Document Detail


Nuclear receptors, Bile acids and Cholesterol Homeostasis Series - Bile Acids and Pregnancy.
MedLine Citation:
PMID:  23159988     Owner:  NLM     Status:  Publisher    
Abstract/OtherAbstract:
Bile acids have been traditionally thought of as having an important role in fat emulsification. It is now emerging that they act as important signalling molecules that not only autoregulate their own synthesis but also influence lipid and glucose metabolism. Although, the mechanisms that underlie the regulation of bile acid homeostasis have been well characterised in normal physiology, the impact of pregnancy on bile acid regulation is still poorly understood. This review summarises the main regulatory mechanisms underlying bile acid homeostasis and discusses how pregnancy, a unique physiological state, can modify them. The fetoplacental adaptations that protect against fetal bile acid toxicity are reviewed. We highlight the importance of bile acid regulation during gestation by discussing the liver disease of pregnancy, intrahepatic cholestasis of pregnancy (ICP) and how genetic, endocrine and environmental factors contribute to the disease aetiology at a cellular and molecular level.
Authors:
Shadi Abu-Hayyeh; Georgia Papacleovoulou; Catherine Williamson
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Publication Detail:
Type:  JOURNAL ARTICLE     Date:  2012-11-15
Journal Detail:
Title:  Molecular and cellular endocrinology     Volume:  -     ISSN:  1872-8057     ISO Abbreviation:  Mol. Cell. Endocrinol.     Publication Date:  2012 Nov 
Date Detail:
Created Date:  2012-11-19     Completed Date:  -     Revised Date:  -    
Medline Journal Info:
Nlm Unique ID:  7500844     Medline TA:  Mol Cell Endocrinol     Country:  -    
Other Details:
Languages:  ENG     Pagination:  -     Citation Subset:  -    
Copyright Information:
Copyright © 2012 Elsevier Ireland Ltd. All rights reserved.
Affiliation:
Institute of Reproductive and Developmental Biology, Dept. of Surgery and Cancer, Faculty of Medicine, Imperial College London, London W12 0NN, United Kingdom.
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