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Excretion bile/biliary

Control of these mechanisms occurs at several levels. The uptake of VLDL remnants and LDL by the apo B/E receptor has been shown to be Unked to the excretion of biliary UC and bile acids [122], whereas the formation of intracellular CE by the ACAT reaction seems to be inversely proportionate to the excretion of the same bile components [123]. The uptake of chylomicron remnants does not seem to be related to bile formation and excretion. Instead, when large amounts of remnant CE enter hepatocytes, as is seen in some species in diet-induced hypercholesterolemia, the CE is hydrolyzed within lysosomes, then reformed by the ACAT reaction and recirculated in the plasma as VLDL CE. Less is known about the control of LCAT secretion by the Ever. In rats and in humans the activity of LCAT in the plasma seems to be hnked not only to the transport of cholesterol, but also to the transport of essential fatty acids [124]. [Pg.113]

Many active substances are eliminated from the body after biotransformation. The metabolites are subsequently cleared via one of the excretion routes or further metabolised to products that can be excreted. The major routes of excretion encompass glomerular filtration followed by excretion into the urine, excretion of the active substance or its metabolites into the faeces (via the liver and bile, biliary excretion) or via... [Pg.335]

Flavonoids are not transported through in the circulatory system and reach body tissues instead, their secondary metabolites formed in the small intestine and hepatic cells elicit antioxidant effects. These reactions favor their excretion via biliary and renal, being the elimination in bile the most important route of elimination for most flavonoids (Cre-spy et al 2003). Flavonoid secondary metaboHtes can be detected in the blood and urine after its ingestion, but only very small fraction of nonconjugated flavonoids in their original form can be found. This implies that these flavonoid secondary metaboHtes rather than the native flavonoids are responsible for the beneficial biological effects in the body (Donovan et al 2006)... [Pg.665]

As described and discussed elsewhere in this volume, the excreted bile enters the gallbladder and after being concentrated is discharged into the duodenum near the pancreatic duct. Mixed with the pancreatic juice and tlie food, the bile is transported down the small intestine. The bile acid conjugates, among other biliary constituents, are partly absorbed from the intestine into the portal vessels and return to the liver to be excreted in the bile again. [Pg.98]

Klaassen, C. D., Watkins, J. B. (1984). Mechanisms of bile formation, hepatic uptake, and biliary excretion. Pharmacol. Rev. 36, 1-67. [Pg.342]

Bile ducts Various intravenous cholegraphic agents, e.g., iodipamide Biligrafin Anion transport Lin SK et al (1977) Iodipamide kinetics Capacity-limited biliary excretion with simultaneous pseudo-first-order renal excretion. J Pharm Sci 66 1670-1674... [Pg.1327]

Finally, the fact that anthocyanins can reach the brain represents a beginning of an explanation of the purported neuroprotection effects of anthocyanins. Anthocyanins may be eliminated via urinary and biliary excretion routes. " The extent of elimination of anthocyanins via urine is usually very low (< 0.2% intake) in rats and in humans, indicating either a more pronounced elimination via the bile route or extensive metabolism. As mentioned earlier, in the colon, non-absorbed or biliary excreted anthocyanins can be metabolized by the intestinal microflora into simpler break-down compounds such as phenolic acids that may be (re)absorbed and conjugated with glycine, glucuronic acid, or sulfate and also exhibit some biological... [Pg.168]

Palmer 1989 Robinson et al.1983). However, the ratio was almost certainly affected by initial chelation with Ca-DPTA, followed by daily intravenous therapy with the chelating agent, Zn-DPTA, treatments that would have increased the urinary excretion of americium (Breitenstein and Palmer 1989). The above not withstanding, the observations made on this subject demonstrate that fecal excretion was an important pathway of excretion in this subject long after mechanical clearance of americium from the respiratory tract would have been complete. This is consistent with observations made in nonhuman primates that show that americium is excreted into bile (see Section 3.4.4.4). However, the extent to which the biliary excretion pathway in humans might resemble that of nonhuman primates is not known. [Pg.72]

The large contribution of the fecal route to excretion of absorbed americium appears to be the result of excretion of americium into the bile. In monkeys that received an intravenous injection of americium citrate,241 Am was detected in gall bladder bile and its concentration increased as the relative rate of fecal excretion increased over time post injection (Durbin 1973). Durbin (1973) estimated that at bile production rates similar to humans, biliary excretion could have accounted for most, if not all, of the fecal excretion of americium observed in the monkeys. [Pg.73]

Studies with rats treated orally with triaryl or trialkyl phosphate esters (which may be found in organophosphate ester hydraulic fluids) indicate that these compounds and their metabolites are readily excreted in the urine, bile, feces and, to a limited extent, in expired air (Kurebayashi et al. 1985 Somkuti and Abou-Donia 1990a Suzuki et al. 1984a Yang et al. 1990). Urinary excretion of metabolites appears to be the predominant elimination route in rats for tri-ort/zo-cresyl phosphate and tri-para-cresyl phosphate, but biliary excretion of parent material and metabolites is also important (Kurebayashi et al. 1985 NTP... [Pg.176]

Several studies in rats have shown that certain acidic and basic compounds can be actively secreted into the bile. Thus, one might expect to see saturation of the biliary excretion process, although data in humans describing this phenomenon have not, as yet, been reported for orally dosed drugs. [Pg.135]

Lead is also eliminated in the bile (Klaassen and Shoeman 1974). In the rat, excretion occurs in the urine, with greater excretion in the feces following intravenous administration (Castellino and Aloj 1964 Klaassen and Shoeman 1974 Morgan et al. 1977). As the dose increases, the proportion of the lead excreted into the gut via bile increases, then plateaus at 3 and 10 mg/kg (Klaassen and Shoeman 1974). Biliary excretion of lead is suggested to be a saturable process (Gregus and Klaassen 1986). Excretion of lead in the bile by dogs amounted to approximately 2% of that by rats, and biliary excretion of lead by rabbits amounted to approximately 40% of that by rats (Klaassen and Shoeman 1974). [Pg.229]

The liver plays an important role in determining the oral bioavailability of drags. Drag molecules absorbed into the portal vein are taken up by hepatocytes, and then metabolized and/or excreted into the bile. For hydrophilic drugs, transporters located on the sinusoidal membrane are responsible for the hepatic uptake [1, 2]. Biliary excretion of many drags is also mediated by the primary active transporters, referred to as ATP-binding cassette transmembrane (ABC) transporters, located on the bile canalicular membrane [1, 3-5], Recently, many molecular biological... [Pg.288]

It is important to establish an in vitro system which will allow in vivo transport across the bile canalicular membrane to be predicted quantitatively. By comparing the transport activity between in vivo and in vitro situations in isolated bile canalicular membrane vesicles, it has been shown that there is a significant correlation for nine types of substrates [90]. Here, in vivo transport activity was defined as the biliary excretion rate, divided by the unbound hepatic concentration at steady-state, whereas in vitro transport activity was defined as the initial velocity for the transport into the isolated bile canalicular membrane vesicles divided by the medium concentration [90]. Collectively, it is possible to predict in vivo canalicular transport from in vitro experiments with the isolated bile canalicular membrane vesicles. [Pg.295]

It is also important to predict the in vivo biliary excretion clearance in humans, and for this purpose MDCK II cell lines expressing both uptake and efflux transporters may be used (Fig. 12.3) [92, 93]. It has been shown that MRP2 is expressed on the apical membrane, whereas OATP2 and 8 are expressed on the basolateral membrane after cDNA transfection (Fig. 12.3) [92, 93]. The transcellular transport across such double-transfected cells may correspond to the excretion of ligands from blood into bile across hepatocytes. Indeed, the vectorial transport from the basal to apical side was observed for pravastatin only in OATP2- and MRP2-expressing... [Pg.296]

MDCK II cells (Fig. 12.3) [93], Kinetic analysis revealed that the Km value for transcellular transport (24 pM) was similar to the Km for OATP2 (34 pM) [93], Moreover, the efflux across the bile canalicular membrane was not saturated under these experimental conditions. These in vitro observations are consistent with in vivo experimental results in rats which showed that the rate-determining process for the biliary excretion of pravastatin is uptake across the sinusoidal membrane. By normalizing the expression level between the double transfectant and human hepatocytes, it might be possible to predict in vivo hepatobiliary excretion. [Pg.297]

Bile salt export pump (BSEP gene symbol ABCB11) mediates the biliary excretion of nonconjugated bile salts, such as taurocholic acid, glycocholic acid and cholic acid, and therefore is responsible for the formation of the bile acid-dependent bile flow [97, 98]. Its hereditary defect results in the acquisition of PFIC2, a potentially lethal disease which requires liver transplantation [17, 81, 82, 99]. As discussed in Section 12.5.2, the inhibition of BSEP following drug administration may result in cholestasis. [Pg.297]

Aoki, J., Suzuki, H., Sugiyama, Y., Quantitative prediction of in vivo biliary excretion clearance across the bile canalicular membrane from in vitro transport studies with isolated membrane vesicles. Abstract of Millennial World Congress of pharmaceutical Sciences, San Francisco, April 16-20, 2000, p. 92. [Pg.307]

Y., Drug—drug interaction at the biliary excretion process prediction of the potential cholestatic activity using bile canalicular membrane vesicles, Jpn. J. Pharmacol. Ther. 2001, 29S, S243-S245. [Pg.309]


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See also in sourсe #XX -- [ Pg.212 , Pg.239 , Pg.292 , Pg.549 ]




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