Literature DB >> 10484008

Sluggish small bowel motility is involved in determining increased biliary deoxycholic acid in cholesterol gallstone patients.

F Azzaroli1, G Mazzella, C Mazzeo, P Simoni, D Festi, A Colecchia, M Montagnani, C Martino, N Villanova, A Roda, E Roda.   

Abstract

OBJECTIVE: Our aim was to establish whether small intestine transit time is defective in subjects with cholesterol gallstones.
METHODS: We enrolled 10 patients (eight women, two men; mean age, 48.7 yr; mean body mass index [BMI], 22.4 Kg/m2) with recently diagnosed cholelithiasis, with no liver pathology, who were not taking any drugs, and 11 comparable healthy volunteers (eight women, three men; mean age, 46.2 yr; mean BMI, 22.7 Kg/m2), who served as controls. All subjects underwent orocecal (by starch breath test technique and serum assays of salazopyrin), oroileal (by serum assays of tauroursodeoxycholic acid), and duodenoileal (by serum assays of taurocholic acid) transit times; cholesterol saturation index; and bile acid composition and gallbladder motility studies (by ultrasound). For serum assays, blood samples were collected over a period of 7 h. Gallbladder motility and orocecal transit time were evaluated simultaneously.
RESULTS: All four means of assessing transit time gave longer times in cholesterol gallstone patients than in controls: orocecal transit time (salazopyrin) = 366 +/- 13 vs 258 +/- 16 min, p < 0.0005; orocecal transit time (starch breath test) = 415 +/- 139 vs 290 +/- 15 min, p < 0.01; duodenoileal transit time: 272 +/- 23 vs 205 +/- 23 min, p < 0.03; and oroileal transit time: 308 +/- 18 vs 230 +/- 19 min, p < 0.009. Cholesterol gallstone patients showed an increase in percent molar biliary deoxycholic acid (30% +/- 4.5% vs 16% +/- 1.3%, p < 0.02) and a decrease in percent molar cholic acid 32% +/- 2.2% vs 40% +/- 1.3%, p < 0.03) and chenodeoxycholic acid (34% +/- 3% vs 41% +/- 1.8%, p < 0.03), compared with controls; patients also had greater percent molar biliary cholesterol. A linear relationship (r2 = 0.6324, p = 0.0012) between biliary deoxycholic acid and small bowel transit time was found. Residual gallbladder volumes were larger in cholesterol gallstone patients (11.38 +/- 1.27 vs 7.55 +/- 0.39 ml, p < 0.04), whereas basal gallbladder volumes, although higher, did not reach statistical significance (24.25 +/- 2.41 vs 19.98 +/- 1.63 ml; p = ns).
CONCLUSIONS: This study confirms that patients with cholesterol gallstones have delayed small bowel transit, defective gallbladder motor function, and increased biliary deoxycholic acid. Delayed small bowel transit may contribute to supersaturation of bile with cholesterol by increasing deoxycholic acid production.

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Year:  1999        PMID: 10484008     DOI: 10.1111/j.1572-0241.1999.01375.x

Source DB:  PubMed          Journal:  Am J Gastroenterol        ISSN: 0002-9270            Impact factor:   10.864


  10 in total

Review 1.  Update on the Molecular Mechanisms Underlying the Effect of Cholecystokinin and Cholecystokinin-1 Receptor on the Formation of Cholesterol Gallstones.

Authors:  Helen H Wang; Piero Portincasa; David Q-H Wang
Journal:  Curr Med Chem       Date:  2019       Impact factor: 4.530

2.  A new oral formulation for the release of sodium butyrate in the ileo-cecal region and colon.

Authors:  Aldo Roda; Patrizia Simoni; Maria Magliulo; Paolo Nanni; Mario Baraldini; Giulia Roda; Enrico Roda
Journal:  World J Gastroenterol       Date:  2007-02-21       Impact factor: 5.742

3.  Deoxycholic acid inhibits pacemaker currents by activating ATP-dependent K+ channels through prostaglandin E2 in interstitial cells of Cajal from the murine small intestine.

Authors:  Jae Yeoul Jun; Seok Choi; In-Youb Chang; Cha Kyung Yoon; Hye-Gwang Jeong; In Deok Kong; Insuk So; Ki Whan Kim; Ho Jin You
Journal:  Br J Pharmacol       Date:  2005-01       Impact factor: 8.739

4.  Ursodeoxycholic acid improves gastrointestinal motility defects in gallstone patients.

Authors:  A Colecchia; G Mazzella; L Sandri; F Azzaroli; M Magliuolo; P Simoni; M L Bacchi-Reggiani; E Roda; D Festi
Journal:  World J Gastroenterol       Date:  2006-09-07       Impact factor: 5.742

5.  Augmented cholesterol absorption and sarcolemmal sterol enrichment slow small intestinal transit in mice, contributing to cholesterol cholelithogenesis.

Authors:  Meimin Xie; Vijay R Kotecha; Jon David P Andrade; James G Fox; Martin C Carey
Journal:  J Physiol       Date:  2012-02-13       Impact factor: 5.182

6.  Effects of cisapride on gall bladder emptying, intestinal transit, and serum deoxycholate: a prospective, randomised, double blind, placebo controlled trial.

Authors:  M J Veysey; P Malcolm; A I Mallet; P J Jenkins; G M Besser; G M Murphy; R H Dowling
Journal:  Gut       Date:  2001-12       Impact factor: 23.059

7.  Targeted disruption of the murine cholecystokinin-1 receptor promotes intestinal cholesterol absorption and susceptibility to cholesterol cholelithiasis.

Authors:  David Q-H Wang; Frank Schmitz; Alan S Kopin; Martin C Carey
Journal:  J Clin Invest       Date:  2004-08       Impact factor: 14.808

8.  High level of deoxycholic acid in human bile does not promote cholesterol gallstone formation.

Authors:  Ulf Gustafsson; Staffan Sahlin; Curt Einarsson
Journal:  World J Gastroenterol       Date:  2003-07       Impact factor: 5.742

9.  Increased cholinergic contractions of jejunal smooth muscle caused by a high cholesterol diet are prevented by the 5-HT4 agonist--tegaserod.

Authors:  Ronald Mathison; Eldon Shaffer
Journal:  BMC Gastroenterol       Date:  2006-02-23       Impact factor: 3.067

Review 10.  An Update on the Lithogenic Mechanisms of Cholecystokinin a Receptor (CCKAR), an Important Gallstone Gene for Lith13.

Authors:  Helen H Wang; Piero Portincasa; Min Liu; Patrick Tso; David Q-H Wang
Journal:  Genes (Basel)       Date:  2020-11-29       Impact factor: 4.096

  10 in total

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