The immunomodulatory property of leptin: Linking plasma leptin status with oxidative stress and inflammation marker in young females of divergent energy states.
26 April 2019 (online)
Leptin is an important adipokin that is synthesized in accordance with the amount of fat stored in adipocytes and contributes centrally to energy homeostasis. However, elevated plasma leptin levels have been shown to adversely influence immune response by enhancing proinflammatory cytokine secretion and thus increasing oxidative stress. Oppositely, immunosuppressive states have been associated with leptin depletion. Most studies dealing with this interconnection focus on obesity, however, there is only few data regarding anorexia nervosa (AN) patients and athletes available. We aimed to evaluate the plasma leptin, inflammation and oxidative stress levels in a cohort of females of divergent energy states.
107 females (18 – 40 years) of various energy status groups (anorexia nervosa AN, normal weight NW, overweight OW, obese OB, and athletes AT) were enrolled. C-reactive protein (CRP) and interleukin 6 (IL-6) were chosen as inflammation marker and determined in plasma by a particle enhanced turbidimetric assay. Total oxidant capacity (T0C) that refers to the total of peroxides and leptin were measured in serum samples by ELISAs.
The BMI range was 13.24 to 46.89 kg/m2. Leptin levels differed significantly between the groups (p < 0.001) and correlated with the BMI (rs= 0.863, p < 0.001), the inflammation marker CRP (rs= 0.576, p < 0.001) and IL-6 (rs= 0.522, p < 0.001), and T0C (rs= 0.387, p < 0.001). Group comparisons revealed significantly higher CRP levels in OB (OB:AN/NW/AT p < 0.001, OB:OW p = 0.003), significantly higher T0C in OB compared to AN (p < 0.001) and NW (p = 0.001) and lower T0C in AN compared to AT (p = 0.021).
In our study population an increase of plasma leptin levels was associated with elevated inflammation markers and oxidative stress, supporting the proposed proinflammatory ability of leptin found in cell and animal models. Although inflammation marker were not elevated in AT, T0C was strikingly high. This might be explained by the enhanced exercise burden. No striking deviations in AN could be observed. Further research in clinical settings focusing on specific immune marker and taking nutritional anti-oxidant status into account is needed to investigate the interconnection of leptin on the immune system.
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