Intestine, cells

Food vitamin B 2 appears to bind to a saUvary transport protein referred to as the R-protein, R-binder, or haptocorrin. In the stomach, R-protein and the intrinsic factor competitively bind the vitamin. Release from the R-protein occurs in the small intestine by the action of pancreatic proteases, leading to specific binding to the intrinsic factor. The resultant complex is transported to the ileum where it is bound to a cell surface receptor and enters the intestinal cell. The vitamin is then freed from the intrinsic factor and bound to transcobalamin II in the enterocyte. The resulting complex enters the portal circulation. 

B. Evaluation of Cell Membrane Affinity In Vivo Interaction with Rat intestinal Cells... 

Importantly, both incretins when secreted by the intestine are rapidly degraded by the dipeptidyl peptidase IV (DPPFV), which removed the two amino-terminus histidine-alanine residues, thereby, inactivating the incretins. This enzyme is present at the surface of the epithelial intestinal cells and capillaries in the vicinity of the K and L cells secreting GIP and GLP-1, respectively. It is also present in the... 

Expression (Mouse) Tissues lungs, Cells myeloid leukocytes, neutrophils, T-cells, macrophages, mast cells, eosinophils Tissues lung, skin, small intestine Cells macrophages, fibroblasts, leukocytes Tissues lung, skin, brain, small intestine, spleen Cells macrophages, fibroblasts, endothelial cells, leukocytes... 

In addition to the described lipid pathways mainly operative in macrophages, two further ABC-transporteis, ABCG5 and ABCG8 have been implicated in the efflux of dietary sterols from intestinal cells back into the gut lumen and from liver to the bile duct (Fig 1). Both ABC-transporters form a functional heterodimer with highest expression levels in liver and intestine and are regulated... 

There are striking similarities in the mechanisms of formation of chylomicrons by intestinal cells and of VLDL by hepatic parenchymal cells (Figure 25—2), perhaps because—apart from the mammary gland—the intestine and liver are the only tissues from which particulate lipid is secreted. Newly secreted or nascent chylomicrons and VLDL contain only a small amount of apolipoproteins C and E, and the frill complement is acquired from HDL in the circulation (Figures 25—3 and 25-4). Apo B is essential for chylomicron and VLDL formation. In abetalipoproteinemia (a rare disease), lipoproteins containing apo B are not formed and lipid droplets accumulate in the intestine and liver. 

Figure 25-2. The formation and secretion of (A) chylomicrons by an intestinal cell and (B) very low density lipoproteins by a hepatic cell. (RER, rough endoplasmic reticulum SER, smooth endoplasmic reticulum G, Golgi apparatus N, nucleus C, chylomicrons VLDL, very low density lipoproteins E, endothelium SD, space of Disse, containing blood plasma.) Apolipoprotein B, synthesized in the RER, is incorporated into lipoproteins in the SER, the main site of synthesis of triacylglycerol. After addition of carbohydrate residues in G, they are released from the cell by reverse pinocytosis. Chylomicrons pass into the lymphatic system. VLDL are secreted into the space of Disse and then into the hepatic sinusoids through fenestrae in the endothelial lining.

Figure 41-14. The transcellular movement of glucose in an intestinal cell. Glucose follows Na+ across the luminal epithelial membrane. The Na+ gradient that drives this symport is established by Na+ -K+ exchange, which occurs at the basal membrane facing the extra-ceiiuiarfiuid compartment. Glucose at high concentration within the ceii moves "downhill" into the extracel-iuiarfiuid by fadiitated diffusion (a uniport mechanism).

The 25-OH-D Is further metabolized In the kidney to 1,25 dlhydroxycholecalclferol (1,25(OH)2D) which Is considered to be the major physiologically Important, tissue-active metabolite of vitamin D. It circulates In extremely low concentrations (< 100 pg/ml of serum). Assay of 1,25(OH)2D Is extremely tedious. It Is done by competitive binding technique using a combined Intestinal cell cytosol and chromatin binding system, biosynthetic 3h-1,25(OH)2D3 as labeled ligand and synthetic 1,25(0H)2D3 as standard (31). 

Based on the limitations of using human subjects, simple alternative in vitro models were developed to investigate mechanisms involved in the intestinal absorption process of a compound of interest and to screen the relative bioavailability of a compound from various food matrices. However, the data generated from in vitro approaches must be taken with caution because they are obtained under relatively simplified and static conditions compared to dynamic physiological in vivo conditions. Indeed, the overall bioavailability of a compound is the result of several complex steps that are influenced by many factors including factors present in the gastrointestinal lumen and intestinal cells as described later. Nevertheless, these in vitro approaches are useful tools for guiding further smdies in humans. 

In the in vitro digestion method, the compound of interest is transferred from the food matrix to a bile salt micelle suspension that simulates the in vivo digestion process. This in vitro digestion procedure was first developed to estimate iron availability from meals and since then has been modified and applied to studying carotenoid bioaccessibility from various food matrices. This approach assesses the bioaccessibility of the compound from a certain meal before it is presented to and taken up by intestinal cells. 

In intestinal cells, carotenoids can be incorporated into CMs as intact molecules or metabolized into mainly retinol (or vitamin A), but also in retinoic acid and apoc-arotenals (see below for carotenoid cleavage reactions). These polar metabolites are directly secreted into the blood stream via the portal vein (Figure 3.2.2). Within intestinal cells, retinol can be also esterified into retinyl esters. 

During, A., Albaugh, G., and Smith, J.C., Characterization of 3-carotene 15,15-dioxygenase activity in TC7 clone of human intestinal cell line Caco-2 cells, Biochem. Biophys. Res. Commun., 249, 467, 1998. 

Ferruzzi, M.G., Failla, M.L., and Schwartz, S.J., Assessment of degradation and intestinal cell uptake of carotenoids and chlorophyll derivatives from spinach puree using an in vitro digestion and Caco-2 cell model, J. Agric. Food Chem., 49, 2082, 2001. 

Chitchumroonchokchai, C., Schwartz, S.J., and Failla, M.L., Assessment of lutein bioavailability from meals and a supplement using simulated digestion and Caco-2 human intestinal cells, J. Nutr, 134, 2280, 2004. 

Although the above profusion of in vivo studies evidence their health potentialities, the problem of the bioavailabihty of proanthocyanidins supplied by dietary supplementation has still not been completely resolved since unequivocal evidence for absorption is missing so far [11]. However, studies carried out using radio-labelled procyanidins revealed that dimers and trimers may be absorbed by intestinal cells, whereas a recent study demonstrated that procyanidin oligomers are readily adsorbed in rats [55], while it has been shown that colon microflora may be able to degrade proanthocyanidins to low-molecular-weight aromatic compounds [56]. 

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... 

There are circumstances, however, where blood flow to the GIT may influence drug absorption. Those compounds absorbed by active or specialized mechanisms require membrane participation in transport, which in turn depends on the expenditure of metabolic energy by intestinal cells. If blood flow and therefore oxygen delivery is reduced, there may be a reduction in... 

The membrane surface facing the lumen is called the apical surface, and the membrane surface on the side facing blood is called the basolateral surface. The intestinal cells are joined at the tight junctions [63,75]. These junctions have pores that can allow small molecules (MW < 200 Da) to diffuse through in aqueous solution. In the jejunum, the pores are 7-9 A in size. In the ileum the junctions are tighter, and pores are 3-4 A in size (i.e., dimensions of mannitol) [63]. 

Dauer larva Lateral hypodermis, SM, VPC, intestinal cells... 

Figure 6 Intestinal cell membrane model with integral membrane proteins embedded in lipid bilayer. The phospholipid bilayer is 30-45 A thick, and membrane proteins can span up to 100 A through the bilayer. The structure of a typical phospholipid membrane constituent, lecithin is illustrated. (From Ref. 76.)...

Zweibaum A, M Laburthe, E Grasset, D Louvard. (1991). Use of cultured cell lines in studies of intestinal cell differentiation and function. In M Field, CA Frizzell, eds. Handbook of Physiology, Section 6, The Gastrointestinal System, Vol. IV, Intestinal Absorption and Secretion. Bethesda, MD Am Physiol Society, pp 223-255. 

O Sullivan, L, Ryan, L, and O Brien, N, 2007. Comparison of the uptake and secretion of carotene and xanthophyll carotenoids by Caco-2 intestinal cells. Br J Nutr 98, 38 -4. 

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