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Intestine secretory cell

INTESTINE Characterization of a membrane potassium ion conductance in intestinal secretory cells using whole cell patch-clamp and calcium-sensitive dye techniques, 192, 309 isolation of intestinal epithelial cells and evaluation of transport functions, 192, 324 isolation of enterocyte membranes, 192, 341 established intestinal cell lines as model systems for electrolyte transport studies, 192, 354 sodium chloride transport pathways in intestinal membrane vesicles, 192, 389 advantages and limitations of vesicles for the characterization and the kinetic analysis of transport systems, 192, 409 isolation and reconstitution of the sodium-de-pendent glucose transporter, 192, 438 calcium transport by intestinal epithelial cell basolateral membrane, 192, 448 electrical measurements in large intestine (including cecum, colon, rectum), 192, 459... [Pg.452]

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]

Figure 7.4 Fate of triacylglycerol that is present in fuel blood after secretion by the intestine. The dietary triacylglycerol in the intestine is hydrolysed to long-chain fatty acids and monoacyl-glycerol, both of which are taken up by the enterocytes in which they are then re-esterified. The triacylglycerol is released in the form of chylomicrons into the blood, from where it is hydrolysed to fatty acids and glycerol by the enzyme lipoprotein lipase in specific tissues (Figure 7.3). The fatty acids are taken up by adipocytes, muscle fibres and secretory cells in the mammary gland. Figure 7.4 Fate of triacylglycerol that is present in fuel blood after secretion by the intestine. The dietary triacylglycerol in the intestine is hydrolysed to long-chain fatty acids and monoacyl-glycerol, both of which are taken up by the enterocytes in which they are then re-esterified. The triacylglycerol is released in the form of chylomicrons into the blood, from where it is hydrolysed to fatty acids and glycerol by the enzyme lipoprotein lipase in specific tissues (Figure 7.3). The fatty acids are taken up by adipocytes, muscle fibres and secretory cells in the mammary gland.
A highly simplified diagram of the intestinal wall and some of the circuitry of the enteric nervous system (ENS). The ENS receives input from both the sympathetic and the parasympathetic systems and sends afferent impulses to sympathetic ganglia and to the central nervous system. Many transmitter or neuromodulator substances have been identified in the ENS see Table 6-1. ACh, acetylcholine AC, absorptive cell CM, circular muscle layer EC, enterochromaffin cell EN, excitatory neuron EPAN, extrinsic primary afferent neuron 5HT, serotonin IN, inhibitory neuron IPAN, intrinsic primary afferent neuron LM, longitudinal muscle layer MP, myenteric plexus NE, norepinephrine NP, neuropeptides SC, secretory cell SMP, submucosal plexus. [Pg.110]

ATP-dependent ABC transporter family. However, it is atypical because it also contains a regulated chloride channel) In secretory epithelia of intestines, pancreas, lungs, sweat glands, and kidneys Cl enters epithelial cells through their basolateral surfaces using an Na+ + K+ + 2 Cl cotransporter and exits the cells through their apical surfaces using the CFTR channel. Absorptive epithelia also contain both the cotransporter and the CFTR channel, but Cl flows into the cells from the exterior surface, and the distribution of the cotransporter and CFTR between basolateral and apical surfaces is opposite to that in secretory cells.1... [Pg.1513]

As mentioned above, the villi of the small intestine (Figure 1.2) house a dynamic, self-renewing population of the epithelial cells that includes absorptive cells (enterocytes), secretory cells, and endocrine cells. The thin lining (height 25 p,M height of the microvilli is 1.5 pM) of the columnar enterocytes is the only barrier between the intestinal lumen and the muscularis mucosa, which represents, in this context, the entire body interior. The entire epithelial lining of the intestine replaces itself every 3-5 d [128], It is the enterocyte and its neighboring cells where absorption processes occur and it will therefore be the focus of the mechanistic discussions below. [Pg.18]

Secretory cells occur in most epithelial surfaces e.g., sweat gland cells in the skin and mucus-secreting cells in the intestine and respiratory tract. [Pg.17]

The gut contains a collection of nerves called the enteric nervous system. Various activities of the gut, such as peristaltic contractions, and certain activities of the pancreas and gall bladder, are controlled in a manner that is relatively independent of the central nervous system. The central nervous system consists of the brain and spinal cord. Five type,s of activity are controlled by the enteric nervous system (1) contraction of smooth muscles that create the peristaltic waves used to mix and propel food through the intestines (2) release of juices by secretory cells (5) release of hormones from endocrine ceils of the gut (4) patterns of blood flow through the arteries of the gut (variations in blood flow occur because of the opening of blood vessels (vasodilation) or the dosing of blood vessels (vasoconstriction)] and (5) activities of immune cells of the gut (GoyaI and Hirano, 1996). [Pg.58]

Cells throughout the gastrointestinal tract release somatostatin. Somatostatin inhibits acid secretion in the stomach and it promotes absorption of sodium, chloride and water in the small intestine and colon (Krejs 1986). The somatostatin analogs octreotide and lanreotide have been shown to decrease intestinal secretion in animal models (Botella et al 1993) and in humans with specific metabolic intestinal secretory disorders however, these drugs are not used widely in human medicine. In one study in horses, octreotide was shown to decrease gastric acidity (Sojka et al 1992) but its effects on intestinal or colonic secretion in horses have not been reported. [Pg.93]

Milano J, McKay J, Dagenais C, et al. Modulation of notch processing by gamma-secretase inhibitors causes intestinal goblet cell metaplasia and induction of genes known to specify gut secretory lineage differentiation. Toxicol Sci. 2004 82(l) 341-358. [Pg.241]

Two phase I clinical trials have tested the regimen of 72-h continuous infusion every two weeks in humans (83, 84). Seventy-six patients were treated in the NCI phase I trial. The dose-limiting toxicity (DLT) was secretory diarrhea with a maximally tolerated dose (MTD) of 50 mg/m2/day for 3 days. Flavopiridol was later found to induce chloride ion secretion in intestinal epithelial cells (85) and to have an enterohepatic circulation that may play a role in potentiating this toxicity (86). With antidiarrheal prophylaxis a higher MTD is reachable at 78 mg/m2/day for 3 days with orthostatic hypotension as the DLT. At the MTD in this study,... [Pg.208]

Only two types of lipoproteins, VLDL and chylomicrons, are fully formed within cells by assembly in the ER, a process that requires the activity of microsomal transfer protein. The assembled particles move through the secretory pathway to the cell surface and are released by exocytosis—VLDL from liver cells and chylomicrons from intestinal epithelial cells (see Figure 18-10b). LDLs, IDLs (intermediate-density lipoproteins), and some HDLs are generated extracellularly in the bloodstream and on the surfaces of cells by the remodeling of secreted VLDLs and chylomicrons. There are four types of modifications ... [Pg.758]


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