2021
DOI: 10.1002/hep.31744
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Abstract: Response to HEP-21-0041 We appreciate the commentary on our study (HEP-20-0294.R1). We do not contest the Sperber hypothesis of osmotically driven water influx in bile formation per se. Rather, our data contests the belief that this water influx occurs in canaliculi to cause a 'canalicular flow'. We refine the Sperber hypothesis by

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“…This zonation creates nontrivial gradient profiles in the canalicular network that complicate deciphering the flux mechanism. A systematic study is under preparation. Estradiol‐17‐glucuronide (E17G)‐induced cholestasis: We discussed E17G‐induced transient cholestasis in a Reply [ 2 ] ; the authors mention observations of bile acid concentrations in extrahepatic bile that neither prove nor disprove the existence of canalicular water flow. Rather, E17G was later shown to inhibit the bile acid transporter BSEP on hepatocytes and several ion pumps required for water efflux on cholangiocytes. Mannitol clearance: Deducing a “canalicular flow” from mannitol clearance assumes its (i) exclusively canalicular permeability and (ii) inertness with respect to bile flow.…”
mentioning
confidence: 99%
“…This zonation creates nontrivial gradient profiles in the canalicular network that complicate deciphering the flux mechanism. A systematic study is under preparation. Estradiol‐17‐glucuronide (E17G)‐induced cholestasis: We discussed E17G‐induced transient cholestasis in a Reply [ 2 ] ; the authors mention observations of bile acid concentrations in extrahepatic bile that neither prove nor disprove the existence of canalicular water flow. Rather, E17G was later shown to inhibit the bile acid transporter BSEP on hepatocytes and several ion pumps required for water efflux on cholangiocytes. Mannitol clearance: Deducing a “canalicular flow” from mannitol clearance assumes its (i) exclusively canalicular permeability and (ii) inertness with respect to bile flow.…”
mentioning
confidence: 99%