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Uptake by enterocyte

COMPETITION DURING UPTAKE BY ENTEROCYTES 18.2.1 Competition between Carotenoids... [Pg.382]

Increasing the uptake of antigens by enterocytes may represent an alternative means for oral vaccine delivery. It is, however, commonly believed that antigen uptake by enterocytes leads to the production of antigen tolerance rather than immunity (Brayden and Baird 2001). [Pg.198]

Matsuno K, Schaffher T, Gerbel HA, et al. Uptake by enterocytes and subsequent translocation to internal organs, EG, the thymus, of percoU microspheres administered per OS to suckling mice. J Reticuloendothelial Soc 1983 33 263-273. [Pg.382]

The claimed health-promoting activities exerted by bifidobacteria are numerous, and include establishment of a healthy microbiota in preterm infants, cholesterol reduction, lactose intolerance, prevention of infectious diarrhea, prevention of cancer, protection against infectious diseases, modulation of mucosal barrier function, amino acid and vitamin production, inhibition of nitrate reduction, stimulation of calcium uptake by enterocytes, short-chain fatty acid production, stimulation of intestinal epithelia through induction of anti-inflammatory c5dokine interleukin (IL)-IO and junctional adhesion molecules. ... [Pg.44]

Production of Mucosal Damage 2.3.1.2.1 Cell culture Stimulated neutrophils are known to be cytotoxic to cells in vitro (Dull et al., 1987 Dallegri et al., 1990 Grisham et al., 1990b). Several in vitro systems have been used to demonstrate oxidative damage to intestinal cells. Xanthine/XO increased Cr release and decreased [ H]thymidine uptake by IEC-18 small intestinal epithelial cell monolayers in a dose-dependent manner (Ma et al., 1991). Rat enterocytes show decreased trypan blue exclusion and increased protein release when incubated with neutrophils stimulated... [Pg.149]

In summary, Caco-2 cells studies strongly suggest that carotenoids interact with each other at the level of cellular uptake by the enterocyte. This phenomenon has been explained by the fact that the uptake of several carotenoids involves, at least in part, the same intestinal membrane transporter the scavenger receptor class B type ISR-BI (Reboul et al. 2005, van Bennekum et al. 2005, Moussa et al. 2008). [Pg.383]

Some of the glutamine that is absorbed is metabolised in the enterocytes. It is used, along with glucose, as a fuel to generate ATP (Chapter 8). The ammonia and the alanine that are produced enter the blood for uptake by the liver. [Pg.81]

B. Dietary lipids are processed by several pancreatic lipases, whose actions facilitate uptake by intestinal epithelial cells (enterocytes). [Pg.103]

Calonge, M.L., Iludian. A., Bolufer, J. (1989). Ionic dependence of glycylsarcosine uptake by isolated chicken enterocytes. J. Cell. Physiol. 138,579-585. [Pg.115]

In case of local gastrointestinal treatments nucleic acid drugs shall be taken up by enterocytes, usually through endocytosis. The route of uptake determines, subsequently, nucleic acid trafficking and lifetime in the cell. Endocytosis is a multistep process involving binding, internalization, formation of endosomes, fusion with lysosomes, and lysis. The low pH and enzymes within... [Pg.225]

Vitamin E, like neutral lipids, requires apoB lipoproteins at every stage of its transport (Fig. 27-2). Dietary vitamin E becomes emulsified in micelles produced during the digestive phase of lipid absorption and permeates the intestinal epithelium, similar to fatty acids and cholesterol. Uptake of vitamin E by enterocytes appears to be concentration dependent. Within intestinal cells, vitamin E is packaged into chylomicrons and secreted into lymph. During blood circulation of chylomicrons, some vitamin E may be released to the tissues as a consequence of partial lipolysis of these particles by endothelial cell-anchored lipoprotein lipase. The rest remains associated with chylomicron remnants. Remnant particles are mainly endocy-tosed by the liver and degraded, resulting in the release of fat-soluble vitamins. [Pg.296]

Uptake of cholesterol by enterocytes is mediated by the transporter NPCILI (Niemann-Pick Cl-like 1), located on the lumen surface. ACAT orchestrates the... [Pg.102]

A second member of the ceruloplasmin family multicopper oxidases with six BCB domains was recently identified as the causative agent of sex-linked anemia (sla) in mice (Vulpe et al., 1993). It was named hephaes-tin and shown to be expressed mostly in the small intestine and the colon, where it is presumably involved in gastrointestinal iron uptake. Hephaes-tin displays a high level of sequence identity to ceruloplasmin and differs from it only by an additional C-terminal transmembrane domain, which anchors the protein to the cell membrane. A 582-nucleotide in-frame deletion in the mRNA for hephaestin sla mice has been identified compared to normal animals. The mice with such a mutation are unable to release iron from enterocytes (intestinal epithelial cells) into the circulation, which results in severe anemia. The GPI-anchored form of ceruloplasmin could potentially also mediate similar cellular iron efflux in the central nervous system. There is a transferrin-independent iron uptake system that requires Fe(III) to be reduced to Fe(II) at the cell surface for uptake to occur (DeSilva et al., 1996). Ceruloplasmin would oxidize Fe and prevent its uptake by this mechanism. Briefly, the role of ceruloplasmin is most likely to prevent excessive intracellular iron accumulation by tightly controlling iron efflux and inhibiting its uptake. [Pg.321]

Biotin uptake into enterocytes is by a sodium-dependent carrier, which also transports pantothenic acid (Section 12.2) and lipoic acid, but is inhibited by biocytin and dethiobiotin. The carrier is found in both the small intestine and the colon, so both biotin and pantothenic acid synthesized by intestinal bacteria can be absorbed (Chatterjee etal., 1999 Ramaswamy, 1999 Said, 1999 Prasad and Ganapathy, 2000). Even at relatively high intakes (up to 80 /rmol), biotin is more-or-less completely absorbed (Zempleni and Mock, 1999b). [Pg.325]

Degradation in the gut is caused by endogenous proteases such as trypsin and a-chymotrypsin. Entrapment of macromolecules in liposomes results in better protection against proteolysis [30], Since lipid-soluble molecules are absorbed quickly in the gut, it could be expected that liposome delivery will give enhanced absorption by diffusion. However, this problem is not simple, as illustrated by the lack of uptake of liposomes by enterocytes [30,31]. Insulin entrapped in liposomes is absorbed in this way [32],... [Pg.13]

The various esters of cholesterol, retinoyl esters, esters of vitamin D and E, probably depend solely on the activity of carboxylester lipase for their hydrolysis. They are, before their uptake by the enterocytes, transformed into the corresponding alcohols to form mixed micelles with bile salts. Carboxylester lipase catalyzes not only the cleavage of esters but also their formation. The most studied example is the reversible esterification of cholesterol, which is favored by low bile salt concentrations and pH [42]. Additionally, the laige specificity of carboxylester lipase probably functions as a first-line detoxification mechanism for a broad variety of orally ingested xenobiotics. [Pg.201]

In the lumen of the small intestine, dietary fat does not only meet bile salt but the much more complex bile in which bile salts are about half saturated with lecithin in a mixed micellar system of bile salt-lecithin-cholesterol. On dilution in the intestinal content, the micelles grow in size as the phase limit is approached and large disk-like micelles form which fold into vesicles [49]. These changes are due to the phase transition that occurs when the bile salt concentration is decreased and the solubility limit for lecithin in the mixed micelles is exceeded. The information is mostly derived from in vitro studies with model systems but most probably is applicable to the in vivo situation. What in fact takes place when the bile-derived lamellar bile salt-lecithin-cholesterol system meets the partly digested dietary fat can only be pictured. Most probably it involves an exchange of surface components, a continuous lipolysis at the interphase by pancreatic enzymes and the formation of amphiphilic products which go into different lamellar systems for further uptake by the enterocyte. Due to the relatively low bile salt concentration and the potentially high concentration of product phases in intestinal content early in fat digestion, the micellar and monomeric concentration of bile salt can be expected to be low but to increase towards the end of absorption. [Pg.410]


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