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rdf:type |
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lifeskim:mentions |
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pubmed:issue |
5
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pubmed:dateCreated |
1992-12-14
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pubmed:abstractText |
Operative liver biopsies were obtained from two male patients who developed gallstone disease during estrogen treatment of metastatic prostatic carcinoma. The heparin-sensitive binding of 125I-low-density lipoprotein (LDL) to liver homogenates (reflecting the expression of the LDL receptor) was determined, together with the activities of the rate-limiting enzymes in cholesterol synthesis [3-hydroxy-3-methylglutaryl-coenzyme A (HMG-CoA) reductase], bile acid production (cholesterol 7 alpha-hydroxylase), and cholesterol esterification (acyl CoA:cholesterol acyl transferase). The results were related to data available in 18 patients (5 male, 13 female) who underwent cholecystectomy because of gallstone disease. The hepatic 125I-LDL-binding activity was increased threefold compared with five controls, and the activity of HMG-CoA reductase was increased twofold. There was no major difference in the activities of cholesterol 7 alpha-hydroxylase or acyl CoA:cholesterol acyl transferase. The concentration of free and total cholesterol in liver microsomes was approximately 30% lower in the estrogen-treated men than in 11 controls. The results indicate that estrogen at pharmacological doses stimulates hepatic LDL-receptor expression and HMG-CoA reductase activity in men. The increased LDL-receptor expression could in part explain the enhanced plasma clearance of injected 125I-LDL and hence the reduction in plasma LDL cholesterol previously shown to occur in estrogen-treated men.
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pubmed:language |
eng
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pubmed:journal |
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pubmed:citationSubset |
AIM
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pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/Cholesterol,
http://linkedlifedata.com/resource/pubmed/chemical/Cholesterol 7-alpha-Hydroxylase,
http://linkedlifedata.com/resource/pubmed/chemical/Estrogens,
http://linkedlifedata.com/resource/pubmed/chemical/Follicle Stimulating Hormone,
http://linkedlifedata.com/resource/pubmed/chemical/Hydroxymethylglutaryl CoA Reductases,
http://linkedlifedata.com/resource/pubmed/chemical/Hydroxymethylglutaryl-CoA-Reductases...,
http://linkedlifedata.com/resource/pubmed/chemical/Lipids,
http://linkedlifedata.com/resource/pubmed/chemical/Lipoproteins,
http://linkedlifedata.com/resource/pubmed/chemical/Luteinizing Hormone,
http://linkedlifedata.com/resource/pubmed/chemical/Prolactin,
http://linkedlifedata.com/resource/pubmed/chemical/Receptors, LDL,
http://linkedlifedata.com/resource/pubmed/chemical/Sterol O-Acyltransferase,
http://linkedlifedata.com/resource/pubmed/chemical/Testosterone
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pubmed:status |
MEDLINE
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pubmed:month |
Nov
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pubmed:issn |
0016-5085
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pubmed:author |
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pubmed:issnType |
Print
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pubmed:volume |
103
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
1657-63
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pubmed:dateRevised |
2006-11-15
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pubmed:meshHeading |
pubmed-meshheading:1426886-Aged,
pubmed-meshheading:1426886-Bile,
pubmed-meshheading:1426886-Cholelithiasis,
pubmed-meshheading:1426886-Cholesterol,
pubmed-meshheading:1426886-Cholesterol 7-alpha-Hydroxylase,
pubmed-meshheading:1426886-Estrogens,
pubmed-meshheading:1426886-Follicle Stimulating Hormone,
pubmed-meshheading:1426886-Humans,
pubmed-meshheading:1426886-Hydroxymethylglutaryl CoA Reductases,
pubmed-meshheading:1426886-Hydroxymethylglutaryl-CoA-Reductases, NADP-dependent,
pubmed-meshheading:1426886-Lipids,
pubmed-meshheading:1426886-Lipoproteins,
pubmed-meshheading:1426886-Liver,
pubmed-meshheading:1426886-Luteinizing Hormone,
pubmed-meshheading:1426886-Male,
pubmed-meshheading:1426886-Microsomes, Liver,
pubmed-meshheading:1426886-Prolactin,
pubmed-meshheading:1426886-Prostatic Neoplasms,
pubmed-meshheading:1426886-Receptors, LDL,
pubmed-meshheading:1426886-Sterol O-Acyltransferase,
pubmed-meshheading:1426886-Testosterone
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pubmed:year |
1992
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pubmed:articleTitle |
Hepatic cholesterol metabolism in estrogen-treated men.
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pubmed:affiliation |
Department of Medicine, Karolinska Institute, Huddinge University Hospital, Sweden.
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pubmed:publicationType |
Journal Article,
Case Reports,
Research Support, Non-U.S. Gov't
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