{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,1,20]],"date-time":"2026-01-20T07:41:06Z","timestamp":1768894866363,"version":"3.49.0"},"reference-count":38,"publisher":"Wiley","issue":"1","license":[{"start":{"date-parts":[[2015,7,28]],"date-time":"2015-07-28T00:00:00Z","timestamp":1438041600000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"},{"start":{"date-parts":[[2015,7,28]],"date-time":"2015-07-28T00:00:00Z","timestamp":1438041600000},"content-version":"tdm","delay-in-days":0,"URL":"http:\/\/journals.sagepub.com\/page\/policies\/text-and-data-mining-license"}],"funder":[{"DOI":"10.13039\/100007582","name":"Alberta Health Services","doi-asserted-by":"publisher","id":[{"id":"10.13039\/100007582","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/501100000024","name":"Canadian Institutes of Health Research","doi-asserted-by":"publisher","id":[{"id":"10.13039\/501100000024","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/501100004073","name":"Killam Trusts","doi-asserted-by":"publisher","id":[{"id":"10.13039\/501100004073","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100008453","name":"American Society for Parenteral and Enteral Nutrition","doi-asserted-by":"publisher","id":[{"id":"10.13039\/100008453","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":["journals.sagepub.com"],"crossmark-restriction":true},"short-container-title":["J Parenter Enteral Nutr"],"published-print":{"date-parts":[[2016,1]]},"abstract":"<jats:p><jats:italic>Background<\/jats:italic>: We aim to study the mechanisms underlying our previous finding that exogenous glucagon\u2010like peptide\u20102 (GLP\u20102) treatment in a preclinical model of neonatal parenteral nutrition\u2013associated liver disease (PNALD) improves cholestasis. <jats:italic>Methods<\/jats:italic>: Neonatal piglets received 17 days of parenteral nutrition (PN) therapy and either saline control (PN\/Saline n = 8) or GLP\u20102 treatment at 11 nmol\/kg\/d (PN\/GLP\u20102, n = 7). At terminal laparotomy, bile and liver samples were collected. The relative gene expression of enzymes involved in bile acid synthesis, regulation, and transport was measured in liver by reverse\u2010transcriptase quantitative polymerase chain reaction. Bile acid composition in bile was determined using tandem mass spectrometry. Data were analyzed using 1\u2010way analysis of variance (ANOVA) or Kruskal\u2010Wallis ANOVA. <jats:italic>Results<\/jats:italic>: GLP\u20102 increased the expression of bile acid export genes: multidrug resistance\u2013associated proteins 2 (MRP2) (<jats:italic>P<\/jats:italic> = .002) and 3 (MRP3) (<jats:italic>P<\/jats:italic> = .037) over saline control. GLP\u20102 increased expression of Farnesoid X receptor (FXR) (<jats:italic>P<\/jats:italic> &lt; .001) and CYP7A1 (cytochrome P450, family 7, subfamily A, polypeptide 1) (<jats:italic>P<\/jats:italic> = .03). GLP\u20102 treatment was associated with decreased concentrations of taurohyocholic acid and conjugates of toxic lithocholic acid (<jats:italic>P<\/jats:italic> &lt; .01). GLP\u20102 treatment increased the liver bile acid content. <jats:italic>Conclusions<\/jats:italic>: GLP\u20102 treatment was associated with alterations in the hepatic expression of genes involved in bile acid metabolism. The transcriptomic results indicate the mechanisms at the transcriptional level acting to regulate bile acid synthesis and increase bile acid export. Differences in bile acid profiles further support a beneficial role for GLP\u20102 therapy in PNALD.<\/jats:p>","DOI":"10.1177\/0148607115595596","type":"journal-article","created":{"date-parts":[[2015,7,28]],"date-time":"2015-07-28T20:49:18Z","timestamp":1438116558000},"page":"22-35","update-policy":"https:\/\/doi.org\/10.1177\/sage-journals-update-policy","source":"Crossref","is-referenced-by-count":21,"title":["Glucagon\u2010Like Peptide\u20102 Alters Bile Acid Metabolism in Parenteral Nutrition\u2013Associated Liver Disease"],"prefix":"10.1002","volume":"40","author":[{"given":"David W.","family":"Lim","sequence":"first","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Paul W.","family":"Wales","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Si","family":"Mi","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Jason Y. 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