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increase the proliferation of PRL-secreting lactotrophs in humans as well as in laboratory animals ( Sarkar et al. 1982 , Gooren et al. 1988 ). Studies of estradiol-induced prolactinomas in estrogen-susceptible rats also identified significant
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. 2005 ). Changes in environment and lifestyle have escalated the rates of type 2 diabetes and obesity ( Zimmet et al . 2005 ). Estrogen deficiency in postmenopausal women contributes to the development of visceral obesity, insulin resistance and the
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Introduction A plethora of evidence has demonstrated that estrogens are involved in many physiological processes in mammals, including developmental features, cellular homeostasis and neurobiological activities ( Kow et al . 2005 , Simpson et al
Department of Pathology,
Division of Biocomputing, Department of Biochemistry and Molecular Biology and
Department of Cell Biology and Physiology, University of New Mexico School of Medicine, Albuquerque, New Mexico 87131, USA
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Department of Pathology,
Division of Biocomputing, Department of Biochemistry and Molecular Biology and
Department of Cell Biology and Physiology, University of New Mexico School of Medicine, Albuquerque, New Mexico 87131, USA
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Department of Pathology,
Division of Biocomputing, Department of Biochemistry and Molecular Biology and
Department of Cell Biology and Physiology, University of New Mexico School of Medicine, Albuquerque, New Mexico 87131, USA
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Department of Pathology,
Division of Biocomputing, Department of Biochemistry and Molecular Biology and
Department of Cell Biology and Physiology, University of New Mexico School of Medicine, Albuquerque, New Mexico 87131, USA
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Department of Pathology,
Division of Biocomputing, Department of Biochemistry and Molecular Biology and
Department of Cell Biology and Physiology, University of New Mexico School of Medicine, Albuquerque, New Mexico 87131, USA
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Department of Pathology,
Division of Biocomputing, Department of Biochemistry and Molecular Biology and
Department of Cell Biology and Physiology, University of New Mexico School of Medicine, Albuquerque, New Mexico 87131, USA
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Department of Pathology,
Division of Biocomputing, Department of Biochemistry and Molecular Biology and
Department of Cell Biology and Physiology, University of New Mexico School of Medicine, Albuquerque, New Mexico 87131, USA
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Department of Pathology,
Division of Biocomputing, Department of Biochemistry and Molecular Biology and
Department of Cell Biology and Physiology, University of New Mexico School of Medicine, Albuquerque, New Mexico 87131, USA
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Introduction The steroid hormone estrogen produces a variety of cell responses, many of which can be attributed to the activation of two known estrogen receptors α and β (ERα and ERβ ), which function as transcription factors
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Introduction The estrogen 17β-estradiol (E 2 ) is a steroid hormone whose actions involve genomic and non-genomic mechanisms ( Bjornstrom & Sjoberg 2005 ). It is generally accepted that the majority of the effects of the hormone are mediated
Department of Biological Sciences, Lock Haven University, Lock Haven, Pennsylvania 17745, USA
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Department of Biological Sciences, Lock Haven University, Lock Haven, Pennsylvania 17745, USA
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Department of Biological Sciences, Lock Haven University, Lock Haven, Pennsylvania 17745, USA
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Department of Biological Sciences, Lock Haven University, Lock Haven, Pennsylvania 17745, USA
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Department of Biological Sciences, Lock Haven University, Lock Haven, Pennsylvania 17745, USA
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, Vale et al. 1994 , Shupnik 1996 ). In most mammals, the estrous cycle is dictated by the bi-modal actions of ovarian-derived estrogens on the HP axis such that moderate levels of E 2 during early folliculogenesis are suppressive to LH secretion
Biochemistry, INRA2006-EA2608, University, Esplanade de la Paix, 14032, CAEN-Cedex, France
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Biochemistry, INRA2006-EA2608, University, Esplanade de la Paix, 14032, CAEN-Cedex, France
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Biochemistry, INRA2006-EA2608, University, Esplanade de la Paix, 14032, CAEN-Cedex, France
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Biochemistry, INRA2006-EA2608, University, Esplanade de la Paix, 14032, CAEN-Cedex, France
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Biochemistry, INRA2006-EA2608, University, Esplanade de la Paix, 14032, CAEN-Cedex, France
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Biochemistry, INRA2006-EA2608, University, Esplanade de la Paix, 14032, CAEN-Cedex, France
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Biochemistry, INRA2006-EA2608, University, Esplanade de la Paix, 14032, CAEN-Cedex, France
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Introduction Although testosterone is recognized as the main sexual steroid in the male, estrogens are also produced in the testis and their concentrations within the male reproductive tract are generally higher than in the general
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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.
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Environmental chemicals which mimic the actions of estrogen have the potential to affect any estrogen responsive tissue. The aim of the present study was to investigate their potential to mimic the effects of 17beta-estradiol (E2) on developing primary rat hypothalamic dopaminergic (DA) neurones maintained in a chemically defined medium. We now show that both E2 and octylphenol (OP), but not the non-aromatizable androgen, dihydrotestosterone, enhanced the uptake of [3H]DA by the cultured cells, whereas they had no effect on the uptake of [14C]GABA. Although the sensitivity of responses may change with the age of the developing cultures, the dose response curves for E2 and OP were typically 'bell-shaped', with a rise in response followed by a decline to control levels with increasing concentrations. Effects were seen as low as 10(-14) M for E2 and 10(-11) M for OP. Responses to E2 (10(-12) M) and OP (10(-9) M) were reversed in the presence of the antiestrogen, ZM 182780 (10(-5) M). This study thus provides direct evidence, using a mechanistic rather than toxicological end-point, in support of the hypothesis that inappropriate exposure to environmental estrogens at critically sensitive stages of development, could potentially perturb the organisational activities of estrogen on selected neuronal populations in the CNS.
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the 17β-HSD family fall into two groups: the reductive and the oxidative 17β-HSDs. The reductive 17β-HSDs produce active androgens and estrogens by catalyzing the formation of the hydroxy group at position 17β of the steroid backbone. The oxidative 17β
