Intestinal cells and

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... 

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.

Moussa, M. et al. (2008). Lycopene absorption in human intestinal cells and in mice involves scavenger receptor class B type I but not Nienmann-Pick Cl-like 1. J. Nutr. 138 1432-1436. 

Satoh, Y., Ishikawa, K., Oomori, Y., Takeda, S. and Ono, K. (1992) Bethanechol and a G-protein activator, NaF/AlC13, induce secretory response in Paneth cells of mouse intestine. Cell and Tissue Research 269, 213-220. 

Trypsin is responsible for the activation of chymotrypsin, as well as for a range of other digestive enzymes synthesized in the pancreas. Trypsin itself is formed from its zymogen via digestion by the enzyme enteropeptidase. Enteropeptidase is secreted from intestinal cells and cleaves trypsinogen to trypsin as soon it travels from the pancreas to the intestine. 

Ingested polysaccharides and disaccharides are converted to monosaccharides by intestinal hydrolytic enzymes, and the monosaccharides then enter intestinal cells and are transported to the liver or other tissues. 

Effect of vitamin D on the intestine 1,25-diOH D3 stimulates intestinal absorption of calcium and phosphate. 1,25-diOH D3 enters the intestinal cell and binds to a cytosolic receptor. The 1,25-diOH D3-receptor complex then moves to the nucleus where it selectively interacts with the cellular DNA. As a result, calcium uptake is enhanced by an increased synthesis of a specific calcium-binding protein. Thus, the mechanism of action of 1,25-diOH D3 is typical of steroid hormones (see p. 238). 

Vitamin D3 is a precursor of the hormone 1,25-dihy-droxyvitamin D3. Vitamin D3 is essential for normal calcium and phosphorus metabolism. It is formed from 7-dehydrocholesterol by ultraviolet photolysis in the skin. Insufficient exposure to sunlight and absence of vitamin D3 in the diet leads to rickets, a condition characterized by weak, malformed bones. Vitamin D3 is inactive, but it is converted into an active compound by two hydroxylation reactions that occur in different organs. The first hydroxylation occurs in the liver, which produces 25-hydroxyvita-min D3, abbreviated 25(OH)D3 the second hydroxylation occurs in the kidney and gives rise to the active product 1,25-dihydroxy vitamin D3 24,25 (OH)2D3 (fig. 24.13). The hydroxylation at position 1 that occurs in the kidney is stimulated by parathyroid hormone (PTH), which is secreted from the parathyroid gland in response to low circulating levels of calcium. In the presence of adequate calcium, 25(OH)D3 is converted into an inactive metabolite, 24,25 (OH)2D3. The active derivative of vitamin D3 is considered a hormone because it is transported from the kidneys to target cells, where it binds to nuclear receptors that are analogous to those of typical steroid hormones. l,25(OH)2D3 stimulates calcium transport by intestinal cells and increases calcium uptake by osteoblasts (precursors of bone cells). 

CM and VLDL secreted by intestinal cells and VLDL synthesized and secreted in the liver have similar metabolic fates. After secretion into the blood, newly formed CM and VLDL take up apoprotein (apo-C) from HDL and are subsequently removed from the blood (plasma half-life of less than 1 h in humans [137]) primarily by the action of lipoprotein lipase (LPL). Lipoprotein lipase is situated mainly in the vascular bed of the heart, skeletal muscle, and adipose tissue and catalyzes the breakdown of core TG to monoglycerides and free fatty acids, which are taken up into adjacent cells or recirculated in blood bound to albumin. The activity of LPL in the heart and skeletal muscle is inversely correlated with its activity in adipose tissue and is regulated by various hormones. Thus, in the fasted state, TG in CM and VLDL is preferentially delivered to the heart and skeletal muscle under the influence of adrenaline and glucagon, whereas in the fed state, insulin enhances LPL activity in adipose tissue, resulting in preferential uptake of TG into adipose tissue for storage as fat. 

It is presumed that dietary consumption of fermented milk products facilitates the interaction of immunoregulatory LAB with cells of the GALT system and there is plenty of evidence for the direct interaction of LAB with intra-intestinal lymphoid foci (De Simone et al. 1987, Yasui and Ohwaki 1991). Recent studies have shown that LAB can potentiate the expression of cytokine receptors on IFN-activated human intestinal cells and can regulate immune phenotype and cytokine expression at intestinal sites following oral delivery in mice (Herias et al. 1999, Maassen et al. 2000). 

CCK-PZ 50 113-116), whose C-terminal pentapeptide sequence is identical with that of gastrin, is discharged into the blood from certain intestinal cells and reaches the gallbladder, where it causes the bile to discharge into the intestine, thus promoting digestion. Cholecystokinin also functions as a cerebral neurotransmitter. 

Lipoproteins are fat carriers in the circulation. Figure 19.3 summarizes human lipoprotein traffic. We focus first on the chylomicrons, which are produced in the intestinal cells and are exported into the general circulation via lymph. Chylomicron metabolism is often referred to as exogenous lipoprotein metabolism. 

Other proteins that interact with biotin including egg yolk biotinbinding proteins and biotin transport components from several systems including yeast, mammalian intestinal cells, and bacteria [70-73]. Note that although there are other proteins (e.g., fibropellins) that have a motif [DENY]-jc(2)-[KRI]-[STA]-x(2)-V-G-jc-[DN]-jc[FW]-T-[KR] in common with strept(avidin), most if not all of these protein do not bind biotin (http //www.expasy.org/prosite/). 

The effect different fatty acids have on cholesterolemia is well known. Whatever the kind of the effect (hyper- or hypocholesterolemic), it seems to be more pronounced when the fatty acids are esterified at the inner than at the outer positions of TAGs. The lower hypercholesterolemic effect of saturated fatty acids at the outer positions (64) can be the result of a combination of different factors such as reduced absorption by unabsorbable soap formation, which in turn interferes with cholesterol absorption in the intestinal lumen, partial desaturation and oxidation in the small intestinal cells, and reduced targeting into the fiver (63). The stronger hypocholesterolemic effect of polyunsamrated fatty acids at the i -2-position (65) could be the result of increased influx in the liver (66). 

Zinc sulfate can cause copper deficiency by inducing the production of metaUothionein in intestinal cells and thus lowering copper absorption copper deficiency can lead in turn to sideroblastic anemia (8), neutropenia, and osteopenia (9). 

B. Palmitate is absorbed into the intestinal cell and utilized to synthesize a triacylglycerol, which is packaged in a nascent chylomicron and secreted via the lymph into the blood. 

Cysteine is oxidized to cystine, which may crystallize, forming kidney stones. In Hartnup s disease, the transport of neutral amino adds is defective in both intestinal cells and kidney tubules, resulting in deficiencies of essential amino acids. 

The homeostasis mechanism permits up to 15% of ingested iron to be absorbed while the average person only excretes 0.01% of the intake. During periods of increased demand, such as pregnancy or childhood, absorption of iron is greatly increased. Normally, excess iron is excreted and some is contained within shed intestinal cells and in bile and urine. Smaller amounts are excreted in sweat, nails. 

Gee, J., Wortley, G., Johnson, I., Price, K., Rutten, A., Houben, G., and Penninks, A. (1996). Effect of saponins and glycoalkaloids on the permeability and viability of mammalian intestinal cells and on the integrity of tissue preparations in vitro. Toxic. In Vitro 10,117-128. Gonzalez, J., Roldan, A., Gallardo, T., and Prado, F. (1989). Quantitative determinations of chemical compounds with nutritional value from INCA crop Chenopodium quinoa. Plant Foods Hum. Nutr. 39, 331-337. 

Pharmacology and Mechanism of Action. Active vitamin D suppresses PTH secretion by stimulating absorption of serum calcium (and phosphorus) by intestinal cells and through direct activity on the parathyroid gland to decrease PTH synthesis. As a result, the serum calcium concentration is raised and the parathyroid glands decrease the rate of secretion and formation of PTH. The set point for calcium (i.e., the calcium concentration at which PTH secretion is... 

Heme, one of the most complex molecules synthesized by mammalian cells, has an iron-containing porphyrin ring. As described previously, heme is an essential structural component of hemoglobin, myoglobin, and the cytochromes. Almost all aerobic cells synthesize heme because it is required for the cytochromes of the mitochondrial ETC. The heme biosynthetic pathway is especially prominent in liver, bone marrow, and intestine cells and in reticulocytes (the nucleus-containing precursor cells of red blood cells). Heme is synthesized from the relatively simple components glycine and succinyl-CoA. 

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