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Small intestine goblet cells

Ishikawa, N., Horii, Y. and Nawa, Y. (1993) Immune mediated alteration of the terminal sugars of goblet cell mucins in the small intestine of Nippostrongylus brasiliensis infected rats. Immunology 78, 303-307. [Pg.370]

Leblond, C.P. and Messier, B. (1958) Renewal of chief cells and goblet cells in the small intestine as shown by radioautography after injection of thymidine-H3 into mice. Anatomical Record 132, 49—58. [Pg.372]

Paulus, U., Loeffler, M., Zeidler, J., Owen, G. and Potten, C.S. (1993) The differentiation and lineage development of goblet cells in the murine small intestinal crypt experimental and modelling studies. Journal of Cell Science 106, 473-484. [Pg.374]

Fig. 1. Small intestine formaldehyde-fixed, paraffin-embedded. Section was stained with Concanavilin A conjngated to 5-nm colloidal gold. The gold was then silver-enhanced. Staining of mucous on the cell snrface and in goblet cells is seen. Fig. 1. Small intestine formaldehyde-fixed, paraffin-embedded. Section was stained with Concanavilin A conjngated to 5-nm colloidal gold. The gold was then silver-enhanced. Staining of mucous on the cell snrface and in goblet cells is seen.
The gastrointestinal system of zebrafish presents clear differences from the human system. The zebrafish does not possess a stomach, the intestine is continuous with the pharynx through a short esophagus, and no sphincters are present [61]. However, zebrafish have most of the cell types observed in the small intestine -absorptive, endocrine, goblet, and interstitial cells of Cajal, although Paneth cells are absent. Gut contractions are under the control of the enteric nervous systems, which respond to different pharmaceuticals in similar way as the mammalian counterpart. For example, zebrafish embryos can be used as predictor of emetic response to pharmaceuticals, one of the most commonly reported clinical adverse effects to be considered in the development of new dmgs [61]. [Pg.408]

The major saccharidase of the small intestine is amylase that digests starch to the disaccharide maltose and the trisaccharide maltotriose. Intestinal mucus is secreted by goblet cells, which either ooze (constitutive basal secretion) or burst as a result of stimuli. In the last mode of secretion condensed mucus gel granules can expand 500-fold within 20 ms [20]. [Pg.7]

Q2 Unlike the small intestinal mucosa, the colonic mucosa does not contain any villi. There are columnar epithelial cells and mucus-secreting goblet cells in the mucosa the columnar epithelium reabsorbs fluid and electrolytes. [Pg.279]

The surface of the mucosa is relatively smooth as there are no intestinal villi. Crypts of Lieberktlhn are present. Goblet cells account for more of the epithehal cells than in the small intestine. The mammalian large intestine is important for the maintenance of water and electrolyte balance. Its primary function is the reabsorption of water, sodium, chloride and volatile fatty acids it secretes potassium and bicarbonate. [Pg.89]

A one-cell thick sheet of epithelial cells covers the surfaces of the villi and lines of crypts. Some of the cell types identified in the epithelial lining of the small intestine are enterocytes (digestion and absorption), goblet cells (mucus secretion), endocrine cells (hormone secretion), and M cells (absorption of food and antigens). [Pg.2714]

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. [Pg.412]

Figure 9.1 shows an overview of protein metabolism in addition to the dietary intake of about 80 g of protein, almost the same amount of endogenous protein is secreted into the intestinal lumen. There is a small faecal loss equivalent to about 10 g of protein per day the remainder is hydrolysed to free amino acids and small peptides, and absorbed (section 4.4.3). The faecal loss of nitrogen is partly composed of undigested dietary protein, but the main contributors are intestinal bacteria and shed mucosal cells, which are only partially broken down, and the protective mucus secreted by intestinal mucosal goblet cells (see Figure 4.2). Mucus is especially resistant to enzymic hydrolysis, and contributes a considerable proportion of inevitable losses of nitrogen, even on a protein-free diet. Figure 9.1 shows an overview of protein metabolism in addition to the dietary intake of about 80 g of protein, almost the same amount of endogenous protein is secreted into the intestinal lumen. There is a small faecal loss equivalent to about 10 g of protein per day the remainder is hydrolysed to free amino acids and small peptides, and absorbed (section 4.4.3). The faecal loss of nitrogen is partly composed of undigested dietary protein, but the main contributors are intestinal bacteria and shed mucosal cells, which are only partially broken down, and the protective mucus secreted by intestinal mucosal goblet cells (see Figure 4.2). Mucus is especially resistant to enzymic hydrolysis, and contributes a considerable proportion of inevitable losses of nitrogen, even on a protein-free diet.

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