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Cholate synthesis

The rate of cholate synthesis in man is about 200-300 mg/day, as measured by isotope dilution studies. The chenodeoxycholate synthesis rate is similar, so that the total primary bile salt synthesis is about 400-600 mg daily for a healthy adult, and when in the steady state this amount is also the daily fecal excretion rate (12). [Pg.58]

Protein Turnover in Liver 586 Some Aspects of Amino Acid Metabolism 587 Hippuric Acid Synthesis Cholate Synthesis Amino Acid Acetylation T ransmethylation... [Pg.538]

Cholic acid may be converted in several steps into the 3,9-epoxy-carboxyIic acid (246) which has the ABC ring system of batrachotoxin. The synthesis of 24-nor-5a-cholic acid from methyl cholate involved the Barbier-Wieland degradation of the side-chain and treatment of the resultant 24-nor-5/3-cholic acid with Raney nickel. A major product of this reaction was the 5a-3-oxo-compound (247) which... [Pg.262]

Brady and Sanders (328) reported the synthesis of dynamic macrolactone libraries based on the thermodynamic transesterification/cyclization of easily accessible cholate monomers 8.117-8.119 (Fig. 8.56). The transesterification conditions were first studied with 8.117, and the mixture of potassium methoxide and a crown ether in toluene was found to be the best thermodynamic protocol. At 5 mM concentration of... [Pg.408]

Figure 8.56 Synthesis of template-assisted, dynamic combinatorial cyclic libraries of oligo-cholates. Figure 8.56 Synthesis of template-assisted, dynamic combinatorial cyclic libraries of oligo-cholates.
The mechanism of the inhibition of the HMG-CoA reductase by bile adds shown in Fig. 14 is a matter of controversy. Weis and Dietschy did not observe any influence of taurocholate on cholesterol synthesis in bile fistula rats fed a cholesterol-free diet, and concluded that the inhibitory effect of bile acids on cholesterol synthesis may be related to the increased absorption of cholesterol by the presence of bile acids in the intestine [247]. However, Hamprecht et al. were able to demonstrate a reduction of HMG-CoA reductase activity in lymph fistula rats infused with cholate [248]. Results by Shefer et al. also indicate that bile acids inhibit HMG-CoA reductase directly [212]. It seems likely that the inhibitory effect of the bile acids on HMG-CoA reductase may involve both direct and indirect effects. It was recently established that the stimulation of HMG-CoA reductase activity in response to treatment with cholestyramine is associated with an increase of the specific mRNA [258]. [Pg.269]

Bile acids in meconium also reflect atypical synthesis. Back and Walter [209] reported on the presence of 14 bile acids obtained from meconium of 6 healthy infants (Table 2B). On the average 21% of chenodeoxycholate and of hyocholate and 8% of cholate were sulfated. Deoxycholate was the major bile acid of the sulfate fraction lithocholate, 3/8-hydroxy-5-cholenate [175] and 3, 12a-dihydroxy-5-cholenate were found only in the sulfate fraction, but quantities of lithocholate (range 0.3-1.4%) and 3i8,12a-dihydroxy-5-cholenate were small. The amount of l, 3tt,7a,12a-tetrahydroxy acid (79% as the taurine conjugate and 21% unconjugated) ranged from 3.6 to 11.1% of the total bile acids [209]. The feta bile adds of a number of animals, normal, adrenalectomized, thyroidectomized, or diabetic, are reviewed by Subbiah and Hassan ]210]. [Pg.324]

Fig. 34.10. Synthesis of bile salts. Two sets of bile salts are generated one with a-hydroxyl groups at positions 3 and 7 (the chenocholate series), and the other with a-hydroxyls at positions 3, 7 and 12 (the cholate series). Fig. 34.10. Synthesis of bile salts. Two sets of bile salts are generated one with a-hydroxyl groups at positions 3 and 7 (the chenocholate series), and the other with a-hydroxyls at positions 3, 7 and 12 (the cholate series).
After cholesterol is formed, it can be converted to other steroids of widely varying physiological function. The smooth ER is an important site for both the synthesis of cholesterol and its conversion to other steroids. Most of the cholesterol formed in the liver, which is the principal site of cholesterol synthesis in mammals, is converted to bile acids, such as cholate and glycocholate (Figure 21.30). These compounds aid in the digestion of lipid droplets by emulsifying them and rendering them more accessible to enzymatic attack. [Pg.633]

Chenodeoxycholate synthesis may possibly proceed along several pathways. As shown in Fig. 2, one route is similar to that for cholate, in which ring alterations are completed before side-chain oxidation. A second suggested route begins with the oxidation of a terminal methyl group of cholesterol, yielding 26-hydroxycholesterol (9,10), which is readily converted to chenodeoxycholate but not cholate in the rat. Such a route involving 26-hydroxy-cholesterol remains speculative in man, however, as this compound has not yet been identified as a metabolite of cholesterol in human bile and there is some recent evidence that 26-hydroxycholesterol is not an important intermediate in bile salt formation (11). [Pg.58]

Values for turnover time, pool size, and half-life of cholate and chenodeoxycholate and the excretion rates for both are given in Table I. When turnover time or synthesis rates are calculated from isotope dilution studies, the values are usually in the same range as those derived from isotope balance studies provided that the latter are done by properly validated and reproducible methods. [Pg.58]

Fasting in obese but otherwise normal subjects results in cessation of cholate turnover (and presumably synthesis) and disappearance of bile salts from the stools (19). [Pg.60]

Patients with hypercholesterolemia do not appear to have significant alterations in bile salt synthesis rates, but patients with combined hypercholesterolemia and hypertriglyceridemia have increased synthesis rates for both cholate and chenodeoxycholate (20). Bile salt synthesis rates are not appreciably changed when nicotinic acid feeding lowers plasma cholesterol concentrations (20). Synthesis rates may also be affected by thyroid hormones. Cholic acid synthesis is decreased and half-life prolonged in hypothyroid subjects. These alterations may be corrected with thyroid hormone (21). Bile acid synthesis is increased in thyrotoxicosis (21). [Pg.60]

As will be discussed in a later section, patients with certain types of liver injury have chenodeoxycholate as the predominant primary bile salt in their serum. Primary bile salt concentration ratios in serum are a fairly accurate reflection of the primary bile salt concentration ratio in bile. The evidence for this is given in Fig. 3, in which the primary bile salt concentration ratio in serum is plotted against that in bile in 14 patients. The correlation coefficient for these two variables is 0.86 (p<0.01). When chenodeoxycholate predominates in bile its metabolites (lithocholate and others) predominate in feces, and when cholate predominates in bile its metabolites (de-oxycholate and others) predominate in feces (27). This relationship is shown in Fig. 4. It thus appears that primary bile salt concentrations in blood and bile are related to their relative synthesis rates and that the predominant bile salt in blood and bile has the greater synthesis rate, since its metabolites predominate in feces. This assumes of course that there is a steady state and... [Pg.61]

It seems quite apparent that 7a-OH-cholesterol serves as a primary intermediate in human chenodeoxycholic acid synthesis (1). 5 -cholestane-3a,7a-diol and, further, dihydroxycoprostanic acid have been found in human bile (17). The latter is known to be converted finally to chenodeoxy-cholate (18). Thus dihydroxycoprostanic acid belongs to the primary human bile acids. [Pg.193]

Studies with radioactive glycocholate or taurocholate demonstrated a virtual absence of the enterohepatic circulation of bile acids in patients with jejunotransversocolostomy (77). The small amount of absorbed bile acids contained some deconjugated cholate and deoxycholate (which had been reconjugated in the liver), indicating a rapid bacterial action during an apparently fast intestinal passage. Under these conditions, steatorrhea is apparently not solely due to bile salt deficiency induced impairment of micelle formation, but reduced absorptive area may play an important contributory role. No direct measurement of bile acid synthesis by fecal determination has been performed in this condition. [Pg.236]

Since, in the rat, cholesterol is eliminated largely in the form of bile acids, it was expected that bile acid secretion in bile would be increased in the hyperthyroid state. Early experiments to test this point indicated that biliary bile acid secretion was actually normal or below normal (2,3). These results can be explained in terms of the inadequate analytical procedures then in use. Only cholate secretion was measured, and the levels of cheno-deoxycholate were not taken into account. When both of these bile acids were determined, it was shown that, in the bile fistula rat, the total production of bile acids was about the same in the hyperthyroid as in the euthyroid state, and lower in the hypothyroid state (4). In addition, in the hyperthyroid state, the normal ratio of cholate/chenodeoxycholate was reversed from approximately 3 1 to 1 3—cholic acid synthesis was decreased, and chenodeoxycholic acid synthesis was increased two- to threefold (4). Identical results were obtained in the bile fistula rat treated with noncalorigenic doses of D-tri-iodothyronine (5,6), suggesting that these effects are not necessarily a function of the basal metabolic rate. [Pg.250]

In intact rats (180-250 g), treatment with thyroid hormones to induce the hyperthyroid state resulted in an increase in total bile acid output. Normal rats produced an average of 3.9 mg of cholate and 1 mg of cheno-deoxycholate per day, while hyperthyroid animals secreted 5.3 mg of cholate and 2.9 mg of chenodeoxycholate per day (7). The synthesis of chenodeoxy-... [Pg.250]

By injecting normal and hypophysectomized rats with i C-labeled cholate and/or chenodeoxycholate, the half-life, turnover rates, and bile acid pool sizes were determined (23-25). In hypophysectomized rats, bile acid synthesis (calculated from the /1/2 and turnover rates) and excretion are reduced to about half when compared to normals. The decrease in bile acid synthesis is reflected in drastically reduced levels of chenodeoxycholate Apparently, the hypophysectomized rat loses its ability to synthesize this bile acid (23,24). Typical values for daily bile acid synthesis expressed in mg/day/100 g rat were 0.55 mg cholate, 0.19 mg chenodeoxycholate for normals, and 0.31 mg cholate, no detectable chenodeoxycholate for hypophysectomized rats. [Pg.253]

In contrast, in ileal absorptive disorders, Garbutt et al. (38) observed an increase in G T ratios of both cholate and deoxycholate, which was attributed to a decrease in enterohepatic recirculation of taurocholate and deoxycholate. It is also interesting to note that a selective conjugation of cholic acid with L-ornithine could be induced in the rat and guinea pig liver by the injection of a toxic capsular polysaccharide of Klebsiella pneumoniae (39). Partial hepatectomy has also been shown to result in a shutdown in the hepatic synthesis of glycine conjugates of bile acids (40). [Pg.265]

FIG. 1 (LEFT). ApH-dependence of the initial rate of ATP-synthesis. The media used for cholate incubation, column centrifugation and acid preincubation (see "Methods") contained 30 mM MBS, 30 mM MOPS, the indicated concentration (in mM) of KCl (x), and (50-x) mM NaCl. Acid preincubation was carried out at pH-8-ApH. [Pg.2048]

It was proved that the reaction effectively occurs within the liposome by radioactive labeling during glycogen synthesis, while the same reaction is prevented in the external medium. The authors additionally showed that DNase I and tRNA molecules could permeate through the POPC/cholate bilayer, but they also observed a critical size of about 70 kDa for which permeation is not possible (for instance, no permeation of phosphorylase and amyloglucosidase were observed). [Pg.3146]

ABSTRACT. Syntheses and binding properties of some supermacrocyclic hosts based on porphyrins and steroids are presented. It is shown that the ligand-binding properties of linear intermediates can be used to control the outcome of the synthesis three distinct rdles for such ligand templates are identified and exploited in the synthesis of a linear poiphyrin octamer. Some chemistry of cyclocholates and cholate-capped poiphyrins is also described, with an emphasis on the control of ring size through steric effects. [Pg.359]


See other pages where Cholate synthesis is mentioned: [Pg.71]    [Pg.587]    [Pg.71]    [Pg.587]    [Pg.116]    [Pg.196]    [Pg.196]    [Pg.161]    [Pg.179]    [Pg.75]    [Pg.179]    [Pg.615]    [Pg.277]    [Pg.310]    [Pg.310]    [Pg.62]    [Pg.90]    [Pg.144]    [Pg.253]    [Pg.71]    [Pg.55]    [Pg.95]    [Pg.129]    [Pg.95]    [Pg.457]    [Pg.136]   
See also in sourсe #XX -- [ Pg.587 ]




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