Glucocorticoid Receptor and Beta-Adrenoceptor Expression in Epididymal Adipose Tissue from Stressed Rats

Authors

  • ELISÂNGELA FARIAS-SILVA,

    1. Department of Physiology and Biophysics, Institute of Biology, State University of Campinas (UNICAMP), Campinas, Brazil
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  • IRAÍDES NUNES DOS SANTOS,

    1. Department of Physiology and Biophysics, Institute of Biology, State University of Campinas (UNICAMP), Campinas, Brazil
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  • MARIA ESMÉRIA COREZOLA DO AMARAL,

    1. Department of Physiology and Biophysics, Institute of Biology, State University of Campinas (UNICAMP), Campinas, Brazil
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  • DORA MARIA GRASSI-KASSISSE,

    1. Department of Physiology and Biophysics, Institute of Biology, State University of Campinas (UNICAMP), Campinas, Brazil
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  • REGINA CELIA SPADARI-BRATFISCH

    Corresponding author
    1. Department of Physiology and Biophysics, Institute of Biology, State University of Campinas (UNICAMP), Campinas, Brazil
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  • *This paper is part of a Ph.D. thesis by Elisângela Farias-Silva.

Address for correspondence: R.C. Spadari-Bratfisch, Laboratório do Estudo do Estresse (LABEEST), Departamento de Fisiologia e Biofísica, Instituto de Biologia, Universidade Estadual de Campinas (UNICAMP), CP 6109, CEP: 13089-970, Campinas, SP, Brasil. Fax: (55) (19) 3788-6185. e-mail: rspabrat@unicamp.br

Abstract

Abstract: Adipocytes isolated from epididymal adipose tissue of foot-shock stressed rats are supersensitive to isoprenaline and subsensitive to norepinephrine. These alterations are probably mediated by a stress-induced increase in plasma corticosterone levels. We investigated whether foot-shock stress modifies the expression of glucocorticoid receptors (GRs) and β-adrenergic protein receptors (β-ARs) in epididymal adipose tissue from rats submitted to one daily foot-shock session on three consecutive days. This stress protocol caused decreases in GR, β1-AR, and β3-AR protein levels, but caused an increase in β2-AR. These results confirm and support previous functional studies. The alterations in protein expression may be modulated by the high corticosterone levels that downregulate the glucocorticoid receptor.

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