Abstract
Obesity per se carries the features of chronic inflammation and oxidative stress that interrelate in a complex network and exert an important role in the onset of several complications such as type 2 diabetes, atherosclerosis and cardiovascular events. On the other hand, it seems that hyperglycemia per se as well as insulin resistance (independent of hyperglycemia), both induce increased oxidative stress. The aim of our study was to analyze proinflammatory and oxidative stress markers in obese patients with and without type 2 diabetes and to verify the hypothesis that type 2 diabetes associated with obesity would promote a higher chronic inflammation and oxidative stress state as compared to obesity alone. We found no differences between the two groups of patients regarding chronic inflammation and oxidative stress markers. Therefore we may conclude that there is no influence of type 2 diabetes on chronic inflammation and oxidative stress in obese patients.
Highlights
Obesity is increasing worldwide at an alarming rate (Low et al, 2009)
Obesity is associated with several diseases such as type 2 diabetes (T2DM), hypertension, dyslipidemia, coronary heart disease, stroke, osteoarthritis, sleep apnea and different malignances which increase cardiovascular risk, mortality and consecutively reduces life expectancy (Buchwald et al, 2004)
A large body of evidence showed that lowgrade chronic inflammation found in obesity increases the expression and activity of prooxidant enzymes including myeloperoxidase and NADPH oxidases and promote the production of reactive free radicals (Park et al, 2007)
Summary
Obesity is increasing worldwide at an alarming rate (Low et al, 2009). In Romania, the available epidemiological data revealed a 20-25% prevalence of obesity (Cinteză et al, 2007). Adipose tissue is known to be an endocrine organ producing adipokines which include hormones such as leptin or adiponectin and inflammatory cytokines such as tumor necrosis factor alpha (TNF-α) or interleukin 6 (IL-6) among others (Wang and Nakayama, 2010; Maury and Brichard, 2010). They are dysregulated in obesity and contribute to the development of obesitylinked metabolic disorders and cardiovascular diseases (Maury and Brichard, 2010; Bullo et al, 2006; Wozniak et al, 2009). Leptin is a hormone secreted by adipocytes in direct proportion to the mass of adipose tissue, promoting oxidative stress and vascular inflammation in obesity, favoring the development of atherosclerosis (Fernández-Sánchez and Madrigal-Santillán, 2011)
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