The Gpbar1 [G-protein-coupled BA (bile acid) receptor 1] is a recently identified cell-surface receptor that can bind and is activated by BAs, but its physiological role is unclear. Using targeted deletion of the Gpbar1 gene in mice, we show that the gene plays a critical role in the maintenance of bile lipid homoeostasis. Mice lacking Gpbar1 expression were viable, developed normally and did not show significant difference in the levels of cholesterol, BAs or any other bile constituents. However, they did not form cholesterol gallstones when fed a cholic acid-containing high-fat diet, and liver-specific gene expression indicated that Gpbar1-deficient mice have altered feedback regulation of BA synthesis. These results suggest that Gpbar1 plays a critical role in the formation of gallstones, possibly via a regulatory mechanism involving the cholesterol 7alpha-hydroxylase pathway.

Previous articleNext article No AccessBooksPrinciples in Conflict Condemned to Repeat? The Paradox of Humanitarian Action. By Fiona Terry. Ithaca: Cornell University Press, 2002. 282 pp.LisaMarkowitzLisaMarkowitzDepartment of Anthropology, University of Louisville, Louisville, KY 40292, U.S.A. ([email protected]). 3 ii 05 Search for more articles by this author Department of Anthropology, University of Louisville, Louisville, KY 40292, U.S.A. ([email protected]). 3 ii 05PDFPDF PLUSFull Text Add to favoritesDownload CitationTrack CitationsPermissionsReprints Share onFacebookTwitterLinkedInRedditEmail SectionsMoreDetailsFiguresReferencesCited by Current Anthropology Volume 46, Number 4August/October 2005 Sponsored by the Wenner-Gren Foundation for Anthropological Research Article DOIhttps://doi.org/10.1086/432825 Views: 73Total views on this site PDF download Crossref reports no articles citing this article.

Culture & AgricultureVolume 26, Issue 1-2 p. 52-52 Guest Editors' Comments: Living with Livestock: Contentments and Contentions Associate Professor Lisa Markowitz, Associate Professor Lisa Markowitz Anthropology at the University of Louisville.Search for more papers by this authorProfessor Valerie Wheeler, Professor Valerie Wheeler Anthropology at California State University-Sacramento.Search for more papers by this author Associate Professor Lisa Markowitz, Associate Professor Lisa Markowitz Anthropology at the University of Louisville.Search for more papers by this authorProfessor Valerie Wheeler, Professor Valerie Wheeler Anthropology at California State University-Sacramento.Search for more papers by this author First published: 28 June 2008 https://doi.org/10.1525/cag.2004.26.1-2.52AboutPDF ToolsExport citationAdd to favoritesTrack citation ShareShare Give accessShare full text accessShare full-text accessPlease review our Terms and Conditions of Use and check box below to share full-text version of article.I have read and accept the Wiley Online Library Terms and Conditions of UseShareable LinkUse the link below to share a full-text version of this article with your friends and colleagues. Learn more.Copy URL Share a linkShare onFacebookTwitterLinked InRedditWechat No abstract is available for this article. Volume26, Issue1-2March 2004Pages 52-52 RelatedInformation

GPR54 is a G-protein-coupled receptor that displays a high percentage of identity in the transmembrane domains with the galanin receptors. The ligand for GPR54 has been identified as a peptide derived from the KiSS-1 gene. KiSS-1 has been shown to have anti-metastatic effects, suggesting that KiSS-1 or its receptor represents a potential therapeutic target. To further our understanding of the physiological function of this receptor, we have generated a mutant mouse line with a targeted disruption of the GPR54 receptor (GPR54 -/-). The analysis of the GPR54 mutant mice revealed developmental abnormalities of both male and female genitalia and histopathological changes in tissues which normally contain sexually dimorphic features. These data suggest a role for GPR54/KiSS-1 in normal sexual development, and indicate that study of the GPR54 mutant mice may provide valuable insights into human reproductive syndromes.