The Hepatokine Leukocyte Cell-Derived Chemotaxin-2 Is Elevated in People with Impaired Glycaemic Regulation and Augmented by Acute Exercise
Buket Engin,
Scott A. Willis,
Sundus Malaikah,
Jack A. Sargeant,
David J. Stensel,
Charlotte Jelleyman,
Gaël Ennequin,
Guruprasad P. Aithal,
Thomas Yates,
James A. King
Affiliations
Buket Engin
National Centre for Sport and Exercise Medicine, School of Sport, Exercise and Health Sciences, Loughborough University, Loughborough LE11 3TU, UK
Scott A. Willis
National Centre for Sport and Exercise Medicine, School of Sport, Exercise and Health Sciences, Loughborough University, Loughborough LE11 3TU, UK
Sundus Malaikah
National Centre for Sport and Exercise Medicine, School of Sport, Exercise and Health Sciences, Loughborough University, Loughborough LE11 3TU, UK
Jack A. Sargeant
NIHR Leicester Biomedical Research Centre, University Hospitals of Leicester NHS Trust and University of Leicester, Leicester LE5 4PW, UK
David J. Stensel
National Centre for Sport and Exercise Medicine, School of Sport, Exercise and Health Sciences, Loughborough University, Loughborough LE11 3TU, UK
Charlotte Jelleyman
Human Potential Centre, School of Sport & Recreation, Auckland University of Technology, Auckland 1010, New Zealand
Gaël Ennequin
Laboratory of the Metabolic Adaptations to Exercise under Physiological and Pathological Conditions (AME2P), Clermont Auvergne University, CRNH Auvergne, 63000 Clermont-Ferrand, France
Guruprasad P. Aithal
Nottingham Digestive Diseases Centre, School of Medicine, University of Nottingham, Nottingham NG5 1PB, UK
Thomas Yates
NIHR Leicester Biomedical Research Centre, University Hospitals of Leicester NHS Trust and University of Leicester, Leicester LE5 4PW, UK
James A. King
National Centre for Sport and Exercise Medicine, School of Sport, Exercise and Health Sciences, Loughborough University, Loughborough LE11 3TU, UK
The hepatokine leukocyte cell-derived chemotaxin-2 (LECT2) promotes insulin resistance and hepatic fibrogenesis. In rodents, acute exercise suppresses circulating LECT2; however, human data are lacking. This study compared circulating LECT2 across populations and explored whether acute exercise impacts circulating LECT2. In Part A (n = 43), data were pooled from three experimental studies, regarding the following groups: healthy individuals, individuals with impaired glycaemic regulation (IGR), and individuals with type 2 diabetes and metabolic dysfunction-associated steatotic liver disease (T2DM-MASLD). Generalised linear models assessed differences in circulating LECT2 among groups. Part B (n = 20) involved exercise (30 min, 65% peak oxygen uptake) and control (resting) trials in the healthy and IGR groups. Circulating LECT2 was measured before and at 0, 1, 2 and 3 h post-exercise. Generalised estimating equations assessed differences in LECT2 responses to the trials among groups. In Part A, circulating LECT2 levels were 28.7% and 37.3% higher in the IGR and T2DM-MASLD groups, vs. healthy individuals (p ≤ 0.038), with BMI identified as the main predictor (p = 0.008). In Part B, average circulating LECT2 levels were 6.3% higher after exercise vs. in the control (p p = 0.829). In the combined cohort, circulating LECT2 levels were elevated 1–3 h after exercise vs. control (p ≤ 0.009). LECT2 is elevated in people with dysglycaemia, with BMI as a leading predictor. Contrary to previous rodent work, acute exercise augments, rather than suppresses, circulating LECT2 in humans.
