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Bile-stimulant

Several studies have been conducted on calcium-fat interactions in human infants (64-70). Low synthesis of bile salts and low pancreatic lipase activity may be responsible for poorer fat utilization in infants than in adults (63,71). Fat from infant formulas may be lower than that from human milk because of the lack of a bile-stimulated lipase in the former (72). In infants, fat absorption tends to decrease with increase in fatty acid length, with lower degree of saturation, and with increase of total fat (3). Triglyceride structure may also influence fat absorption in the infant and, thus, indirectly, might also affect calcium absorption in the infant. [Pg.180]

Fig. 9.1. Evagination of protoscoleces of Echinococcus granulosus with and without bile treatment. Although bile stimulates immediate evagination, the percentage of worms finally evaginating is almost the same, with or without bile. (After Smyth, 1967.)... Fig. 9.1. Evagination of protoscoleces of Echinococcus granulosus with and without bile treatment. Although bile stimulates immediate evagination, the percentage of worms finally evaginating is almost the same, with or without bile. (After Smyth, 1967.)...
Several references on herbal safety contraindicate the use of turmeric in persons with biliary tract obstruction (Brinker 2001 De Smet 1993 Mills and Bone 2005) due to reported bile-stimulating activity (De Smet 1993) observed in rats administered the compound curcumin (Bhat et al. 1984), and gallbladder contraction (50% contraction after 40 mg dose) observed in humans administered the compound curcumin (Rasyid et al. 2002). Such concerns are theoretical, and no clinical evidence for turmeric has been reported to support or refute these concerns. [Pg.291]

Although ginger has been reported to have antiplatelet activity (Srivastava 1984), thus slowing blood clotting, human studies have not demonstrated any antiplatelet activity (Bordia et al. 1997 Janssen et al. 1996 Lumb 1994 Srivastava 1989). Bile-stimulating effects have been reported in animal studies (Srinivasan and Sambaiah 1991 Yamahara et al. 1985). [Pg.949]

The mechanism by which sucralfate accelerates healing of duodenal ulcers has not been determined. It does not have significant antisecretory, acid neutralizing activity or direct stimulation of ulcer healing. It is known that the mechanism is local rather than systemic. Binding of pepsin or bile salts may contribute to its effect. It is indicated for the short-term therapy of active duodenal ulcers and for maintenance at reduced dosage. [Pg.199]

It is important to note that diet is a complex mixture that contain compounds with varying activity. Chemical stimulators of colon cancer growth include bile acids, 1,2-diglycerides and prostaglandins which stem from consumption of fat. In contrast, fruits and vegetables contain substances such as carotenoids, flavonoids and fibre, which may inhibit cancer cell growth, and the risk of colon cancer appears to be mirrored by the ratio of plant sterols to cholesterol in the... [Pg.126]

Proton Pump Inhibitors and Acid Pump Antagonists retinoid X receptor (RXR) and is also activated by various lipophilic compounds produced by the body such as bile acids and steroids. PXR heterodimerized with RXR stimulates the transcription of cytochrome P450 3A monooxygenases (CYP3A) and other genes involved in the detoxification and elimination of the... [Pg.998]

Phytochemicals influence other digestive secretions. Several traditional herbal medicines stimulate gastric mucous secretion, providing protection (Sairam et al., 2001). The secretion and recycling of bile are also responsive to phytochemicals. The way in which certain polysaccharides increase fecal concentrations of bile acids (DalT Angelo and Lino van Poser, 2000) and thereby influence recycling and synthesis is particularly noteworthy. [Pg.166]

Dietary fats, libers, and other carotenoids have been reported to interfere with carotenoid bioaccessibility. It is clear that by their presence in the gut, lipids create an environment in favor of hydrophobic compounds such as carotenoids. When arriving in the small intestinal lumen, dietary fats stimulate bile flow from the gallbladder and therefore enhance the micelle formation, which in turn could facilitate the emulsification of carotenoids into lipid micelles. Without micelle formation, carotenoids are poorly absorbed a minimum of 3 g of fat in meal is necessary for an efficient absorption of carotenoids, except for lutein esters that require higher amounts of fat. ... [Pg.159]

Craven, P.A., Pfanstiel, J. and DeRubertis, F.R. (1986). Role of reactive oxygen in bile salt stimulation of colonic epithelial proliferation. J. Clin. Invest. 77, 850-859. [Pg.162]

Mechref, Y., Chen, P, and Novotny, M. V., Structural characterization of the N-linked oligosaccharides in bile salt-stimulated lipase originated from human breast milk, Glycobiology, 9, 227, 1999. [Pg.311]

Ursodiol may slow progression of liver disease. It improves bile flow and may displace toxic bile acids that accumulate in a cholestatic liver, stimulate bicarbonate secretion into the bile, offer a cytoprotective effect, and reduce elevated liver tests. Ursodiol is typically dosed at 15 to 20 mg/kg per day in two divided doses and may be rounded to the nearest tablet size.5,7... [Pg.253]

Secretin Endocrine cells in mucosa of duodenum Acid in duodenum Inhibits gastric emptying and gastric secretion stimulates secretion of bicarbonate from pancreas stimulates secretion of bicarbonate-rich bile from liver... [Pg.284]

The return of the bile salts to the liver from the small intestine is the most potent stimulus of bile secretion. In fact, these bile salts may cycle two to five times during each meal. The intestinal hormone secretin, which is released in response to acid in the duodenum, enhances aqueous alkaline secretion by the liver. Secretin has no effect on the secretion of bile salts. During the cephalic phase of digestion, before food even reaches the stomach or intestine, parasympathetic stimulation, by way of the vagus nerve, promotes bile secretion from the liver. [Pg.297]

The primary action of BARs is to bind bile acids in the intestinal lumen, with a concurrent interruption of enterohepatic circulation of bile acids, which decreases the bile acid pool size and stimulates hepatic synthesis of bile acids from cholesterol. Depletion of the hepatic pool of cholesterol results in an increase in cholesterol biosynthesis and an increase in the... [Pg.116]

The metabolites and metabolic pathway of a new anticonvulsant drug, sodium valproate, in rats were investigated using carbon-14 labeled sodium valproate. Most of the metabolites in urine and bile were a glucuronide conjugate of valproic acid. Free sodium valproate was as little as one-seventh of the total metabolites. In feces, only free sodium valproate was detected, and the possibility of enterohepatic circulation of sodium valproate was presumed. A part of dosed sodium valproate was excreted in expired air in the form of CO2. This degradative reaction took place in liter mitochondria and required CoA and oxygen. It was stimulated by ATP... [Pg.548]

Warded, J.M., Wright, A.J., Bardsley, W.G. and D Souza, S.W. (1984) Bile salt-stimulated lipase and esterase activity in human milk after collection, storage, and heating nutritional implications. Pediatr. Res. 18, 382-386. [Pg.342]

Bile flow and secretion are stimulated by fats and certain other foods. Bile salts may enhance or delay absorption depending on whether they form insoluble complexes with drugs or enhance the solubility of agents. [Pg.464]

The overall metabolism of vitamin A in the body is regulated by esterases. Dietary retinyl esters are hydrolyzed enzymatically in the intestinal lumen, and free retinol enters the enterocyte, where it is re-esterified. The resulting esters are then packed into chylomicrons delivered via the lymphatic system to the liver, where they are again hydrolyzed and re-esterified for storage. Prior to mobilization from the liver, the retinyl esters are hydrolyzed, and free retinol is complexed with the retinol-binding protein for secretion from the liver [101]. Different esterases are involved in this sequence. Hydrolysis of dietary retinyl esters in the lumen is catalyzed by pancreatic sterol esterase (steryl-ester acylhydrolase, cholesterol esterase, EC 3.1.1.13) [102], A bile salt independent retinyl-palmitate esterase (EC 3.1.1.21) located in the liver cell plasma hydrolyzes retinyl esters delivered to the liver by chylomicrons. Another neutral retinyl ester hydrolase has been found in the nuclear and cytosolic fractions of liver homogenates. This enzyme is stimulated by bile salts and has properties nearly identical to those observed for... [Pg.51]


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