Glucocorticoid regulation of beta-adrenergic receptors in 3T3-L1 preadipocytes.
Abstract
Treatment of 3T3-L1 preadipocytes (fibroblasts) with 250 nM dexamethasone for 48 hr caused a doubling of total beta-adrenergic receptors and an increase in beta 2-adrenergic receptor subtype proportion from approximately 50% in controls to 85% in treated cells. The responses to epinephrine and norepinephrine in a whole cell cAMP accumulation assay reflected these changes. The effects of dexamethasone on beta-adrenergic receptors were mediated through the glucocorticoid receptor and were time and dose dependent with an EC50 of 2.77 +/- 0.73 nM for an increase in the proportion of beta 2-adrenergic receptors. The rank order of potency of steroids to effect these changes (betamethasone = dexamethasone greater than fludrocortisone greater than hydrocortisone = triamcinolone greater than aldosterone) correlated with their glucocorticoid potency. [3H]Dexamethasone binding to intact cells yielded a KD value of 3.47 +/- 0.38 nM for binding to the glucocorticoid receptor which correlated well with the EC50 for dexamethasone to alter beta-adrenergic receptors. Inhibition of [3H]dexamethasone binding by other steroids confirmed that the ability of steroids to regulate beta-adrenergic receptors correlated with the affinity of each compound for the 3T3-L1 glucocorticoid receptor. Progesterone, which can bind to the glucocorticoid receptor but has only weak agonist activity, competitively inhibited the ability of dexamethasone to alter beta-adrenergic receptors. Protein synthesis, RNA synthesis, and N-linked glycosylation appeared to be necessary for the change in receptor subtype expression and the increase in beta-adrenergic receptor number induced by dexamethasone. The present study suggests that regulation of beta-adrenergic receptor expression in 3T3-L1 preadipocytes by dexamethasone is a glucocorticoid-specific effect which may require gene activation.
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Cortisol and noradrenaline support each other in release of energy-rich fuels or calcium/phosphorus from stores.
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From Interaction of the endocrine system with inflammation: a function of energy and volume regulation (2014) · cites this paper as [56]
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“Although this supplement is regarded as one of the most widely used com - ponents, dexamethasone (as a glucocorticoid) is known to affect β2-adrenergic receptor density and expression [ 102, 103 ].”
- Authors
- Nakada, M. T., Stadel, J. M., Poksay, K. S., & Crooke, S. T.
- ORCID
- Crooke, S T
- Venue
- Molecular Pharmacology
- Publisher
- Elsevier BV
- Published
- 1987-04
- Volume
- 31
- Issue
- 4
- Pages
- 377-384
- ISSN
- 0026-895X (ISSN-L)
- OpenAlex
- W2280222586
- Cited by
- 78
- References
- 0
- Citations by year
- 2026: 2 · 2025: 3 · 2022: 2 · 2020: 2 · 2019: 1 · 2018: 2 · 2017: 1 · 2016: 2 · 2015: 3 · 2014: 6 · 2013: 1 · 2012: 1
- FWCI
- 1.79
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Molecular Pharmacology (publishedVersion)
- PubMed (publishedVersion)
- PubMed
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Receptor Mechanisms and Signaling
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Genetics › Estrogen and related hormone effects
- Health Sciences › Medicine › Physiology › Adipose Tissue and Metabolism
- Keywords
- glucocorticoid regulation, beta-adrenergic receptors, 3T3-L1 preadipocytes, dexamethasone, glucocorticoid receptor, epinephrine, norepinephrine, cAMP accumulation, steroid potency, progesterone, receptor expression, gene activation, protein synthesis, RNA synthesis, N-glycosylation
- MeSH terms
- Cyclic AMP, Adipose Tissue, Alprenolol, Animals, Binding, Competitive, Cell Line, Cycloheximide, Dactinomycin, Dexamethasone, Epinephrine, Colforsin, Glucocorticoids, Kinetics, Membranes, Norepinephrine, Pindolol, Receptors, Adrenergic, beta, Tunicamycin, Iodocyanopindolol, Mice
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