Estrogen interacts with glucocorticoids in the regulation of lipocalin 2 expression in human adipose tissue. Reciprocal roles of estrogen receptor α and β in insulin resistance?

التفاصيل البيبلوغرافية
العنوان: Estrogen interacts with glucocorticoids in the regulation of lipocalin 2 expression in human adipose tissue. Reciprocal roles of estrogen receptor α and β in insulin resistance?
المؤلفون: Kristina E. Almby, Prasad G. Kamble, Maria J. Pereira, Jan W. Eriksson
المصدر: Molecular and Cellular Endocrinology. 490:28-36
بيانات النشر: Elsevier BV, 2019.
سنة النشر: 2019
مصطلحات موضوعية: Adult, Male, 0301 basic medicine, medicine.medical_specialty, medicine.drug_class, Adipokine, Adipose tissue, Estrogen receptor, 030209 endocrinology & metabolism, Lipocalin, Biochemistry, Dexamethasone, 03 medical and health sciences, 0302 clinical medicine, Endocrinology, Insulin resistance, Lipocalin-2, Internal medicine, medicine, Estrogen Receptor beta, Humans, Glucocorticoids, Molecular Biology, Aged, Chemistry, Estrogen Receptor alpha, Estrogens, Middle Aged, medicine.disease, Postmenopause, 030104 developmental biology, Adipose Tissue, Gene Expression Regulation, Premenopause, Estrogen, Female, Insulin Resistance, Glucocorticoid, medicine.drug
الوصف: 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-β-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) α antagonist alone but not with ERβ antagonist, suggesting that E2 effects on LCN2 are mediated via ERβ pathway. Dexamethasone alone or E2+dexamethasone had no significant effect on LCN2. However, E2+dexamethasone increased LCN2 expression with ERα-blockade. Dexamethasone reduced ERα but increased ERβ expression. Dexamethasone can regulate LCN2 expression via inhibition of ERα and stimulation of ERβ and may contribute to the development of glucocorticoid-induced insulin resistance in human AT. In conclusion, ERβ and ERα pathways have opposite effects on LCN2 expression and they interact with glucocorticoid action.
تدمد: 0303-7207
الوصول الحر: https://explore.openaire.eu/search/publication?articleId=doi_dedup___::3bd0ef07fed0e8f14410238ea543764fTest
https://doi.org/10.1016/j.mce.2019.04.002Test
حقوق: CLOSED
رقم الانضمام: edsair.doi.dedup.....3bd0ef07fed0e8f14410238ea543764f
قاعدة البيانات: OpenAIRE