Enterocytes duodenal

Nakamura, T., Sakaeda, T., Ohmoto, N., Tamura, T., Aoyama, N. et al., Real-time quantitative polymerase chain reaction for MDR1, MRP1, MRP2, and CYP3A-mRNA levels in Caco-2 cell lines, human duodenal enterocytes, normal colorectal tissues, and colorectal adenocarcinomas, Drug Metab. Dispos. 2002, 30, 4—6. 

There is one known pathway for cellular iron export, involving the export of iron into the plasma from the basolateral membrane of duodenal enterocytes, from macrophages, hepatocytes and a number of other cell types. This involves the protein known as IREG1 or ferroportin described already in Chapter 7. We will discuss ferroportin in more detail in the next section on iron homeostasis, since ferroportin is the target of hepcidin, a recently described iron regulatory peptide. 

Nakamura T, Sakaeda T, Horinouchi M, Tamura T, Aoyama N, Shirakawa T, Matsuo M, Kasuga M, Okumura K. Effect of the mutation (C3435T) at exon 26 of the MDR1 gene on expression level of MDR1 messenger ribonucleic acid in duodenal enterocytes of healthy Japanese subjects. Clin Pharmacol Ther 2002 71(4) 297-303. 

Iron levels are tightly regulated through control of dietary absorption of iron. The duodenum and upper jejunum are the only areas of the body where this occurs. Since nonheme iron forms insoluble complexes when ingested, it must first be converted into soluble complexes. This is accomplished on the apical surface of duodenal villus enterocytes by duodenal ferric reductase, which converts insoluble duodenal ferric (Fe3+) iron into soluble and absorbable ferrous (Fe2+) iron. Iron is then transported across the membrane to the cytoplasm through a transporter known as the divalent metal transporter 1 (DMT-l), a proton sym-porter (Harrison and Bacon, 2003). 

Figure 31-1. A schematic model of HFE regulation of iron transport in duodenal ente-rocytes. A and B correspond to villus and cryptal enterocytes, respectively. As noted, HFE lies at the center of regulation of iron absorption through its role in sensing body iron stores in the villus enterocyte. It communicates this information to the crypt ente-rocyte indirectly through regulation of development of ferroportin and DMT-1. Reprinted with permission from Parkkila et al. (2001). 2001, American Gastroenterological Association.

Trinder, D., Oates, P. S., Thomas, C., Sadleir, J., and Morgan, E. H. (2000). Localisation of divalent metal transporter 1 (DMTl) to the microvillus membrane of rat duodenal enterocytes in iron deficiency, but to hepatocytes in-iron overload [See comments]. Gut 46, 270-276. 

Intestinal absorption of dietary iron. Ferrous iron is absorbed by the duodenal villus tip enterocytes mediated by divalent metal transporter-1 (DMTI). Iron transport mediated by DMTl of the apical surface and the basolateral tran.sporter at the basolateral surface are coupled to ferric reductase and ferroxidase that change the iron oxidation state, respectively. The degree of iron entry is determined by the level of DMTl and its level of expression is programmed in the crypt cells. The programming of the crypt cells is coupled to the body iron stores via transferrin-mediated and HFE protein-modulated iron transport. [Modified and reprinted with permission from B. R. Bacon, L. W. Powell,... 

Dietary riboflavin is present mostly as a phosphate, which is rapidly hydrolyzed before absorption in the duodenum.In humans, the rapid, saturable absorption of riboflavin following an oral dose suggests that it is transported by a carrier-mediated pathway located predominantly in duodenal enterocytes. The process may be sodium-dependent. Bile salts enhance absorption of riboflavin. Fecal riboflavin is derived from the intestinal mucosa and the intestinal flora. This is the predominant excretory route for the vitamin. 

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. 

It has recently been discussed [61-63] whether the diffusional barrier at the intestinal surface can be accounted for solely by an unstirred water layer. It has been proposed that the mucus layer overlying the enterocytes should be regarded as an important diffusion barrier for uptake of lipid solutes from the luminal contents. The mucus adherent to the rat duodenal wall has been found to be approximately 80 jam thick in the fasted state [64]. The intestinal mucus coat is formed by proteoglycans produced by goblet cells, but so far very little is known about the molecular structure of the mucus layer [65]. The possible interaction between mucus constituents and luminal lipid solutes needs to be investigated in detail, since it might reveal key factors which constitute the diffusional barrier of the small intestine. 

Ferrireductases and ferroxidases Ceruloplasmin (Cp) Duodenal cytochrome b Hephaestin Steap proteins Plasma protein with ferroxidase activity involving in cellular iron export Membrane ferric reductase involving in cellular iron uptake Membrane Cp homolog functioning in enterocyte iron export Ferrireductases required for iron uptake in Tf cycle... 

Tekaya, L. Ayadi, A. et al. (2005). "Selective mineral elements concentration of the intestinal mucosa role of the lysosomes of duodenal enterocytes in the handling of mineral elements after intragastric administration." Cell Mol Biol, (Noisy-le-grand), 51, Suppl OL819-27. 

Dietary retinyl esters must be hydrolyzed in the lumen of the small intestine before retinol is absorbed, while carotenoids must be absorbed into the intestinal mucosa before being cleaved intracel-lularly. Several enzymes with retinyl ester hydrolase (REH) activity are present in pancreatic juice or on the brush border of duodenal and jujenal enterocytes (Figure 3). Retinol and carotenoids must be solubilized in the lumen in mixed micelles composed of bile acids and products of lipid digestion prior to their uptake into enterocytes. These processes require the release of an adequate amount of bile... 

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