Please use this identifier to cite or link to this item: http://hdl.handle.net/10553/53296
Title: The estradiol induction of the microsomal low-affinity glucocorticoid binding sites (LAGS) in the male rat liver is independent of the endocrine status
Authors: Chirino, R. 
Fernández, L. 
López, A.
Navarro, D.
Rivero, J. F.
Díaz-Chico, J. C. 
Díaz-Chico, B. N. 
UNESCO Clasification: 32 Ciencias médicas
Keywords: Dexamethasone Binding
Estrogen-Receptor
Mammalian Liver
Sex
Issue Date: 1992
Journal: Journal of Steroid Biochemistry and Molecular Biology 
Abstract: The low-affinity glucocorticoid binding sites (LAGS) are entities present in the microsomal fraction of the rat liver, capable of binding several glucocorticoids and progesterone with low affinity. The present work focuses on the demonstration that estradiol exerts a powerful stimulatory effect on the LAGS concentration. For this purpose, we studied the effect of this hormone in immature, hypothyroid, and hypophysectomized rats, three experimental models which present a very low level of LAGS. In all of them, estradiol showed ability to significantly increase the level of LAGS. The positive results obtained in hypophysectomized rats point to a direct action of estradiol on the liver. In immature rats, the estradiol induction of the LAGS was shown to be especially slow, 3-4 days after estradiol administration being necessary to obtain a significant rise in the level of LAGS. Moreover, the dose of estradiol necessary to obtain the LAGS induction in these rats (0.5 mg/100 g body weight) was clearly supraphysiological. From these data we concluded that: (A) estradiol is a powerful stimulator of the LAGS concentration, its effect probably being exerted directly on the liver; and (B) to elicit its effect, estradiol does not need the participation of other hormones known to be implicated in the endocrine regulation of the LAGS.
URI: http://hdl.handle.net/10553/49848
ISSN: 0960-0760
DOI: 10.1016/0960-0760(92)90418-I
Source: Journal Of Steroid Biochemistry And Molecular Biology[ISSN 0960-0760],v. 41 (3-8), p. 757-760
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