Abstract
Amongst other immune cells, neutrophils play a key role in systemic inflammation leading to cardiovascular disease and can release inflammatory factors, including lipocalin-2 (LCN2). LCN2 drives cardiac hypertrophy and plays a role in maladaptive remodelling of the heart and has been associated with renal injury. While lifestyle factors such as diet and exercise are known to attenuate low-grade inflammation, their ability to modulate plasma LCN2 levels is unknown. Forty-eight endurance athletes and 52 controls (18–55 years) underwent measurement for various cardiovascular health indicators, along with plasma LCN2 concentration. No significant difference in LCN2 concentration was seen between the two groups. LCN2 was a very weak predictor or absent from models describing blood pressures or predicting athlete status. In another cohort, 57 non-diabetic overweight or obese men and post-menopausal women who fulfilled Adult Treatment Panel III metabolic syndrome criteria were randomly allocated into either a control, modified Dietary Approaches to Stop Hypertension (DASH) diet, or DASH and exercise group. Pre- and post-intervention demographic, cardiovascular health indicators, and plasma LCN2 expression were measured in each individual. While BMI fell in intervention groups, LCN2 levels remained unchanged within and between all groups, as illustrated by strong correlations between LCN2 concentrations pre- and 12 weeks post-intervention (r = 0.743, P < 0.0001). This suggests that circulating LCN2 expression are stable over a period of at least 12 weeks and is not modifiable by diet and exercise.
Highlights
High body mass index (BMI) and obesity promote a low-grade chronic systemic inflammatory state, triggering a systemic acute phase response[1]
In the context of cardiac remodelling, LCN2 has been shown to preserve the enzymatic activity of matrix metalloprotease-9 (MMP9), a protein heavily involved in the breakdown of the interstitium[20,21]
The analysis showed that athlete status could be predicted correctly in 94.8% of individuals using BMI, sex, age, andV O2peak as predictors, with the model having an overall Cox & Snell β value of 0.683
Summary
High body mass index (BMI) and obesity promote a low-grade chronic systemic inflammatory state, triggering a systemic acute phase response[1]. Among a variety of inflammatory factors, neutrophils release lipocalin-2 (LCN2, otherwise known as neutrophil gelatinase-associated lipocalin or NGAL), a 25 kDa protein that is upregulated during the acute phase response, and primarily contributes to innate immunity through its function as an iron c helator[11,12]. It has been used clinically as a marker of renal failure and, more recently, as a marker of increased cardiovascular risk[13,14,15]. We aimed to determine if LCN2 plasma levels are modulated by physical fitness and diet, and to investigate whether LCN2 levels are stable over time
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