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Blockade of mineralocorticoid receptor ameliorates oral contraceptive-induced insulin resistance by suppressing elevated uric acid and glycogen synthase kinase-3 instead of circulating mineralocorticoid.

Authors
  • Adeyanju, O A1, 2
  • Michael, O S1, 3
  • Soladoye, A O1, 3
  • Olatunji, L A1
  • 1 HOPE Cardiometabolic Research Team, Department of Physiology, University of Ilorin, Ilorin, Nigeria. , (Niger)
  • 2 Cardiometabolic Research Unit, Department of Physiology, College of Medicine and Health sciences, Afe Babalola University, Ado-Ekiti, Nigeria. , (Niger)
  • 3 Cardiometabolic Research Unit, Department of Physiology, College of Health sciences, Bowen University, Iwo, Nigeria. , (Niger)
Type
Published Article
Journal
Archives of physiology and biochemistry
Publication Date
Jul 01, 2020
Volume
126
Issue
3
Pages
225–234
Identifiers
DOI: 10.1080/13813455.2018.1509220
PMID: 30318954
Source
Medline
Keywords
Language
English
License
Unknown

Abstract

Context: Estrogen-progestin combined oral contraceptive (COC) has been connected to mineralocorticoid receptor (MR) activation and adverse cardiometabolic events. We consequently hypothesised that insulin resistance (IR), hyperuricemia, and elevated circulating GSK-3 induced by COC is through activation of MR via mineralocorticoid and glucocorticoid pathways.Methods: Female Wistar rats aged 12 weeks received (po) vehicle and COC (1.0 μg ethinylestradiol plus 5.0 μg levonorgestrel) with or without MR blocker (0.25 mg/kg spironolactone; Spl), daily for eight weeks.Results: Data showed that COC treatment led to increased IR, 1-hour postload glucose level, insulinemia, triglyceride/HDL-cholesterol ratio, total cholesterol/HDL-cholesterol ratio, uric acid, GSK-3, aldosterone, corticosterone values, impaired glucose tolerance and pancreatic β-cell function. However, MR blockade by Spl ameliorated all these alterations except that of aldosterone.Conclusion: The results demonstrate that COC induces IR, hyperuricemia and high GSK-3 levels through activation of MR via glucocorticoid dependent pathway.

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