The influence of acute moderate-intensity exercise on circulating fibroblast growth factor (FGF) 21 and fetuin-A concentrations in lean and overweight men.

Background & Aim: FGF21 and fetuin-A are liver-secreted proteins (hepatokines) that modulate peripheral glucose metabolism. Hepatokine secretion is altered by hepatic steatosis which has prompted interest surrounding their role in Non-Alcoholic Fatty Liver Disease pathophysiology1,2. Circulating FGF21 and fetuin-A concentrations may be influenced by exercise but evidence in humans is limited. We sought to examine the impact of acute exercise on circulating FGF21 and fetuin-A; and explore any mediating effect of BMI. Objective: To characterise the effects of acute moderate-intensity exercise on plasma concentrations of FGF21 and fetuin-A in lean and overweight men. Material & Methods: Fourteen, age-matched (44 ± 17 years; mean ± SD), healthy men were recruited into lean and overweight groups (BMI: 23.4 ± 1.5 vs. 28.6 ± 3.0 kg/m2). Participants completed exercise and control trials in a randomised, counterbalanced order, each lasting seven hours. In the exercise trial, participants performed continuous treadmill exercise (60% VO2peak) during the first hour then rested. Participants rested throughout the control trial. Plasma concentrations of FGF21 and fetuin-A were measured at 0, 1, 1.5, 2.75, 4 and 7 hours via ELISA (R & D Systems, UK). Results: Fasting FGF21 concentrations were higher in overweight versus lean individuals (184 ± 29 vs 81 ± 22 pg/mL, P=0.02), however BMI did not modulate responses over time nor the impact of exercise (P≥0.20). Subsequently, with groups combined, exercise significantly increased plasma concentrations of FGF21 versus control (P=0.02) with pairwise comparisons revealing significant elevations at 1, 1.5, 2.75 and 4 hours (P≤0.04). Conversely, fetuin-A was unaffected by exercise (P=0.52). Conclusions: This study demonstrates that acute moderate-intensity exercise transiently increases circulating concentrations of FGF21 but not fetuin-A; findings are not mediated by BMI. References: 1. Iroz A, Couty J-P, Postic C. (2015). Diabetologia.1699-1703. 2. Stefan N, Häring H-U. (2013). Nat. Rev. Endocrinol. 9(3):144-52. Acknowledgements: This study was supported by the NIHR, Leicester-Loughborough Diet, Lifestyle and Physical Activity Biomedical Research Unit based at University Hospitals Leicester and Loughborough University. Conflicts of Interest & Funding Disclosures: The authors have no conflicts of interest to declare.