The lack of adequate physical activity and obesity created a worldwide pandemic. Obesity is characterized by the deposition of\r\nadipose tissue in various parts of the body; it is now evident that adipose tissue also acts as an endocrine organ capable of secreting\r\nmany cytokines that are though to be involved in the pathophysiology of obesity, insulin resistance, and metabolic syndrome.\r\nAdipokines, or adipose tissue-derived proteins, play a pivotal role in this scenario. Increased secretion of proinflammatory\r\nadipokines leads to a chronic inflammatory state that is accompanied by insulin resistance and glucose intolerance. Lifestyle change\r\nin terms of increased physical activity and exercise is the best nonpharmacological treatment for obesity since these can reduce\r\ninsulin resistance, counteract the inflammatory state, and improve the lipid profile. There is growing evidence that exercise exerts\r\nits beneficial effects partly through alterations in the adipokine profile; that is, exercise increases secretion of anti-inflammatory\r\nadipokines and reduces proinflammatory cytokines. In this paper we briefly describe the pathophysiologic role of four important\r\nadipokines (adiponectin, leptin, TNF-??, and IL-6) in the metabolic syndrome and review some of the clinical trials that monitored\r\nthese adipokines as a clinical outcome before and after exercise.
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