Enterohepatic circulation of bile acids after cholecystectomy.

Roda, Enrico; Aldini, Rita; Mazzella, Giuseppe; Roda, Aldo; Sama, C; Festi, Davide; Barbara, L

doi:10.1136/gut.19.7.640

Cited by 102 publications

(49 citation statements)

References 33 publications

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“…Only in a group ofItalian gallstone patients the reduction ofthe CA pool was caused by a combination ofreduced synthesis and enhanced turnover (32). In our study and in studies of American whites (1,3,4) and American Indians (33) gallstone patients had normal hepatic synthesis of bile acids.…”

Section: Discussionmentioning

confidence: 57%

Disorders of bile acid metabolism in cholesterol gallstone disease.

Berr

Pratschke²,

Fischer³

et al. 1992

J. Clin. Invest.

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The aim of the study was to evaluate the metabolism of individual bile acids in patients with cholesterol gallstone disease. Therefore, we determined pool size and turnover of deoxycholic (DCA), cholic (CA), and chenodeoxycholic acid (CDCA) in 23 female gallstone patients classified according to their gallbladder function and in 15 healthy female controls. Gallstone patients had normal hepatic bile acid synthesis, but, depending on gallbladder function, differed with respect to turnover and size of the bile acid pools: Patients with well-emptying gallbladder (group A, n = 9) had enhanced turnover and reduced pools of CA (-46%; P < 0.01 vs. controls) and CDCA (-24%; P < 0.05), but normal input and size of the DCA pool. With reduced gallbladder emptying (< 50% of volume; group B, n = 6), turnover and pools of CA, CDCA, and DCA were similar as in controls. Patients with loss ofgallbladder reservoir (group C, n = 8) had increased input (+100%; P < 0.01) and pool size of DCA (+45%; P = 0.07) caused by rapid conversion of CA to DCA, while the pools of CA (-71%; P < 0.001 vs. controls) and CDCA (-36%; P < 0.05) were reduced by enhanced turnover. Thus, in patients with cholesterol gallstones, the pools of primary bile acids are diminished, unless gallbladder emptying is reduced. Furthermore, in a subgroup of gallstone patients, who had completely lost gallbladder function, the CA pool is largely replaced by DCA owing to rapid transfer of CA to the DCA pool. This probably contributes to supersaturation of bile with cholesterol. (J. Clin. Invest. 1992. 90:859-868.) Key words: bile acid metabolism * cholesterol gallstone disease * deoxycholic acid -gallbladder emptying . cholesterol saturation of bile IntroductionIn most nonobese patients with cholesterol gallstones, the pools of cholic acid (CA)' and chenodeoxycholic (CDCA) are reduced ( 1-6), and deoxycholic acid (DCA) is often increased in bile (7). Both changes could contribute to supersaturation of bile with cholesterol ( 1, 7, 1. Abbreviations used in this paper: CA, cholic acid; CCK, cholecystokinin; CDCA, chenodeoxycholic acid; DCA, deoxycholic acid; FTR, fractional turnover rate. circulation (9), the increase ofDCA by raising biliary secretion of cholesterol ( 10).The small pools ofCA and CDCA may be caused by a small gallbladder reservoir ( 1 1), by enhanced turnover (2, 5), or by inhibition of bile acid synthesis by an oversensitive feedback mechanism ( 1 2) or by elevated levels of DCA ( 13,14). An increased fraction ofDCA in bile could be caused by high input and large pool size of DCA. CA is nearly completely 7a-dehydroxylated to DCA by anaerobic bacteria in the colon (7,15,16), but only 30-40% of this DCA is absorbed from the intestine ( 17 ). The DCA pool could be expanded by increased input of DCA owing to increased synthesis ofthe precursor CA or to an increased fraction of CA transferred to the DCA pool.It is still unclear which of the above factors account(s) for the reduction in CA and CDCA pool size and which for an increase in biliary DCA. ...

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Section: Discussionmentioning

confidence: 57%

Disorders of bile acid metabolism in cholesterol gallstone disease.

Berr

Pratschke²,

Fischer³

et al. 1992

J. Clin. Invest.

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“…During fetal and neonatal life, synthesis of BA has been postulated to occur via an alternate pathway, which has lithocholic acid and 3 8-hydroxy-5 cholenoic acid as intermediates (16)(17)(18)(19)(20)(21)(22)(23)(24)(25)(26)(27)(28). There appears to be synthesis via the usually accepted pathway as well, however, the alternate pathway seems to be of major importance in fetal life (1 3).…”

Section: Discussionmentioning

confidence: 99%

Correlation between Fetal and Maternal Serum Bile Acid Concentrations

Colombo

Roda

et al. 1985

Pediatr Res

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“…After RNAse treatment of samples, tracted with chloroform-methanol (2:1, vol/vol) and analyzed for chohybrids were precipitated and collected on glass filters. The slopes of lesterol 12 and phospholipids. 13 The total bile acid concentration was the linear hybridization signals were calculated by the least-squares determined in another portion by an enzymatic method.…”

Section: Methodsmentioning

confidence: 99%

Hepatic cholesterol metabolism in human obesity

et al. 1997

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an elevated hepatic synthesis of cholesterol, and a reduced Hepatic cholesterol metabolism was studied in operaconversion of cholesterol to bile acids or to a decreased esteritive liver biopsies from 17 morbidly obese subjects and fication rate of hepatic cholesterol. 5 Obese subjects have an compared with that in samples from 15 nonobese conincreased synthesis of cholesterol that has been established trols. The aim was to understand the mechanisms causin several previous studies. [6][7][8] In a previous study, we assayed ing the hypersecretion of cholesterol into bile. The conthe activity of the microsomal enzyme 3-hydroxy-3-methyltent of cholesteryl esters was increased threefold in the glutaryl coenzyme A (HMG CoA) reductase, that regulates liver of obese subjects compared with that of the conthe synthesis of cholesterol, and showed that the liver is a trols (P õ .0001). The activity and the messenger RNA major contributor to the increased cholesterol production in (mRNA) level of 3-hydroxy-3-methylglutaryl coenzyme obesity. 9 Bile acid formation and pool size have been reported A (HMG CoA) reductase, the rate limiting enzyme for to be normal or enhanced in obesity. 1,3,4,8 No information is cholesterol synthesis, were higher in the obese subjects available on the activity of the microsomal cholesterol 7a-compared with the nonobese subjects (75% and 140%, hydroxylase, the rate determining enzyme for catabolism of respectively; P õ .01). In the obese subjects, the activity cholesterol to bile acids, in obesity. In a recent study of obese and mRNA level of cholesterol 7a-hydroxylase, which subjects, we found the activity of the microsomal acyl coenregulates the catabolism of cholesterol to bile acids, zyme A:cholesterol acyltransferase (ACAT) which catalyzes were also increased by 140% (P õ .05) and 180% (P Å .06), the esterification of cholesterol, to be normal but the content respectively, as compared with the controls. There was of esterified cholesterol in liver homogenates was elevated in a significant correlation between the activities and the comparison with nonobese controls. 10 mRNA levels of cholesterol 7a-hydroxylase among theThe aim of the present study was to elucidate possible obese subjects (r Å /0.65, P õ .01). The activities of acylmechanisms responsible for the previously reported hypersecoenzyme A:cholesterol acyltransferase (ACAT), which cretion of biliary cholesterol in obesity. We, therefore, considgoverns cholesteryl ester formation, in obese and nonered it important to thoroughly study the hepatic metabolism obese patients were 12.5 { 1.7 and 8.1 { 1.2 pmol/min/ of cholesterol in obese subjects. We have assayed the activimg protein, respectively (P õ .05), and the low-density ties of the following three important rate-limiting enzymes: lipoprotein (LDL) receptor mRNA levels were 5.3 { 0.7 HMG CoA reductase, cholesterol 7a-hydroxylase, and ACAT. and 4.5 { 0.9 molecules of mRNA/mg of RNA, respectively.In addition, we have quantitated the mRNA levels for HMG We conclude that the activities ...

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Enterohepatic circulation of bile acids after cholecystectomy.

Cited by 102 publications

References 33 publications

Disorders of bile acid metabolism in cholesterol gallstone disease.

Disorders of bile acid metabolism in cholesterol gallstone disease.

Correlation between Fetal and Maternal Serum Bile Acid Concentrations

Hepatic cholesterol metabolism in human obesity

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