| http://purl.uniprot.org/citations/1420288 | http://www.w3.org/1999/02/22-rdf-syntax-ns#type | http://purl.uniprot.org/core/Journal_Citation |
| http://purl.uniprot.org/citations/1420288 | http://www.w3.org/2000/01/rdf-schema#comment | "Rats were treated with hydrocortisone, dexamethasone or triamcinolone for 4 days. The effect of treatment on hepatic lipase and lecithin:cholesterol acyltransferase (LCAT) mRNA levels and catalytic activities was determined. Hepatic lipase mRNA was not affected by hydrocortisone, but was decreased after dexamethasone (-28%) and triamcinolone (-54%). Hepatic lipase activity followed the same pattern, it was not affected by hydrocortisone and lowered by dexamethasone (-38%) and triamcinolone (-70%). The LCAT mRNA level in the liver was also not affected by hydrocortisone, but increased upon treatment with dexamethasone (+22%) and triamcinolone (+72%). Plasma LCAT, determined with an excess exogenous substrate (designated LCAT-II), tended to decrease after hydrocortisone treatment (-11%) and was higher after dexamethasone (+21%) and triamcinolone (+22%). The plasma cholesterol esterification rate (designated LCAT-I), determined by incubation of the plasma at 37 degrees C, followed the same pattern. The activity ratio of hepatic lipase/LCAT-II decreased from 1 in the controls to 0.51 after dexamethasone and 0.25 in the triamcinolone-treated animals. The plasma HDL cholesterol concentration in the different groups changed oppositely to the hepatic lipase/LCAT activity ratio. It is concluded that HDL cholesterol is raised by synthetic glucocorticoids due, among other factors, to a lowered hepatic lipase and an increased plasma LCAT activity. The influence of glucocorticoids on these enzymes is, at least partly, explained by the effects on the hepatic mRNA contents."xsd:string |
| http://purl.uniprot.org/citations/1420288 | http://purl.org/dc/terms/identifier | "doi:10.1016/0005-2760(92)90305-f"xsd:string |
| http://purl.uniprot.org/citations/1420288 | http://purl.uniprot.org/core/author | "Auwerx J."xsd:string |
| http://purl.uniprot.org/citations/1420288 | http://purl.uniprot.org/core/author | "Staels B."xsd:string |
| http://purl.uniprot.org/citations/1420288 | http://purl.uniprot.org/core/author | "Jansen H."xsd:string |
| http://purl.uniprot.org/citations/1420288 | http://purl.uniprot.org/core/author | "Skretting G."xsd:string |
| http://purl.uniprot.org/citations/1420288 | http://purl.uniprot.org/core/author | "van Tol A."xsd:string |
| http://purl.uniprot.org/citations/1420288 | http://purl.uniprot.org/core/date | "1992"xsd:gYear |
| http://purl.uniprot.org/citations/1420288 | http://purl.uniprot.org/core/name | "Biochim Biophys Acta"xsd:string |
| http://purl.uniprot.org/citations/1420288 | http://purl.uniprot.org/core/pages | "181-185"xsd:string |
| http://purl.uniprot.org/citations/1420288 | http://purl.uniprot.org/core/title | "Opposite regulation of hepatic lipase and lecithin: cholesterol acyltransferase by glucocorticoids in rats."xsd:string |
| http://purl.uniprot.org/citations/1420288 | http://purl.uniprot.org/core/volume | "1128"xsd:string |
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