Obesity may induce the onset of other conditions leading to overt cardiovascular disease, such as glucose intolerance, dyslipidemia, impaired glucose tolerance and type 2 diabetes, hypertension, and kidney failure ( Martin-Rodriguez et al., 2015 Soares et al., 2015). The worldwide prevalence of obesity has nearly doubled in the past decades (World Health Organization). Obesity is a challenge for global public health. Given the crucial role of autonomic dysfunction in the pathophysiology of obesity and its cardiovascular complications, vagal nerve modulation and sympathetic inhibition may serve as therapeutic targets in this condition. Weight loss is able to reverse metabolic and autonomic alterations associated with obesity. Selective leptin resistance, obstructive sleep apnea syndrome, hyperinsulinemia and low ghrelin levels are possible mechanisms underlying sympathetic activation in obesity. Furthermore, an increased sympathetic activity has been demonstrated in obese patients, particularly in the muscle vasculature and in the kidneys, possibily contributing to increased cardiovascular risk. This article will review current evidence about the role of the ANS in short-term and long-term regulation of energy homeostasis. On the other hand, the excess weight induces ANS dysfunction, which may be involved in the haemodynamic and metabolic alterations that increase the cardiovascular risk of obese individuals, i.e., hypertension, insulin resistance and dyslipidemia. Indeed, alterations of the ANS might be involved in the pathogenesis of obesity, acting on different pathways. The autonomic nervous system (ANS) dysfunction has a two-way relationship with obesity. Obesity is reaching epidemic proportions globally and represents a major cause of comorbidities, mostly related to cardiovascular disease.
3Scuola Superiore Sant'Anna, Pisa, Italy.2Institute of Clinical Physiology of CNR, Pisa, Italy.
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