Obesity, characterized by weight gain caused by excessive fat accumulation, is a global problem [1] and considered to be a primary factor in the etiology of several diseases [2]. Inflammation and oxidative stress are associated with obesity [3], which induce several changes in the body, such as an inflammatory response [4-7]. Moreover,there exists a correlation between oxidative stress and obesity [3]. Oxidative stress is caused by an increase in the concentration of reactive oxygen species (ROS) and is responsible for various diseases, such as arteriosclerosis, malignant tumors, and autoimmune diseases [8-12].

Diacron-reactive oxygen metabolite (d-ROMs) is a common biomarker that can be used as an index of the products from ROS. d-ROM indicates the level of hydroperoxides, a type of fairly stable reactive oxygen metabolite [13]. However, the association of abdominal obesity with d-ROM concentration and biological antioxidant potential (BAP), and its usability as an index of antioxidant potential in Korean adults, has not yet been proved.

The aim of this study was to evaluate the association among dROMs, BAP levels, and abdominal obesity in Korean adults using clinically available data.

Our results demonstrated that patients with abdominal obesity presented significantly higher d-ROM levels. Obesity is known to be related to minute chronic systemic inflammation in adipose tissues. This arises though the inducing triggering of the innate immune system in adipose tissues, which promotes the proinflammatory condition and oxidative stress, giving rise to an acute systemic inflammation. Moreover, several chronic diseases, such as diabetes mellitus, metabolic syndrome, cardiovascular diseases, and cancer, are a result of obesity and also related to oxidative stress [2]. Thus, it is inferred that the inflammation of adipose tissues in an obese person plays an important role in the etiology of obesity-related diseases [21].

Obesity affects the production of adipokines [5]. Consequently, blood flow is diminished and hypoxia follows, caused by a progressive increase in the number of adipocytes and amount of adipose tissues. Hypoxia is associated with necrosis and macrophage infiltration into adipose tissues. Infiltrated macrophages form crown-like constructions that surround adipocytes and lead to the overproduction of adipokines and inflammatory mediators, such as interleukin (IL)-6, IL-1β, and tumor necrosis factor-α [5,6]. Although C-reactive protein is associated with insulin resistance, IL-6 has the potential to confuse insulin signal transduction, due to the production of proteins that attach to the insulin receptor [22]. At the systemic level, altered adipokine secretion may result in increased food intake and reduced energy expenditure owing to processes in the hypothalamus and decreased liver insulin sensitivity [23].

Moreover, necrosis is an additional pathway of cellular apoptosis related to the accumulation of ROS and depends on functional mitochondria [24]. Disruption of inter-endothelial junctions between endothelial cells; a significant increase in the production of ROS and inflammation mediators which originate from inflamed endothelial cells; a change in the balance between nitric oxide (NO) synthesis and ROS, insulin signaling, and NO production; and change in L-arginine level, are all associated with endothelial dysfunction during obesity [25].

A limitation of our study is that we voluntarily analyzed data from participants who visited the health promotion center. Thus, our study group may not represent the general population. Secondly, other oxidative stress measurement methods are also available, but we used the measurement method used by Ajou University Hospital. This method has the advantage of being able to obtain a lot of data with ease, but is less stable compared to other technologies. Another limitation is the lack of research on other factors that affect oxidative stress. Regardless of these limitations, our study is valuable because it is the first to evaluate the importance of the association between oxidative stress and abdominal obesity. Another advantage of this study is that it provides insights on the effect of antioxidants for obesity-related diseases.

In conclusion, we observed a positive association between abdominal obesity and d-ROMs. The present analysis shows that abdominal obesity can increase oxidative stress and may affect the development of the pathways involved in obesity, such as the inflammatory pathway. The results of this study are helpful in revealing the cause of oxidative stress and methods to reduce oxidative stress.