Regulation of hepatocyte bile salt transporters during hepatic regeneration

Richard M. Green*, John L. Gollan, Bruno Hagenbuch, Peter J. Meier, David R. Beier

*Corresponding author for this work

Research output: Contribution to journalArticlepeer-review

3 Scopus citations


Bile formation is an essential liver-specific function, and the hepatic regeneration that occurs in response to hepatocellular injury is often associated with cholestasis. We have employed a partial hepatectomy model to examine the effect of hepatic regeneration on tissue-specific bile salt transporters and on Na+-K+-adenosinetriphosphatase (ATPase). Liver-specific sodium-dependent taurocholate uptake by basolateral plasma membrane vesicles was undetectable 24 h after hepatectomy. Basolateral membrane protein expression of the sodium-taurocholate cotransporter and gene expression of Ntcp were decreased by >90% 24 h after partial hepatectomy. In vitro transcription assays demonstrated that Ntcp gene transcription was also markedly reduced. In contrast, hepatic Na+-K+-ATPase activity, protein expression, and gene expression were unaffected by partial hepatectomy. Similarly, protein and gene expression of the ectoATPase, a putative canalicular bile salt transporter, and canalicular ATP-dependent taurocholate uptake remained unchanged. Partial hepatectomy results in a marked reduction in the gene transcription and expression of the liver-specific Ntcp, as well as a decrease in protein expression and loss of transport activity. These changes provide a potential mechanism for the decrease in hepatocellular bile salt transport that is associated with hepatic regeneration. cholestasis; liver; taurocholate

Original languageEnglish (US)
Pages (from-to)E650-E654
JournalAmerican Journal of Physiology
Issue number3 PART 1
StatePublished - Dec 1 1997

ASJC Scopus subject areas

  • Physiology (medical)


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