Cited by 119Metabolism, Diabetes, and CancerIon Transport and Channel RegulationEstrogen and related hormone effects

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Dexamethasone causes translocation of glucose transporters from the plasma membrane to an intracellular site in human fibroblasts

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Horner, H C, Munck, A, Lienhard, G E·1987·Journal of Biological Chemistry

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Abstract

To investigate the mechanism by which glucocorticoids inhibit glucose transport in peripheral tissues, we have used a monoclonal antibody directed against the human glucose transporter to measure the relative amounts of glucose transporter polypeptide in various cell fractions of human foreskin fibroblasts after treatment with and without dexamethasone. In cells treated for 4 h with 100 nM dexamethasone, a decrease of 48% in glucose transport was accompanied by a decrease of 40% in the amount of glucose transporter polypeptide in a plasma membrane fraction enriched 10-fold in 5'-nucleotidase activity and a 78% increase in the amount of transporter polypeptide in a fraction of putative intracellular membranes, designated P2. There was no significant change in the amount of transporter polypeptide in whole cell lysates. Insulin (200 nM) stimulated glucose transport in basal fibroblasts by only 9%. However, addition of insulin for 30 min to cells that had been treated for 4 h with dexamethasone completely reversed the dexamethasone-induced decrease in glucose transport and also reversed the dexamethasone-induced changes in glucose transporter polypeptide content of the plasma membrane and P2 fractions. From these observations we conclude that dexamethasone decreases glucose transport by causing translocation of glucose transporters from the plasma membrane to an internal location and that insulin reverses the dexamethasone effect by reversing the translocation.

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Authors: Horner, H. C., Munck, A., & Lienhard, G. E.
Affiliations: Dartmouth College (US)
Venue: Journal of Biological Chemistry
Publisher: Elsevier BV
Published: 1987-12
Volume: 262
Issue: 36
Pages: 17696-17702
ISSN: 0021-9258 (ISSN-L)
DOI: 10.1016/s0021-9258(18)45435-x
OpenAlex: W1524260356
Cited by: 119
References: 46
Citations by year: 2025: 2 · 2022: 3 · 2021: 3 · 2020: 1 · 2019: 3 · 2018: 4 · 2017: 1 · 2016: 1 · 2015: 1 · 2014: 1 · 2013: 2 · 2012: 1
FWCI: 2.96
Type: journal article
Language: en
Open access: hybrid
doi.org
Licence: cc-by
www.elsevier.com/tdm/userlicense/1.0/ (tdm)
www.elsevier.com/legal/tdmrep-license (tdm)
creativecommons.org/licenses/by/4.0/ (vor, 12008 d)
Locations: Journal of Biological Chemistry (publishedVersion, cc-by)
PubMed (publishedVersion)
Funders: National Institutes of Health (2r01am003535-27)
National Cancer Institute (CA 23 108)
National Institute of General Medical Sciences (GM 22996)
Topics: Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Metabolism, Diabetes, and Cancer
Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Ion Transport and Channel Regulation
Life Sciences › Biochemistry, Genetics and Molecular Biology › Endocrinology › Estrogen and related hormone effects
Keywords: dexamethasone, glucose transport, glucose transporters, glucocorticoids, insulin, human foreskin fibroblasts, plasma membrane
MeSH terms: Cell Membrane, Cells, Cultured, Deoxyglucose, Dexamethasone, Dose-Response Relationship, Drug, Fibroblasts, Humans, Insulin, Monosaccharide Transport Proteins, Nucleotidases, Time Factors, 5'-Nucleotidase

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Dexamethasone causes translocation of glucose transporters from the plasma membrane to an intracellular site in human fibroblasts

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