of the evidence of biliary secretion. If there was lack of the evidence of the biliary secretion, endoscopy was removed and repeated the examination with some pause. Results: There are lack of the evidence of biliary secretion in all infants with BA. In non-BA group, 8 out of the 10 infants showed biliary secretion on the first trial, however one (Alagille syndrome) of the two infants without evidence of biliary secretion, finally exhibited biliary secretion on the second trial. The above observations resulted in the diagnostic accuracy of 96.3% with 100.0% sensitivity and 90.0% specificity. Conclusion: In light of the results from our relatively small study, endoscopy is a convenient, and relative inexpensive procedure. we strongly support the use of endoscopy for the diagnosis of BA in the screening and evaluation of infantile cholestasis.
the exocrine pancreatic secretion is an important factor in the maintenance of zinc homeostasis. The daily pancreatic secretion of zinc into the gastrointestinal tract may be two or more times the daily dietary zinc intake. The objective of this study was to examine the distribution of proteins and zinc in pancreatic/biliary fluid following intraperitoneal {TEX}${65}^Zn${/TEX} injection into dietary prepared Sprague-Dawly rats. Distribution of zinc-binding protein in Sephadex G-75 subfractions showed a peak corresponding to the high molecular weight protein standard(<66kDa) in the pancreatic/biliary fluid. Zinc also was associated with the 29~35kDa mole-cular weight proteins. These are similar in size with zinc-containing enzymes, carboxypeptidase A and car-boxypeptidase B. A more remarkable small molecular weight fraction eluted beyond the 6.5kDa standard pro-tein peak. These results show the presence of small molecular weight compound in pancreatic/biliary fluid associated with zinc . These small molecular weight compounds may serve as zinc-binding ligands for the secretion of enogenous zinc into the duodenum. These findings suggest that these lignads may dissociate zinc in the duodenum thus making it vulnerable to complexation with phytate in the upper gastrointestinal tract rendering the zinc unavailable for reabsorption.
The pancreas is an important organ in the maintenance of zinc homeostasis. Endogenous zinc is con-tinuously secreted via pancreatic exocrine fluid or to a lesser extent in bile. Much of the endogenous secretion must be reabsorbed to sustain zinc homeostasis. The objective of this study was to estimate the relative size of the pancreatic/biliary zinc pool in comparision to the dietary zinc intake, and to study the effect of the phytate and calcium on the zinc homeostasis using a rat model. At the termination of the experiment, pan-creatic/biliary fluid was collected from the rats. Both radioactivity and total zinc were measured and the relative size of the pancreatic/biliary zinc pool was estimated. To determine the effect of phytate and calcium on zinc homeostsis, dietary zinc intake, the amount of zinc in pancreatic.biliary fluid and fecal zinc excretion were measured. The flow rate of pancreatic/biliary fluid, as corrected for tubing constriction, gives the corrected zinc concentration in the pancreatic/biliary fluid was 2.2 times higher than dietary zinc intake. To maintain zinc homeostasis, zinc absorption/reabsorption was very efficient in the current model; 76%, 88% of absorption/reabsorption for low calcium group and high calcium group 81% for phytate group and non-phytate group, respectively.
A study on the mechanism of biliary and urinary excretion of chloramphenicol has been performed in the dog. 1) Chloramphenicol administered intravenously to dogs with ligated renal pedicle, readily appeared in bile greater than in plasma. 6.9% of a 50mg /kg i. v. dose of chloramphenicol were excreted into bile within 100 minutes. During the same periods of above experiment, the bile/plasma concentration ratios(B/P ratios) were 46 to 87. 2) Chloramphenicol injected into the vein of dog was rapidly excreted into urine. 18% of the administered dose were excreted into urine within 70 minutes. In the same periods of this experiment, Ccm/Ccr ratios were greater than 1.0 in most cases. 3) In experiment of simultaneous measurement of biliary and urinary excretion of chloramphenicol, Ccm/Ccr ratios were less than 1.0 and B/P ratios were 50 to 52. 4) In experiment measured simultaneously biliary and urinary excretion both Ccm/Ccr and $C^Hcm$(hepatic clearance) were significantly declined by probenecid, but not affected by 2,4-DNP and aminophylline although 2,4-DNP increased only bile flow and aminophylline both bile and urine volume. 5) Ccm/Ccr and $C^Hcm$ were increased in proportion to increment of plasma concentration ranging from 3.3 to 30 mg% of chloramphenicol. But when plasma concentration were increased to 70mg %, Ccm/Ccr were not increased and $C_Hcm$ were reduced about 30% in comparison with values obtajned at 30mg% of chloramphenicol. 6) Free/Bound(free to bouid from) ratios ranging from 1.0 to 90.0mg% of chloramphenicol were 76.2+3.72% $(mean{\pm}S.E.)$ Above results suggest that chloramphenicol is excreted into bile by a process of active trasport, that excretion of chloramphenicol into urine was made up with dual process, reabsorption and secretion, and that renal secretion was attained by active trasport process although renal reabsorption process could not understand.
Bile formation is a complex process comprised of three separate physiologic mechanism operating at two anatomical sites. At present time, it was known that at least two processes are responsible for total canalicular secretion at the bile canaliculus. One of the processes is bile salt-dependent secretion (BSDS) hypothesis that the active transport of bile salts from plasma to bile provided a primary stimulus for bile formation: the osmotic effect of actively transported bile acid was responsible for the movement of water and ions into bile. The other process is bile salt-independent secretion (ESIS), which is unrelated to bile salt secretion at the canaliculus and which may involve the active transport of sodium. The third process for bile formation involves the biliary ductal epithelium. Secretin-stimulated bile characteristically contained bicarbonate in high concentration. Therefor, it was suggested that secretin stimulated water and bicarbonate secretion from the biliary ductules. One the other hand, it was found that a large amounts of cAMP was present in canine bile but no apparent relationship between bile salt secretion and cAMP content in dog bile. However, bile flow studies in human have demonstrated that secretin and glucagon increase bile cAMP secretion as does secretin in baboons. Secretin increases baboon bile duct mucosal cAMP levels in addition to bile CAMP levels suggesting that in that species secretin-stimulated bile flow may be cAMP mediated. It has been postulated that glucagon and theophylline which increase the bile salt-independent secretion in dogs might act through an increased in liver cAMP content. In a few studies, the possible role of cAMP on bile formation has teen tested by administration of an exogenous derivative of cAMP, dibutyryl cAMP. In the rat, DB cAMP did not modify bile flow, but injection of DB cAMP in the dog promoted an increase in the bile salt-independent secretion. Because of these contradictory results, this study was carried out to examine the relationship between cyclic nucleotides and bile flow due to various bile salts as well as secretin or theophylline. Experiments were performed in rabbits with anesthesia produced by the injection of seconal(30 mg/kg). Rabbits had the cystic duct ligated and the proximal end of the divided common duct cannulated with an appropriately sized polyethylene catheter. A similar catheter was placed into the inferior vena cava for administration of drugs. Bile was collected for determination of cyclic nucleotides and total cholate in 15 min. intervals for a few hours. The results are summerized as followings. 1) Administrations of taurocholic acid or chenodeoxycholic acid increased significantly the concentrations of cAMP and cGMP in bile of rabbits. 2) Concentration of cAMP in bile during the continuous infusion of ursodeoxycholic acid, was remarkedly increased in accordance with the increase of bile flow, while on the contrary concentration of cGMP in bile was decreased significantly. 3) Dehydrocholic acid and deoxycholic acid significantly increased bile flow, total cholate output and cyclic nucleotides in bile. 4) Only cAMP concentration in bile was significantly increased from control value by secretin, while theophylline increased cAMP as well as cGMP in rabbit bile. 5) In addition, the administration of secretin to taurocholic acid-stimulated bile flow increased cAMP while theophylline produced the increases of cAMP and cGMP in bile. 6) The administration of insulin to taurocholic acid-stimulated bile flow decreased cAMP concentration, while on the contrary cGMP was remarkedly increased in rabbit bile.
This study was done to investigate the effect of vitamin C on hepatic biliary and microsomal function during ischemia and reperfusion. Rats were treated with vitamin C(20, 100, 400, 1600 mg/kg) or with vehicle(saline) and then subjected to 60 min no-flow hepatic ischemia in vivo. Control animals were time-matched sham ischemic animals. After 1 or 5 hr of reperfusion, bile was collected, blood was obtained from the abdominal aorta, and liver microsomes were isolated. In vehicle-treated ischemic rats, serum ALT and AST levels peaked at 5 hr and were significantly attenuated by vitamin C 20 mg/kg and 100 mg/kg treatment. Similarly, hepatic wet weight-to-dry weight ratio was decreased in the vehicle-treated ischemic group. Vitamin C 20 mg/kg and 100 mg/kg treatment minimized the increase in this ratio. Lipid peroxidation was elevated in vehicle-treated ischemic group, but this elevation was also inhibited by vitamin C 20 mg/kg and 100 mg/kg treatment. Bile flow and cholate output, but not bilirubin output, were markedly decreased by ischemia/reperfuzion. Vitamin C 20 mg/kg and 100mg/kg treatment restored the secretion but vitamin C 1600 mg/kg reduced the cholate output. Cytochrome P-450 content was decreased by ischemia/reperfusion and restored by vitamin C 20 mg/kg and 100 mg/kg treatment to the level of sham operated group but decreased by vitamin C 1600 mg/kg. Aminopyrine N-demethylase activity was decreased and aniline p-hydroxylase activity was increased by ischemia/reperfusion. The changes in the activities of aminopyrine were prevented by vitamin C 20 mg/kg and 100 mg/kg treatment, but not by 400 mg/kg and 1600 mg/kg treatment. Our findings suggest that ischemia/reperfusion diminishes hepatic secretory functions as well as microsomal drug metabolizing systems, small doses(20, 100 mg/kg) of vitamin C significantly ameliorates and large doses(400, 1600 mg/kg) of vitamin C aggravated these ischemia/reperfusion-induced changes.
The histological change of the billary mucosa in clonorchiasis is characterized as adenomatous hyperplasia, and cross-sectioned mucosa looks like intestinal mucosa. In addition to the glandular hyperplasla, the metaplasia of mucin secreting cells is also known. The present study investigated the presence of intestinal secretion from the biliary mucosal cells of rabbits and rats with Clonorchis sinensis infection. The rabbit was infected with 300 and the rat was infected with 100 metacercariae of C. sinensif. A part of the animals were followed up after praziquantel treatment. The rabbit livers were prepared for histochemistry to observe any endocrine secretion and the bile duct mucosa of the mice was processed far the activity of brush border membrane (BBM)-bound enzymes of the small intestine. Immunohistochemistry with the polyclonal antibodies and biotin-streptavidin-peroxidase staining kit showed no positive cells for gastrin and secretin, but a few cells were positive for serotonin. The proliferated billiw mucosa of the mice revealed no activity of dissaccharidases and aminopeptidase. Only alkaline phosphatase activity was found both in the control and the infected. The hyperplastic billary mucosal cells showed no gastrointestinal secretory functions. The serotonin secreting cells may be one of the inflammatory cells.
No evidence has accumulated that lead compound is an essential component for biological function in animals. Lead is absorbed primarily through the epithelial mucosal cells in duodenum and the absorption can be enhanced by the substances which bind lead and increase its solubility. Iron, zinc and calcium ions, however, decrease the absorption of lead without affecting its solubility, probably by competing for shared absorptive receptors in the intestinal mucosa. Therefore, the absorption of lead is increased in iron deficient animals. Lead shows a strong affinity for ligands such as phosphate, cysteinyl and histidyl side chains of proteins, pterins and porphyrins. Hence lead can act on various active sites of enzymes, inhibiting the enzymes which has functional sulfhydryl groups. lead inhibits the activity of ${\delta}$-aminolevulinic acid dehydratase for the biosynthesis of hemoproteins and cytochrome, which catalyzed the synthesis of monopyrrole prophobilinogen from ${\delta}$-aminolevulinic acid. Accordingly lead decrease hepatic cytochrome p-450 content, resulting an inhibition of the activity of demethylase and hydroxylase in liver. Little informations are available on the effect of lead on digestive system although the catastrophic effects of lead intoxication are well documented. The present study was, therefore, attempted to investigate the effect of lead on pancreaticobiliary secretion in rats. Albino rats of both sexes weighing $170{\sim}230g$ were used for this study. The animals were divided into one control and three treated groups, i.e., control (physiologic saline 1.5ml/kg i.p.), lead acetate $(l0{\mu}mole/kg/day\;i.p.)$, $Pb(Ac)_2$ and EDTA$(each\;10{\mu}mole/kg/day\;i.p.)$, $Pb(Ac)_2$ and $FeSO_4(each\;l0{\mu}mole/kg/day\;hp)$. The pancreatico-biliary juice was collected under urethane anesthesia, and activities of amylase and lipase were determined by employing Sumner's and Cherry and Crandall's methods. The summarized results are follows. 1) In the experiment for acute toxicity of lead acetate, 20% of mortality was observed in rat treated with lead acetate as well as inhibition of the activity of amylase in the juice at the 3 rd day of the treatment. 2) No increases in body weight were observed in rats treated with lead acetate, while in control group the significant increases were observed. However, the body weights of animals were increased in the group lead acetate plus EDTA or $FeSO_4$. 3) Lead acetate decreased significantly the volume of pancreatico-biliary juice whereas additional treatment of EDTA and $FeSO_4$ prevented it. 4) Total activity of amylase was markedly reduced due to lead acetate treatment, but no change was showed following additional treatment with EDTA and $FeSO_4$. 5) No changes in the cholate and lipase output were observed in rats treated with lead acetate as compared with that of control rats. 6) Increase in bilirubin output in rats treated with lead acetate was shown on the 2nd and 3rd weeks treatment. 7) In the case of in vitro experiment, lead acetate also markedly inhibited release of amylase from pancreatic fragment. 8) Histologic finding indicated that acini vacuolation was induced in the pancreatic tissue of rat treated with lead acete. From the above results, it might be concluded that lead acetate decreases the volume of pancreatico-biliary secretion and inhibits the amylase activity, by acting directly on pancreatic cells.
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