Obesity-related metabolic syndrome: mechanisms of sympathetic overactivity

Abstract

The prevalence of the metabolic syndrome has increased worldwide over the past few years. Sympathetic nervous system overactivity is a key mechanism leading to hypertension in patients with the metabolic syndrome. Sympathetic activation can be triggered by reflex mechanisms as arterial baroreceptor impairment, by metabolic factors as insulin resistance, and by dysregulated adipokine production and secretion from visceral fat with a mainly permissive role of leptin and antagonist role of adiponectin. Chronic sympathetic nervous system overactivity contributes to a further decline of insulin sensitivity and creates a vicious circle that may contribute to the development of hypertension and of the metabolic syndrome and favor cardiovascular and kidney disease. Selective renal denervation is an emerging area of interest in the clinical management of obesity-related hypertension. This review focuses on current understanding of some mechanisms through which sympathetic overactivity may be interlaced to the metabolic syndrome, with particular regard to the role of insulin resistance and of some adipokines.

Figure 1

In obesity, infiltration of inflammatory cells in the white adipose tissue disturbs the secretion of adipokines and increases the activity of adipocyte renin-angiotensin system. Increased secretion of leptin and proinflammatory cytokines and decreased amounts of adiponectin contribute to the development of obesity-related hypertension.