The lack of adequate physical activity and obesity created a worldwide pandemic. Obesity is characterized by the deposition of adipose tissue in various parts of the body; it is now evident that adipose tissue also acts as an endocrine organ capable of secreting many cytokines that are though to be involved in the pathophysiology of obesity, insulin resistance, and metabolic syndrome. Adipokines, or adipose tissue-derived proteins, play a pivotal role in this scenario. Increased secretion of proinflammatory adipokines leads to a chronic inflammatory state that is accompanied by insulin resistance and glucose intolerance. Lifestyle change in terms of increased physical activity and exercise is the best nonpharmacological treatment for obesity since these can reduce insulin resistance, counteract the inflammatory state, and improve the lipid profile. There is growing evidence that exercise exerts its beneficial effects partly through alterations in the adipokine profile; that is, exercise increases secretion of anti-inflammatory adipokines and reduces proinflammatory cytokines. In this paper we briefly describe the pathophysiologic role of four important adipokines (adiponectin, leptin, TNF-α, and IL-6) in the metabolic syndrome and review some of the clinical trials that monitored these adipokines as a clinical outcome before and after exercise. 1. Introduction The metabolic syndrome refers to a group of symptoms including obesity, high blood pressure, insulin resistance, and hyperlipidemia, in which the role of central obesity is critical [1, 2]. The increased prevalence of obesity in both industrialized and developing countries is associated with a surge in the preponderance of metabolic syndrome. In North America, 55% of 97 million adults are either overweight or obese (with a body mass index (BMI) ≥25) [3]. In a study of 12363 US men and women using the National Cholesterol Education Program Adult Treatment Panel III guidelines, the metabolic syndrome was diagnosed in 22.8% and 22.6% of the men and women, respectively [4]. The metabolic syndrome can be present in different forms, according to the combination of the various components of the syndrome, and it is well established that the metabolic syndrome increases the risk for the development of cardiovascular disease, type II diabetes, and cancer [5–7]. It is not yet known how the metabolic syndrome is triggered or how the different components are causally linked, but insulin resistance is strongly suspected as a common pathophysiologic link [8, 9]. It is clear that there is a positive correlation
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