Glucocorticoid exposure causes disrupted glucoregulation, cardiac inflammation and elevated dipeptidyl peptidase-4 activity independent of glycogen synthase kinase-3 in female rats

Abstract

Objective: We tested the hypothesis that glucocorticoid (GC) exposure in female rats would lead to glucose dysregulation and elevated cardiac inflammatory biomarkers, which are dipeptidyl peptidase-4 (DPP-4)- and glycogen synthase kinase-3 (GSK-3)-dependent.

Methods: Female Wistar rats received vehicle (control; n = 6) or GC (dexamethasone; n = 6; 0.2 mg/kg; p.o.) for six days. Insulin resistance was determined by HOMA-IR. DPP-4 activity was determined by fluorescence method, whereas vascular cell adhesion molecule-1 (VCAM-1), uric acid, malondialdehyde (MDA), lactate dehydrogenase (LDH) and nitric oxide (NO) from plasma and cardiac homogenate were estimated as cardiac pro-inflammatory biomarkers.

Results: Results showed that GC exposure resulted in glucose dysregulation and increased plasma and cardiac pro-inflammatory markers which are associated with elevated DPP-4 activity but reduced GSK-3.

Conclusions: The present results demonstrate that GC exposure would cause glucose dysregulation, increased DPP-4 activity and cardiac inflammation that is independent of GSK-3.

Keywords:

• Dexamethasone
• DPP-4
• GSK-3
• glucose homeostasis
• VCAM-1

Acknowledgements

The authors are also appreciative of the facilities made available by HOPE Cardiometabolic Research Team, Ilorin, Nigeria.

Disclosure statement

No potential conflict of interest was reported by the authors.

Additional information

Funding

This research was supported by Association of African Universities (AAU; 2017/2018) and International Society of Hypertension (ISH) grant for mentors (2017).