Effect of estrogen on scavenger receptor BI expression in the rat
Autor: | Liqing Yu, Herbert Stangl, Gregory A. Graf, Guoqing Cao, K L Wyne |
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Rok vydání: | 2002 |
Předmět: |
CD36 Antigens
Male medicine.medical_specialty Hypophysectomy medicine.drug_class Endocrinology Diabetes and Metabolism medicine.medical_treatment Endogeny Adrenocorticotropic hormone Biology Ethinyl Estradiol Dexamethasone Rats Sprague-Dawley Endocrinology Adrenocorticotropic Hormone Internal medicine Adrenal Glands medicine Animals Scavenger receptor Receptors Immunologic Glucocorticoids Receptors Lipoprotein Receptors Scavenger Membrane Proteins Scavenger Receptors Class B Indirect effect Rats Cholesterol Liver Receptors LDL Estrogen LDL receptor hormones hormone substitutes and hormone antagonists medicine.drug |
Zdroj: | The Journal of endocrinology. 175(3) |
ISSN: | 0022-0795 |
Popis: | High-dose 17alpha-ethinyl estradiol treatment is associated with increased adrenal and decreased hepatic levels of scavenger receptor class B type 1 (SR-BI) in rats. In this paper we explored the mechanisms responsible for the differential regulation of SR-BI by estrogen in these two tIssues. Previously it was shown that estrogen-treated rats are profoundly hypolipidemic due to increased hepatic low density lipoprotein receptor (LDLR) activity, and that this effect is not maintained with hypophysectomy. To determine if the reduction in hepatic SR-BI was a direct or indirect effect of estrogen, we treated hypophysectomized rats with high-dose estrogen; the levels of SR-BI expression did not change in the livers or adrenals of these animals. To determine if the absence of response to estrogen in the adrenals of hypophysectomized animals was due to the absence of adrenocorticotropic hormone (ACTH), we examined the effect of estrogen treatment on SR-BI expression in animals treated with dexamethasone, which inhibits endogenous ACTH production. The administration of dexamethasone completely inhibited the increase in SR-BI expression in the adrenals of estrogen-treated rats. From these studies we conclude that estrogen does not have a direct effect on SR-BI expression in either the liver or the adrenals. In the liver, the decrease in SR-BI is dependent on the estrogen-induced increase in LDLR activity, and in the adrenal glands, ACTH is required for the estrogen-associated increase in expression of SR-BI. |
Databáze: | OpenAIRE |
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