Integrated haematological profiles of redox status, lipid, and inflammatory protein biomarkers in benign obesity and unhealthy obesity with metabolic syndrome

The pathogenesis of obesity (OB) and metabolic syndrome (MetS) is thought to imply free radical-, oxidized lipid- and inflammatory cytokine-mediated altered pathways in target organs, primarily adipose tissue. Key elements of the transition from benign OB to unhealthy OB+MetS remain un-clear. Here, we measured an extensive panel of redox, antioxidant, and inflammation blood markers in the groups of N=112 OB patients (67 with, 45 without MetS) and 90 controls in order to distin-guish the two groups. Both OB groups displayed heavy oxidative stress (OS) evidenced by reduced vs. normal levels of glutathione, downregulated glutathione-S-transferase, increased 4-hydroxynonenal protein adducts, reactive oxygen species (ROS), and membrane-bound monoun-saturated fatty acids (MUFA). In the unhealthy OB+MetS, elevated glutathione peroxidase (GPX) activity accounted for advanced lipid peroxide (LOOH) formation, with elevated plasmatic tumor necrosis factor-α, and other pro-inflammatory cytokines/chemokines/growth factors and adipokines produced by adipose tissues and circulating leukocytes primed by LOOH. High adipokine plasmin-ogen activator inhibitor-1 and MUFA were consistent with increased cardio-vascular risk. The un-complicated OB group showed features of adaptation to OS such as decreased levels of vitamin E, activated superoxide dismutase and inhibited catalase, suggesting elevated hydrogen peroxide pro-duction. Pro-inflammatory cytokine profile was similar to controls, except few markers like RANTES, a suitable candidate for therapeutic approaches to prevent a setting of MetS by inhibition of LOOH primed leukocyte chemotaxis and recruitment to target tissues.