Glucocorticoid-induced insulin resistance is related to macrophage visceral adipose tissue infiltration

The Journal of Steroid Biochemistry and Molecular Biology
Thi Thu Huong DoBuyse Marion

Abstract

Insulin resistance is frequently present in patients with glucocorticoid (GC) excess (Cushing's syndrome) or treated with high doses of GCs. Furthermore, others similarities between metabolic syndrome (visceral obesity, elevated blood glucose levels, dyslipidemia) and Cushing's syndrome suggest that GCs could play a role in obesity-linked complications. Here we reported that long-term corticosterone (CORT) exposure in mice induced weight gain, dyslipidemia as well as hyperglycaemia and systemic insulin resistance. CORT-treated mice exhibited an increased 11β-Hsd1 expression and corticosterone levels in fat depots but a specific upregulation of glucocorticoid receptor (Gr) and hexose-6-phosphate dehydrogenase only in gonadal adipose tissue, suggesting that GC could act differentially on various fat depots. Despite fat accumulation in all depots, an increased expression of adipogenic (Pparγ, C/ebpα) and lipogenic (Acc, Fas) key genes was restricted to gonadal adipose tissue. Hypertrophied adipocytes observed in both visceral and subcutaneous depots also resulted from reduced lipolytic activity due to CORT treatment. Surprisingly, GC treatment promoted macrophage infiltration (F4/80, Cd68) within all adipose tissues along with pre...Continue Reading

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Citations

Jun 12, 2019·International Journal of Molecular Sciences·Adrián Hernández-DíazcouderFausto Sánchez-Muñoz
Nov 30, 2018·International Journal of Molecular Sciences·Emira AyroldiCarlo Riccardi
Sep 12, 2019·Frontiers in Immunology·Jan M EhrchenKatarzyna Barczyk-Kahlert
Jul 17, 2020·Frontiers in Molecular Neuroscience·Lorraine SieboldStephen Ashwal
Jan 14, 2021·International Journal of Molecular Sciences·Carine BeaupereGhislaine Guillemain
Sep 7, 2021·The Journal of Clinical Endocrinology and Metabolism·Guillermo García-EgurenFelicia A Hanzu

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