Association of the Ala16Val MnSOD gene polymorphism with plasma leptin levels and oxidative stress biomarkers in obese patients.

Chronic oxidative stress is a major characteristic of obesity. Manganese superoxide dismutase (MnSOD) is an antioxidant enzyme known to be present within mitochondria and is considered a main defense against oxidative stress. The aim of this study was to investigate the association between the MnSOD gene Ala16Val polymorphism in obesity in terms of body mass index (BMI), lipid parameters, plasma leptin levels, homeostasis model assessment of insulin resistance (HOMA-IR), and oxidative stress biomarkers. The study included 150 obese and 120 non-obese subjects. The MnSOD Ala16Val polymorphism was determined by polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP). Plasma leptin levels, serum lipid, superoxide dismutase (SOD), malondialdehyde (MDA), and anthropometric parameters were measured. No association was found between the MnSOD gene Ala16Val polymorphism and BMI in the study or control group. Strikingly, in the study group, obese subjects with the VV genotype had significantly higher plasma leptin levels (p<0.001) than those with the AA and AV genotypes. Serum total cholesterol (p<0.01) and MDA (p<0.001) levels were significantly higher in subjects with the VV genotype for MnSOD in the obese and non-obese groups. In the obese group, subjects with the VV genotype had significantly lower SOD (p<0.001) activity than the AA and AV genotypes. Our results suggest that the MnSOD gene polymorphism was associated with leptin levels and superoxide dismutase activity in the obese group but had no direct association with obesity. Moreover, the Ala16Val polymorphism has a significant effect on lipid profiles and MDA levels in both obese and non-obese subjects.