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Record Nr. |
UNINA9910790494903321 |
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Autore |
Häussinger D (Dieter), <1951-> |
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Titolo |
Hepatobiliary transport in health and disease [[electronic resource] /] / edited by Dieter Häussinger, Verena Keitel and Ralf Kubitz |
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Pubbl/distr/stampa |
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Berlin, : De Gruyter, c2012 |
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ISBN |
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1-283-85800-2 |
3-11-027934-7 |
3-11-027935-5 |
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Descrizione fisica |
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1 online resource (312 p.) |
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Altri autori (Persone) |
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HäussingerD <1951-> (Dieter) |
KeitelVerena |
KubitzRalf |
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Disciplina |
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Soggetti |
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Liver - Metabolism - Disorders |
Biliary tract - Metabolism - Disorders |
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Lingua di pubblicazione |
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Formato |
Materiale a stampa |
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Livello bibliografico |
Monografia |
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Note generali |
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Description based upon print version of record. |
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Nota di bibliografia |
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Includes bibliographical references and index. |
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Nota di contenuto |
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Sodium-dependent bile salt uptake -- Sodium-independent bile salt uptake into hepatocytes -- Bile salt export across the canalicular membrane -- Bile salt salvage systems. |
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Sommario/riassunto |
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One major function of the liver is the uptake of endo- and xenobiotics from the bloodstream and their excretion into bile. The transport systems involved in hepatobiliary transport have been recently cloned and characterized at the molecular level and it is becoming clear that mutations and polymorphisms of individual transporter molecules underlie a variety of liver diseases. Furthermore, new research has shown that bile acids, whose function in digestion is long known, also behave as signal molecules in a variety of organs, including the intestinal and biliary epithelia, sinusoidal endothelial and immune cells. This book provides indepth surveys on the structure and function of transport molecules involved in hepatobiliary transport, on the role of different bile acids receptors in various organs and their function in health and disease, the mechanisms of bile salt-induced apoptosis and hepatocyte protection, and the role of transporter mutations as causes and modifiers of liver diseases. The book will be of interest not only for |
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