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Oxidative Medicine and Cellular Longevity
Volume 2015, Article ID 490613, 14 pages
Research Article

Integrated Haematological Profiles of Redox Status, Lipid, and Inflammatory Protein Biomarkers in Benign Obesity and Unhealthy Obesity with Metabolic Syndrome

1Section of Medical Pathophysiology, Endocrinology and Food Science, Department of Experimental Medicine, “Sapienza” University, “Umberto I” Polyclinic, Viale Regina Elena 324, 00161 Rome, Italy
2Department of Life Sciences and Biotechnology, University of Ferrara, Via Luigi Borsari 46, 44100 Ferrara, Italy
3Department of Food and Nutrition, Kyung Hee University, 26 Kyungheedae-ro, Dongdaemun-gu, Seoul 130-701, Republic of Korea
4Active Longevity Clinic “Institut Krasoty na Arbate”, 8 Maly Nikolopeskovsky Lane, Moscow 119002, Russia
5Centre of Innovative Biotechnological Investigations (Cibi-NanoLab), 197 Vernadskogo Prospekt, Moscow 119571, Russia

Received 15 December 2014; Revised 11 April 2015; Accepted 20 April 2015

Academic Editor: Antonio Ayala

Copyright © 2015 Carla Lubrano et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


The pathogenesis of obesity (OB) and metabolic syndrome (MetS) implies free radical-, oxidized lipid- (LOOH-), and inflammatory cytokine-mediated altered pathways in target organs. Key elements of the transition from benign OB to unhealthy OB+MetS remain unclear. Here, we measured a panel of redox, antioxidant, and inflammation markers in the groups of OB patients (67 with, 45 without MetS) and 90 controls. Both OB groups displayed elevated levels of adipokines and heavy oxidative stress (OS) evidenced by reduced levels of glutathione, downregulated glutathione-S-transferase, increased 4-hydroxynonenal-protein adducts, reactive oxygen species, and membrane-bound monounsaturated fatty acids (MUFA). Exclusively in OB+MetS, higher-than-normal glutathione peroxidase activity, tumor necrosis factor-α, and other proinflammatory cytokines/chemokines/growth factors were observed; a combination of high adipokine plasminogen activator inhibitor-1 and MUFA was consistent with increased cardiovascular risk. The uncomplicated OB group showed features of adaptation to OS such as decreased levels of vitamin E, activated superoxide dismutase, and inhibited catalase, suggesting H2O2 hyperproduction. Proinflammatory cytokine pattern was normal, except few markers like RANTES, a suitable candidate for therapeutic approaches to prevent a setting of MetS by inhibition of LOOH-primed leukocyte chemotaxis/recruitment to target tissues.