Crosstalk between Oxidative Stress and Inflammation in Obesity

Abstract

Obesity is a multifactorial disease in which oxidative stress and inflammation play important roles. The aim of our study was to evaluate oxidative stress levels and inflammation markers in obese subjects vs. controls and to investigate the relationship between these values. We found increased levels of reactive oxygen species and inflammation markers (fibrinogen, ferritin, CRP, NLR) and decreased levels of antioxidants in obese subjects vs. controls.Obesity is a multifactorial disease, characterized by the accumulation of abnormal or excessive fat. Considered a global health problem, obesity is involved in the development of a myriad of health issues, such as diabetes mellitus, cardiovascular disease, cancer, infertility, asthma, sleep disorders, irritable bowel syndrome, hepatic and renal dysfunctions. According to the World Health Organization (WHO) definition of overweight and obesity, an overweight subject has a body mass index (BMI) of 25 to 29.9 kg/m 2 , whereas the BMI of an obese subject exceeds 30 kg/m 2 . Recent studies have underlined that, in obese subjects, the adipose tissue dysfunction derives also from the interplay between reactive oxygen species (ROS) signalling and inflammatory response pathways [1][2][3][4][5][6][7][8][9].Oxidative stress, defined as the imbalance between the production of ROS and the levels of antioxidants in the body, is a key element in the development of obesity and many obesity-related comorbidities. The main ROS involved in this process are the superoxide anion • O2 -, the hydrogen peroxide H2O2 and the hydroxyl radical • OH, whereas antioxidant enzymes, i.e. superoxide dismutase (SOD), catalase (CAT) and glutathione peroxidase (GPx), uric acid, cofactors (e.g. NADPH), vitamin E, vitamin C, thioredoxin and glutathione (GSH) and trace metals (e.g. selenium) counteract pro-oxidant effects of ROS. Oxidative stress can also be induced by obesity per se by several mechanisms such as oxidative phosphorylation in the mitochondria, oxidation of fatty acids, over-consumption of oxygen, protein kinase C activation, hyperleptinemia, postprandial ROS generation due to lipid-rich and carbohydrate-rich diets, low antioxidant defenses, endothelial dysfunction due to reduced bioavailability of nitric oxide and increased levels of endothelium-derived contractile factors, and chronic inflammation [10][11][12][13][14][15][16][17][18].In the adipose tissue, local hypoxia and the hypertrophy of adipocytes resulted during the overgrowth of fat cells can act as inflammation triggers. Hypoxia is correlated with the macrophage infiltration into the fat tissue and with an excess of pro-inflammatory cytokines (TNF-α, IL-1β, IL-6). Thus, in the adipose tissue, low-grade localized inflammation can develop and then lead to systemic inflammation which acts as an essential element in the development of many obesityassociated comorbidities [9]. TNF-α is a pro-inflammatory cytokine which binds to specific receptors and is involved in immunity, adipose cell apoptosis, lipid metabolism, insulin signallin...

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