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.