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Cited by 321Liver Disease and TransplantationGut microbiota and healthGastrointestinal motility and disorders

Oral bile acids reduce bacterial overgrowth, bacterial translocation, and endotoxemia in cirrhotic rats

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Lorenzo-Zúñiga, Vicente, Bartolí, Ramón, Planas, Ramón, Hofmann, Alan F., Viñado, Belén, Hagey, Lee R., Hernández, José M., Mañé, Josep +3 more·2003·Hepatology
DOI 10.1053/jhep.2003.50116
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Abstract

Experiments were performed to test whether conjugated bile acid administration would decrease bacterial overgrowth, bacterial translocation, and endotoxemia in ascitic cirrhotic rats. Cholylsarcosine, a deconjugation–dehydroxylation resistant and cholylglycine, a deconjugation–dehydroxylation susceptible bile acid were used. Rats with CCl 4 –induced cirrhosis and ascites were fed cholylsarcosine, cholylglycine (both at 70 mg/kg/d), or placebo for 2 weeks. Healthy rats, as controls, were treated similarly. In cirrhotic rats receiving placebo, bile secretion from an acute biliary fistula was lower than in healthy rats (27.2 ± 6.5 vs. 53.0 ± 3.1 μL/kg/min; mean ± SE, P < .05). The administration of conjugated bile acids to cirrhotic rats normalized bile secretion (cholylsarcosine, 51.8 ± 6.29; cholylglycine, 52.72 ± 8.9 μL/kg/min). Total ileal bacterial content was 6–fold higher in ascitic cirrhotic rats than in healthy rats. Conjugated bile acid administration reduced bacterial content to normal levels. Bacterial translocation was less in cirrhotic animals receiving conjugated bile acids (cholylsarcosine, 33%; cholylglycine, 26%) than in animals receiving placebo (66%). Endotoxemia was decreased in cirrhotic rats by conjugated bile acid feeding (cholylsarcosine, 0.098 ± 0.002; cholylglycine 0.101 ± 0.007 EU/mL) compared with placebo (0.282 ± 0.124, P < .001). Survival was greater in animals receiving conjugated bile acids (cholylsarcosine, 10/15; cholylglycine, 11/15; placebo, 5/15). In conclusion, the administration of conjugated bile acids to ascitic cirrhotic rats increased bile acid secretion, eliminated intestinal bacterial overgrowth, decreased bacterial translocation, decreased endotoxemia, and increased survival. Oral conjugated bile acids may be useful in preventing bacterial translocation, endotoxemia, and spontaneous bacterial perotonitis in cirrhotic patients.

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Crossref · 10.1053/jhep.2003.50116

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  • Deficits in luminal bile acid levels are associated with small intestine bacterial overgrowth, activation of inflammation, and subsequent damage to the epithelium.

    “Deficits in luminal bile acid levels have been associated with small intestine bacterial overgrowth, activation of inflammation, and subsequent damage to the epithelium (Inagaki et al., 2006;Lorenzo-Zuniga et al., 2003).”

    From The Microbiota-Gut-Brain Axis (2019) · cites this paper as Lorenzo-Zuniga et al., 2003

    The introductory passage (section C; page unavailable) proposes that reduced intraluminal bile acids in cirrhosis may promote small-intestinal bacterial growth. It describes bacterial translocation across the epithelial barrier and subsequent endotoxemia, but does not establish the claimed activation of inflammation or subsequent epithelial damage. (LLM, conf=0.87)

    Experimental — accuracy not yet measured

  • Bile acids can eliminate bacterial overgrowth and reduce bacterial translocation and endotoxemia.

    “Bile acids can, moreover, eliminate bacterial overgrowth and reduce bacterial translocation and endotoxemia.208”

    From The role of gut dysbiosis in Parkinson’s disease: mechanistic insights and therapeutic options (2021) · cites this paper as [208]

    The Abstract (p. 551) reports that oral conjugated bile acids eliminated intestinal bacterial overgrowth and decreased bacterial translocation and endotoxemia in ascitic cirrhotic rats. The citing sentence omits that experimental population and the fact that the administered bile acids were conjugated, making the claim broader than the result shown. (LLM, conf=0.84)

    Experimental — accuracy not yet measured

  • Decreased bile secretion in rodents after common bile duct ligation or cirrhosis contributes to bacterial translocation through intestinal bacterial overgrowth and increased gut permeability.

    “Decreased bile secretion in rodents by either ligation of the common bile duct or induction of cirrhosis contributes to bacterial translocation, which is not only caused by intestinal bacterial overgrowth but also by increased gut permeability20,28,134.”

    From The gut microbiome and liver cancer: mechanisms and clinical translation (2017) · cites this paper as [134]

  • Oral bile acid administration attenuates these effects in experimental cirrhotic models.

    “Notably, these effects are attenuated after oral administration of bile acids in different experimental cirrhotic models20,134,135.”

    From The gut microbiome and liver cancer: mechanisms and clinical translation (2017) · cites this paper as [134]

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Cites

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Research works printed but not linked: 4

  1. [1]1. Conn HO. Spontaneous bacterial peritonitis and bacteriemia in LaennecЈs cirrhosis caused by enteric organisms. A relatively common but rarely recognized syndrome. Ann Intern Med 1964;60:568-580
  2. [15]15. Hylemon PB. Metabolism of bile acids in intestinal microflora. In: Danielsson H, Sjovall J, eds. Sterols and Bile Acids. New York: Elsevier, 1985:331-343.
  3. [35]35. Kallner A. On the biosynthesis and metabolism of allodeoxycholic acid in the rat. Acta Chem Scand 1967;21:315-321.
  4. [47]47. Ricci P, Hofmann AF, Hagey LR, Jorgensen RA, Lindor KD. Adjuvant cholylsarocosine during ursodeoxycholic acid treatment of primary biliary cirrhosis. Dig Dis Sci 1998;43:1292-1295.

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Authors
Lorenzo-Zúñiga, V., Bartolí, R., Planas, R., Hofmann, A. F., Viñado, B., Hagey, L. R., Hernández, J. M., Mañé, J., Alvarez, M. A., Ausina, V., & Gassull, M. A.
Affiliations
  • Hospital Universitari Germans Trias i Pujol (ES)
  • University of California San Diego (US)
  • Zoological Society of San Diego (US)
Corresponding author
Planas, Ramón
ORCID
Venue
Hepatology
Publisher
Ovid Technologies (Wolters Kluwer Health)
Published
2003-03
Volume
37
Issue
3
Pages
551-557
ISSN
0270-9139 (ISSN-L)
DOI
10.1053/jhep.2003.50116
OpenAlex
W2164410979
Semantic Scholar
0959b5153c2c625df9ca8067b5a6329269b3bb70
Cited by
321
References
52
Citations by year
2026: 12 · 2025: 11 · 2024: 20 · 2023: 18 · 2022: 27 · 2021: 20 · 2020: 21 · 2019: 23 · 2018: 14 · 2017: 20 · 2016: 18 · 2015: 16 · 2014: 12 · 2013: 9 · 2012: 12
FWCI
6.55
Type
journal article
Language
en
Open access
Licence
doi.wiley.com/10.1002/tdm_license_1.1 (tdm, 4567 d)
Locations
  • Hepatology (publishedVersion)
  • PubMed (publishedVersion)
Funders
  • Falk Foundation
  • Baylor University
  • National Institutes of Health
  • University of California, San Diego
  • Baylor University Medical Center
  • National Institute of Diabetes and Digestive and Kidney Diseases (DK 37172)
Topics
  • Health Sciences › Medicine › Hepatology › Liver Disease and Transplantation
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Gut microbiota and health
  • Health Sciences › Medicine › Gastroenterology › Gastrointestinal motility and disorders
Keywords
liver cirrhosis, ascites, bacterial overgrowth, bacterial translocation, endotoxemia, bile acid conjugates, cholylglycine, bile secretion, intestinal bacteria, survival, CCl4-induced cirrhosis, biliary fistula, sepsis
MeSH terms
Animals, Bacteria, Bile, Bile Acids and Salts, Cholic Acids, Glycocholic Acid, Ileum, Intestines, Liver Cirrhosis, Experimental, Male, Placebos, Sarcosine, Rats, Sprague-Dawley, Bacterial Translocation, Endotoxemia, Rats

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