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Estrogen interacts with glucocorticoids in the regulation of lipocalin 2 expression in human adipose tissue. Reciprocal roles of estrogen receptor alpha and beta in insulin resistance?
Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Medical Sciences, Clinical diabetology and metabolism.
Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Medical Sciences, Clinical diabetology and metabolism.ORCID iD: 0000-0001-5498-3899
Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Medical Sciences, Clinical diabetology and metabolism.
Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Medical Sciences, Clinical diabetology and metabolism.ORCID iD: 0000-0002-2639-9481
2019 (English)In: Molecular and Cellular Endocrinology, ISSN 0303-7207, E-ISSN 1872-8057, Vol. 490, p. 28-36Article in journal (Refereed) Published
Abstract [en]

The adipokine lipocalin 2 (LCN2) is linked to insulin resistance. Its expression in human adipose tissue (AT) can be regulated in a sex-specific manner by a synthetic glucocorticoid, dexamethasone, suggesting an underlying role of sex steroids. We show that 17-beta-estradiol (E2) dose-dependently increased LCN2 gene expression in subcutaneous AT from postmenopausal women. This was also seen in the presence of estrogen receptor (ER) alpha antagonist alone but not with ER beta antagonist, suggesting that E2 effects on LCN2 are mediated via ER beta pathway. Dexamethasone alone or E2 + dexamethasone had no significant effect on LCN2. However, E2+ dexamethasone increased LCN2 expression with ER alpha-blockade. Dexamethasone reduced ER alpha but increased ER beta expression. Dexamethasone can regulate LCN2 expression via inhibition of ER alpha and stimulation of ER beta and may contribute to the development of glucocorticoid-induced insulin resistance in human AT. In conclusion, ER beta and ER alpha pathways have opposite effects on LCN2 expression and they interact with glucocorticoid action.

Place, publisher, year, edition, pages
ELSEVIER IRELAND LTD , 2019. Vol. 490, p. 28-36
Keywords [en]
Human adipose tissue, Estrogen, Glucocorticoids, Lipocalin2
National Category
Endocrinology and Diabetes
Identifiers
URN: urn:nbn:se:uu:diva-384989DOI: 10.1016/j.mce.2019.04.002ISI: 000467539600004PubMedID: 30953748OAI: oai:DiVA.org:uu-384989DiVA, id: diva2:1324029
Funder
Swedish Diabetes AssociationEXODIAB - Excellence of Diabetes Research in SwedenErnfors FoundationAvailable from: 2019-06-13 Created: 2019-06-13 Last updated: 2019-06-13Bibliographically approved

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Kamble, Prasad G.Pereira, Maria JAlmby, Kristina E.Eriksson, Jan

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