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Dynamics of glucocorticoid receptor and induction of tyrosine aminotransferase in rat liver.
Endocrinol Jpn. 1982 Apr; 29(2):209-18.EJ

Abstract

In order to better understand the role of glucocorticoid receptor in the hormonal action of glucocorticoid, depletion and replenishment of the cytoplasmic receptor and kinetics of induction of tyrosine aminotransferase (TAT) in rat liver were examined after administration of dexamethasone (Dex) and prednisolone. The extent of the receptor depletion and the duration of the depletion period were dose-dependent and were well correlated not only with the biological potency of the steroids administered but also with the kinetics of TAT induction. A linear relationship between the amount of depleted receptor and the kinetics of TAT induction was observed. Pretreatment of animals with a large dose of Dex reduced the response of TAT induction by Dex which was administered 24 h later. This seems to be attributable, at least in part, to the incomplete replenishment of the receptor and also to the increased rate of replenishment of the receptor. The reduced affinity of the partially replenished receptor to glucocorticoid might also participate in lowering the response to the second injection. In conclusion, depletion and replenishment of the cytoplasmic glucocorticoid receptor appeared to be directly responsible for the physiological action of glucocorticoid.

Authors

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Pub Type(s)

Journal Article

Language

eng

PubMed ID

6127207

Citation

Izawa, M, et al. "Dynamics of Glucocorticoid Receptor and Induction of Tyrosine Aminotransferase in Rat Liver." Endocrinologia Japonica, vol. 29, no. 2, 1982, pp. 209-18.
Izawa M, Yoshida A, Ichii S. Dynamics of glucocorticoid receptor and induction of tyrosine aminotransferase in rat liver. Endocrinol Jpn. 1982;29(2):209-18.
Izawa, M., Yoshida, A., & Ichii, S. (1982). Dynamics of glucocorticoid receptor and induction of tyrosine aminotransferase in rat liver. Endocrinologia Japonica, 29(2), 209-18.
Izawa M, Yoshida A, Ichii S. Dynamics of Glucocorticoid Receptor and Induction of Tyrosine Aminotransferase in Rat Liver. Endocrinol Jpn. 1982;29(2):209-18. PubMed PMID: 6127207.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Dynamics of glucocorticoid receptor and induction of tyrosine aminotransferase in rat liver. AU - Izawa,M, AU - Yoshida,A, AU - Ichii,S, PY - 1982/4/1/pubmed PY - 1982/4/1/medline PY - 1982/4/1/entrez SP - 209 EP - 18 JF - Endocrinologia japonica JO - Endocrinol Jpn VL - 29 IS - 2 N2 - In order to better understand the role of glucocorticoid receptor in the hormonal action of glucocorticoid, depletion and replenishment of the cytoplasmic receptor and kinetics of induction of tyrosine aminotransferase (TAT) in rat liver were examined after administration of dexamethasone (Dex) and prednisolone. The extent of the receptor depletion and the duration of the depletion period were dose-dependent and were well correlated not only with the biological potency of the steroids administered but also with the kinetics of TAT induction. A linear relationship between the amount of depleted receptor and the kinetics of TAT induction was observed. Pretreatment of animals with a large dose of Dex reduced the response of TAT induction by Dex which was administered 24 h later. This seems to be attributable, at least in part, to the incomplete replenishment of the receptor and also to the increased rate of replenishment of the receptor. The reduced affinity of the partially replenished receptor to glucocorticoid might also participate in lowering the response to the second injection. In conclusion, depletion and replenishment of the cytoplasmic glucocorticoid receptor appeared to be directly responsible for the physiological action of glucocorticoid. SN - 0013-7219 UR - https://www.unboundmedicine.com/medline/citation/6127207/Dynamics_of_glucocorticoid_receptor_and_induction_of_tyrosine_aminotransferase_in_rat_liver_ L2 - https://joi.jlc.jst.go.jp/JST.Journalarchive/endocrj1954/29.209?from=PubMed DB - PRIME DP - Unbound Medicine ER -