{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,14]],"date-time":"2026-10-14T18:01:26Z","timestamp":1792000886579,"version":"4.4.0"},"reference-count":50,"publisher":"Ovid Technologies (Wolters Kluwer Health)","issue":"3","license":[{"start":{"date-parts":[[2015,9,1]],"date-time":"2015-09-01T00:00:00Z","timestamp":1441065600000},"content-version":"tdm","delay-in-days":4567,"URL":"http:\/\/doi.wiley.com\/10.1002\/tdm_license_1.1"}],"content-domain":{"domain":["lww.com","ovid.com"],"crossmark-restriction":true},"short-container-title":[],"published-print":{"date-parts":[[2003,3]]},"abstract":"<jats:sec>\n                    <jats:title\/>\n                    <jats:p>\n                      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\u2013dehydroxylation resistant and cholylglycine, a deconjugation\u2013dehydroxylation susceptible bile acid were used. Rats with CCl\n                      <jats:sub>4<\/jats:sub>\n                      \u2013induced 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 \u00b1 6.5 vs. 53.0 \u00b1 3.1 \u03bcL\/kg\/min; mean \u00b1 SE,\n                      <jats:italic toggle=\"yes\">P<\/jats:italic>\n                      &lt; .05). The administration of conjugated bile acids to cirrhotic rats normalized bile secretion (cholylsarcosine, 51.8 \u00b1 6.29; cholylglycine, 52.72 \u00b1 8.9 \u03bcL\/kg\/min). Total ileal bacterial content was 6\u2013fold 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 \u00b1 0.002; cholylglycine 0.101 \u00b1 0.007 EU\/mL) compared with placebo (0.282 \u00b1 0.124,\n                      <jats:italic toggle=\"yes\">P<\/jats:italic>\n                      &lt; .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.\n                    <\/jats:p>\n                  <\/jats:sec>","DOI":"10.1053\/jhep.2003.50116","type":"journal-article","created":{"date-parts":[[2003,3,15]],"date-time":"2003-03-15T07:29:29Z","timestamp":1047713369000},"page":"551-557","update-policy":"https:\/\/doi.org\/10.1097\/lww.0000000000001000","source":"Crossref","is-referenced-by-count":297,"title":["Oral Bile Acids Reduce Bacterial Overgrowth, Bacterial Translocation, and Endotoxemia in Cirrhotic Rats"],"prefix":"10.1097","volume":"37","author":[{"given":"Vicente","family":"Lorenzo-Z\u00fa\u00f1iga","sequence":"first","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Ram\u00f3n","family":"Bartol\u00ed","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Ram\u00f3n","family":"Planas","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Alan F.","family":"Hofmann","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Bel\u00e9n","family":"Vi\u00f1ado","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Lee R.","family":"Hagey","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Jos\u00e9 M.","family":"Hern\u00e1ndez","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Josep","family":"Ma\u00f1\u00e9","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Marco A.","family":"Alvarez","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Vicente","family":"Ausina","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Miquel Angel","family":"Gassull","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"276","reference":[{"key":"10.1053\/jhep.2003.50116-BIB1","doi-asserted-by":"crossref","first-page":"568","DOI":"10.7326\/0003-4819-60-4-568","volume":"60","author":"Conn","year":"1964","journal-title":"Ann Intern Med"},{"key":"10.1053\/jhep.2003.50116-BIB2","first-page":"257","volume":"21","author":"Garc\u00eda-Tsao","year":"1992","journal-title":"Dis Clin North Am"},{"key":"10.1053\/jhep.2003.50116-BIB3","doi-asserted-by":"crossref","first-page":"403","DOI":"10.1128\/IAI.23.2.403-411.1979","volume":"23","author":"Berg","year":"1979","journal-title":"Infect Immun"},{"key":"10.1053\/jhep.2003.50116-BIB4","doi-asserted-by":"crossref","first-page":"792","DOI":"10.1016\/S0168-8278(94)80241-6","volume":"21","author":"Runyon","year":"1994","journal-title":"J Hepatol"},{"key":"10.1053\/jhep.2003.50116-BIB5","first-page":"1861","volume-title":"Oxford Textbook of Clinical Hepatology","author":"Rimola","year":"1999","unstructured":". 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