Objectives
Elevated lipocalin-2 (LCN2) is associated with increased risk of cardio-metabolic disease. LCN2 has different forms including a polyaminated (hLCN2), secreted by osteoblasts, and non-polyaminated (C87A and R81E), secreted by adipocytes. Glucocorticoids negatively affect bone and energy metabolism while exercise improves energy metabolism. As such, both glucocorticoids and exercise potentially regulate circulating LCN2. We hypothesised that glucocorticoids would suppress LCN2 and its forms, at baseline and following exercise
Methods
In a double-blind, randomised crossover design, nine young, healthy males (aged 27.8 ± 4.9 years, BMI 24.4 ± 2.4 kg/m2) completed 30 mins of high intensity aerobic exercise (4 sets x 4 mins at 90-95% HRR) after glucocorticoid (20 mg prednisolone) or placebo treatments. Blood was collected at baseline, immediately post-exercise, 1 h post-exercise (variant analyses only), and 3 h post-exercise. LCN2 was analysed using commercially available ELISA (LCN2 Abcam – primary outcome) and different forms of LCN2 (hLCN2, C87A and R81E) using in-house assays previously validated, secondary outcomes.
Results
LCN2 (Abcam) was elevated after prednisolone compared with placebo (main treatment effect of ~10%; p = 0.015). Prednisolone treatment had no effect on individual LCN2 forms (all p > 0.53). Regardless of treatment, or assay used, LCN2, C87A, R81E, and hLCN2 increased immediately after exercise (all p < 0.033). LCN2, but not the forms, remained elevated at 3 h post-ex (p = 0.048).
Conclusion
In contrast to our hypothesis, prednisolone had a limited effect on LCN2, however, both LCN2 and its forms are transiently increased by acute exercise in young healthy males, independent of assay used. The role of LCN2 and it forms in exercise and glucose metabolism warrant further investigation.