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Sterols fecal neutral

Various mechanisms have been proposed to explain the hypocholesterolemic effect of GA (Annison et al., 1995 Tiss et al., 2001). Some studies have suggested that the viscosity of fermentable dietary fiber contributes substantially to the reduction of lipids in animals and humans (Gallaher et al., 1993 Moundras et al., 1994). However, other studies suggested that this property is not related to plasma lipids (Evans et al., 1992). The mechanism involved is clearly linked to increased bile acid excretion and fecal neutral sterol or a modification of digestion and absorption of lipids (Moundras et al., 1994). [Pg.9]

An interrupted enterohepatic circulation of cholesterol itself is seen in malabsorption (119), very little extra bile salts being lost. Under these conditions, the bile acid fluxes to and from the liver are probably normal, the return of cholesterol being markedly reduced and the biliary secretion normal or increased. Thus (a) cholesterol synthesis is increased, (b) bile acid synthesis is normal or slightly elevated, and (c) serum cholesterol is low due to augmented catabolism of cholesterol via fecal neutral sterol excretion. The relationship between bile acid and cholesterol metabolism under different conditions in which cholesterol synthesis is altered is illustrated in Table I. [Pg.204]

Cholesterol and fat-soluble vitamins require bile acid induced micellar solubilization for absorption, which takes place in the upper small intestine (c/. 32,116-118). Accordingly, in bile salt deficiency states, cholesterol absorption should be markedly impaired and fecal neutral sterol excretion increased. The fact that fecal neutral steroid excretion on a low-cholesterol diet is actually normal, as after ileal resection, ileal bypass, and cholestyramine treatment, or even decreased, as in cirrhosis of the liver or biliary occlusion (11), is due to a markedly reduced biliary secretion of cholesterol. In gluten enteropathy, in which no excessive bile salt loss usually exists, fecal neutral sterol excretion is markedly augmented (119). However, in occasional cases in which fecal bile salt elimination is markedly enhanced, the fecal neutral steroid excretion is quite normal, probably owing to decreased biliary cholesterol secretion as a consequence of low biliary bile salt secretion. Detailed information on the role of bile salts in both intraluminal and mucosal phases of fat and sterol absorption is presented in many recent reviews (6,10,113,114,117). [Pg.206]

Fecal bile acid elimination is markedly reduced in patients with liver cirrhosis (11,182,191), even if icterus and signs of biliary obstruction are absent (11,182). Since, in addition, the urinary excretion of bile acids is quantitatively, if not proportionally (81), negligible, it can be concluded that the overall bile acid synthesis is markedly depressed in liver cirrhosis (182). The administration of cholestyramine, which is associated with reduction of both serum bile acids (188,192,193) and urinary bile acids (88,182), augmented the fecal bile acid excretion to a very small extent only (182). This indicates that the ability of the parenchymal cells to increase their bile acid production is clearly decreased compared to that of normal subjects. Though the fecal neutral sterol excretion was also increased by cholestyramine, only a relatively small decrease in serum cholesterol was found, suggesting that the patients still were able to increase their cholesterol production (182). [Pg.223]

Cholestyramine is a high molecular weight anionic exchange resin which, as the chloride salt, is used to absorb bile acids. In the dog (26), this material, when fed at the level of 25 g/day, was shown to increase fecal sterols by 85 % and fecal bile acids by 160% and to reduce cholesterol levels by 22%. Rate fed 2 % of cholestyramine in the diet showed a three- to fourfold increase in bile acid excretion, and the increase was all in the dihydroxycholanic acid fraction (27). In mice (28), this resin decreased the time for bile acid turnover from 5 to 1.25 days. Fecal neutral sterols were increased by 37%. Pigs fed 2-4% cholestyramine showed a marked increase in bile acid excretion (29). [Pg.276]

Number of rats Endogenous fecal neutral sterol 12 12 14... [Pg.297]

Mice fed agar showed significantly more colon tumors per animal (twice as many) as those fed diets without agar. Agar-fed animals also showed decreased levels of fecal neutral sterol and bile acid concentrations. When fed to rats at 5% and 15% levels of the diet. [Pg.10]

B. S. Reddy and E. L. Wynder, Metabolic epidemiology of colon cancer. Fecal bile acids and neutral sterols in colon cancer patients and patients with adenomatous polyps. Cancer, 1977, 39(6), 2533. [Pg.70]

Czubayko F, Beumers B, Lammsfuss S, Lutjohann D, von Bergmann (1991) A simplified micro-method for quantification of fecal excretion of neutral and acidic sterols for outpatient studies in humans. J Lipid Res 32 1861-1867... [Pg.662]

The ring structure of cholesterol cannot be metabolized to C02 and HfeO in humans. Rather, the intact sterol nucleus is eliminated from the body by conversion to bile acids and bile salts, which are excreted in the feces, and by secretion of cholesterol into the bile, which transports it to the intestine for elimination. Some of the cholesterol in the intestine is modified by bacteria before excretion. The primary compounds made are the isomers coprostanol and cholestanol, which are reduced derivatives of cholesterol. Together with cholesterol, these compounds make up the bulk of (neutral fecal sterols. [Pg.222]

Degradation of choles terol Mechanisms of choles terol disposal DEGRADATION OF CHOLESTEROL (p. 222) The ring structure of cholesterol can not be metabolized in humans. Cholesterol can be elim inated from the body either by conversion to bile salts or by secretion into the bile. Intestinal bacteria can reduce cholesterol to coprostanol and cholestanol, which together with cholesterol make up the bulk of neutral fecal sterols. [Pg.488]

Jenkins, K.J. and Atwal, A.S. 1994. Effects of dietary saponins on fecal bile acids and neutral sterols, and availability of vitamins A and E in the chick. J. Nutr. Biochem. 5, 134-137. [Pg.198]

The mass of bile acids per 0.5 g feces = mass in 1 ml methanol x dpm 14C-taurocholate added/dpm recovered in 1 ml methanol. As for neutral sterols, the total excreted per 3 days is calculated from the total fecal mass collected and data are reported as mass (or moles) excreted per day per gram body weight. [Pg.174]

PLASMA AND LIVER LIPID CONCENTRATIONS AND FECAL OUTPUT OF NEUTRAL STEROLS ... [Pg.110]

Most of the bile acids which escape from the terminal ileum into the colon undergo under normal conditions a transformation to secondary bile acids via the action of colonic bacteria (1,4). The amount of primary bile acids in feces is thus negligible, if any, the mixture of fecal bile acids consisting of compounds with a wide range of polarity (38-41). However, in contrast to neutral sterols, bile acids are not degraded to any appreciable extent into undetectable metabolites during the intestinal passage (42). [Pg.194]

Elimination of cholesterol from the human body takes place primarily by the fecal route as bile acids and neutral sterols, viz. cholesterol, coprosta-nol, and coprostanone. About one-third of cholesterol is normally catabo-lized by way of bile acids (11). As will be shown later, the amount of the latter depends on the body size, so that the weight correlates with the fecal bile acids, the average daily output of 250 mg corresponding to about 4 mg/ kg. The factors regulating hepatic bile acid production under normal conditions are, however, unknown in many respects. [Pg.199]

Administration of cholestyramine to triglyceridemic patients usually has no effect on serum cholesterol. Yet a marked increase is seen in fecal bile acid elimination, the increment showing, in contrast to the results in Fig. 3, no distinct positive correlation with initial bile acid values (88). Furthermore, a cholestyramine-induced increase in fecal bile acid excretion was almost constantly associated with a decrease in neutral sterol elimination despite an apparent reduction of cholesterol absorption. Thus, under these conditions, biliary secretion of cholesterol was probably markedly decreased, particularly because cholesterol production in the intestinal mucosa was obviously enhanced by the reduction of intraluminal bile salt concentration (92,98). [Pg.219]

Nichols, Comparison of patterns of fecal bile acid and neutral sterol between children and adults. Am.J.Clin.Nutr., 29 1196 (1976). [Pg.125]


See other pages where Sterols fecal neutral is mentioned: [Pg.138]    [Pg.203]    [Pg.208]    [Pg.229]    [Pg.239]    [Pg.287]    [Pg.37]    [Pg.43]    [Pg.45]    [Pg.51]    [Pg.163]    [Pg.135]    [Pg.452]    [Pg.239]    [Pg.157]    [Pg.174]    [Pg.305]    [Pg.563]    [Pg.88]    [Pg.120]    [Pg.144]    [Pg.205]    [Pg.230]    [Pg.276]    [Pg.277]    [Pg.169]    [Pg.226]    [Pg.133]    [Pg.22]    [Pg.87]    [Pg.129]   
See also in sourсe #XX -- [ Pg.43 , Pg.45 , Pg.46 , Pg.50 , Pg.51 ]




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Fecal sterols

Sterols neutral

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