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Enterocytes jejunal

Although infection with C. parvum is considered predominantly secretory, histopathologic studies have revealed varying degrees of villous atrophy and infiltration of inflammatory cells beneath the epithelial mucosa [85, 86], Prostaglandins, which are known to induce cAMP-mediated apical chloride secretion and inhibit electroneutral sodium chloride and water absorption in enterocytes, have been demonstrated to be elevated in a porcine model of cryptosporidiosis [87], Inflammatory cytokines such as IL-1, IL-8 and TNF-a are induced in intestinal epithelial cell lines infected with Cryptosporidium and in animal models of cryptosporidiosis and have been postulated to play a role in pathogenesis [88, 89], Expression of TNF-a and IL-1 mRNA in the majority of jejunal biopsies of adult volunteers after experimental infection were also observed, although this did not correlate with the enteric symptoms [90]. [Pg.28]

Duszka, C., Grolier, P, Azim, E., Alexandte-Couabau, M.-C Bore), P and A ais-Braesco, V. (1996). Rat intestinal -caroteoe ctioxygenase activity is located primarily in the cytosol of mature jejunal enterocytes. /. jVirfr. 126,2550-2556. [Pg.659]

Shed enterocytes constitute a very elegant cellular in vitro model of human gut metabolism [133]. About 15-30 million enterocytes are shed per minute into the lumen of the gastrointestinal tract, and these cells can be collected by segmental jejunal perfusion from healthy volunteers. The majority of shed enterocytes collected this way were nonapoptotic and metabolically fully competent. Obstacles to more widespread use of this tool are the still very limited availability and very high price. [Pg.345]

Intestinal Receptor for IF-B 2 Complex. Although this receptor is not, strictly speaking, a cobalamin-binding protein, it is essential for normal absorption of dietary cobalamin. It is present on the membrane of microvilli of ileal but not jejunal or duodenal cells, with the highest concentration in the distal 60-cm portion of the small intestine. The purified receptor is composed of two subunits (M.W. 90,(X)0 and 140,000) and binds free IF and IF-B12 complex, although free IF binds more slowly. Subsequent transport of cobalamin into enterocytes is accomplished by an active process. [Pg.922]

Recent data indicate that ezetimibe inhibits a specific transport process in jejunal enterocytes, which take up cholesterol from the lumen. The putative transport protein is Niemann-Pick Cl-hke 1 protein (NPCILI). In wild-type mice, ezetimibe inhibits cholesterol absorption by about 70% in NPCILI knockout mice, cholesterol absorption is 86% lower than in wild-type mice, and ezetimibe has no effect on cholesterol absorption. Ezetimibe does not affect intestinal triglyceride absorption. In human subjects, ezetimibe reduced cholesterol absorption by 54%, precipitating a compensatory increase in cholesterol synthesis, which can be inhibited with a cholesterol synthesis inhibitor such as a statin. There is also a substantial reduction of plasma levels of plant sterols (campesterol and sitosterol concentrations are reduced by 48 and 41%, respectively), indicating that ezetimibe also inhibits intestinal absorption of plant sterols. [Pg.261]

Both ischaemia (clamping of the superior mesenteric artery for 30,60, 90 min) and ischaemia/reperfusion affected respiratory function of isolated rat enterocyte mitochondria as compared to control (Madesh et al. 2000). Preconditioning with nitric oxide donor, sodium nitroprusside (1 mM, given into the proximal jejunal lumen at a rate of 1 ml/ min), significantly enhanced the recovery of the respiratory control rate. Mitochondrial lipid changes suggestive of activation of phospholipase... [Pg.623]

Ezetimibe is a selective inhibitor of the Niemaim-Pick Cl like 1 cholesterol transporter protein, which is expressed on the brush border membrane of the small intestine, and blocks the transport of dietary and biliary cholesterol into the jejunal enterocyte without reducing the absorption of fat-soluble vitamins, TG or bile acids. Ezetimibe may also block the hepatic reabsorption of biliary cholesterol and further augment the elimination of cholesterol. [Pg.677]


See other pages where Enterocytes jejunal is mentioned: [Pg.177]    [Pg.167]    [Pg.170]    [Pg.178]    [Pg.178]    [Pg.179]    [Pg.46]    [Pg.482]    [Pg.494]    [Pg.495]    [Pg.2715]    [Pg.136]    [Pg.197]    [Pg.199]    [Pg.205]    [Pg.206]    [Pg.206]    [Pg.208]    [Pg.418]    [Pg.54]    [Pg.30]    [Pg.374]    [Pg.380]    [Pg.11]    [Pg.132]   
See also in sourсe #XX -- [ Pg.177 ]




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