Abstract
SUMMARYPrader-Willi syndrome (PWS) represents the most common form of genetic obesity. Several studies confirm that obesity is associated with inflammation, oxidative stress and impairment of antioxidant systems; however, no data are available concerning PWS subjects. We compared levels of plasma lipids and C-reactive protein (CRP) in 30 subjects of ‘normal’ weight (18.5–25 kg/m2), 15 PWS obese (>30 kg/m2) subjects and 13 body mass index (BMI)-matched obese subjects not affected by PWS. In all subjects, we evaluated the levels of lipid hydroperoxides and the activity of paraoxonase-1 (PON1), an enzyme involved in the antioxidant and anti-inflammatory properties exerted by high-density lipoproteins (HDLs). Furthermore, using the fluorescent molecule of Laurdan, we investigated the physicochemical properties of HDLs isolated from normal weight and obese individuals. Altogether, our results demonstrated, for the first time, higher levels of lipid hydroperoxides and a lower PON1 activity in plasma of obese individuals with PWS with respect to normal-weight controls. These alterations are related to CRP levels, with a lower PON1:CRP ratio in PWS compared with non-PWS obese subjects. The study of Laurdan fluorescence parameters showed significant modifications of physicochemical properties in HDLs from PWS individuals. Whatever the cause of obesity, the increase of adiposity is associated with inflammation, oxidative stress and alterations in HDL compositional and functional properties.
Highlights
Environmental and genetic factors are involved in the development of human obesity, a predisposing factor for cardiovascular diseases (CVDs) (Zalesin et al, 2011)
In the present study we confirmed a significant increase in lipid hydroperoxides and a decrease in the activity of the antioxidant and anti-inflammatory enzyme PON1 in plasma of non-Prader-Willi syndrome (PWS) obese individuals with respect to normalweight subjects, in good agreement with previous studies carried out by us and by other authors (Higdon and Frei, 2003; Ferretti et al, 2005; Vincent and Taylor, 2006; Ferretti et al, 2010b; BondiaPons et al, 2012)
We demonstrate an increase in the levels of lipid hydroperoxides and a decrease in the activity of the enzyme PON1 in plasma of PWS obese subjects, in the absence of significant changes of plasma lipids [total cholesterol (TC), cholesterol associated with low-density lipoprotein (LDL) (LDL-C), TG]
Summary
Environmental and genetic factors are involved in the development of human obesity, a predisposing factor for cardiovascular diseases (CVDs) (Zalesin et al, 2011). Prader-Willi syndrome (PWS), a complex disorder associated with elevated morbidity and mortality both in paediatric and in adult ages (Whittington et al, 2001), is the most common form of genetic obesity. Adults with PWS die prematurely from complications conventionally related to obesity, including type 2 diabetes mellitus (DM2), respiratory insufficiency and CVD (Einfeld et al, 2006; Patel et al, 2007). In this respect, we have previously demonstrated a cardiac cause of death in 58% of adults with PWS (Grugni et al, 2008)
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