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http://purl.uniprot.org/citations/14962946http://www.w3.org/1999/02/22-rdf-syntax-ns#typehttp://purl.uniprot.org/core/Journal_Citation
http://purl.uniprot.org/citations/14962946http://www.w3.org/2000/01/rdf-schema#comment"

Objective

Cholesterol 7alpha-hydroxylase (cyp7a1) catalyzes the rate-limiting step in conversion of cholesterol to bile acids. To study the relationship between bile acid biosynthesis and triglyceride metabolism, we cross-bred mice lacking cyp7a1 on a hyperlipidemic APOE*3-Leiden background.

Methods and results

Female mice received a chow or lipogenic diet. On both diets, fecal bile acid excretion was 70% decreased concomitantly with a 2-fold increased neutral sterol output. The differences in bile acid biosynthesis did not change plasma cholesterol levels. However, plasma triglyceride levels decreased by 41% and 38% in the cyp7a1-/-. APOE*3-Leiden mice as compared with APOE*3-Leiden mice on chow and lipogenic diet, respectively. Mechanistic studies showed that very-low-density lipoprotein (VLDL)-apolipoprotein B and VLDL-triglyceride production rates were reduced in cyp7a1-/-. APOE*3-Leiden mice as compared with APOE*3-Leiden mice (-34% and -35%, respectively). Cyp7a1 deficiency also increased the hepatic cholesteryl ester and triglyceride content (2.8-fold and 2.5-fold, respectively). In addition, hepatic anti-oxidative vitamin content, which can influence VLDL-production, was lower. Hepatic mRNA analysis showed decreased expression of genes involved in lipogenesis including srebf1.

Conclusions

Cyp7a1 deficiency in APOE*3-Leiden mice decreases the VLDL particle production rate, as a consequence of a strongly reduced bile acid biosynthesis, leading to a decrease in plasma triglycerides. These data underscore the close relationship between bile acid biosynthesis and triglyceride levels."xsd:string
http://purl.uniprot.org/citations/14962946http://purl.org/dc/terms/identifier"doi:10.1161/01.atv.0000121572.21122.59"xsd:string
http://purl.uniprot.org/citations/14962946http://purl.uniprot.org/core/author"Solaas K."xsd:string
http://purl.uniprot.org/citations/14962946http://purl.uniprot.org/core/author"Post S.M."xsd:string
http://purl.uniprot.org/citations/14962946http://purl.uniprot.org/core/author"Rensen P.C."xsd:string
http://purl.uniprot.org/citations/14962946http://purl.uniprot.org/core/author"Princen H.M."xsd:string
http://purl.uniprot.org/citations/14962946http://purl.uniprot.org/core/author"Groenendijk M."xsd:string
http://purl.uniprot.org/citations/14962946http://purl.uniprot.org/core/date"2004"xsd:gYear
http://purl.uniprot.org/citations/14962946http://purl.uniprot.org/core/name"Arterioscler Thromb Vasc Biol"xsd:string
http://purl.uniprot.org/citations/14962946http://purl.uniprot.org/core/pages"768-774"xsd:string
http://purl.uniprot.org/citations/14962946http://purl.uniprot.org/core/title"Cholesterol 7alpha-hydroxylase deficiency in mice on an APOE*3-Leiden background impairs very-low-density lipoprotein production."xsd:string
http://purl.uniprot.org/citations/14962946http://purl.uniprot.org/core/volume"24"xsd:string
http://purl.uniprot.org/citations/14962946http://www.w3.org/2004/02/skos/core#exactMatchhttp://purl.uniprot.org/pubmed/14962946
http://purl.uniprot.org/citations/14962946http://xmlns.com/foaf/0.1/primaryTopicOfhttps://pubmed.ncbi.nlm.nih.gov/14962946
http://purl.uniprot.org/uniprot/#_A1L3S6-mappedCitation-14962946http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/14962946
http://purl.uniprot.org/uniprot/#_Q64505-mappedCitation-14962946http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/14962946
http://purl.uniprot.org/uniprot/A1L3S6http://purl.uniprot.org/core/mappedCitationhttp://purl.uniprot.org/citations/14962946
http://purl.uniprot.org/uniprot/Q64505http://purl.uniprot.org/core/mappedCitationhttp://purl.uniprot.org/citations/14962946