Obesity and adipokines: effects on sympathetic overactivity

Abstract

Excess body weight is a major risk factor for cardiovascular disease, increasing the risk of hypertension, hyperglycaemia and dyslipidaemia, recognized as the metabolic syndrome. Adipose tissue acts as an endocrine organ by producing various signalling cytokines called adipokines (including leptin, free fatty acids, tumour necrosis factor-α, interleukin-6, C-reactive protein, angiotensinogen and adiponectin). A chronic dysregulation of certain adipokines can have deleterious effects on insulin signalling. Chronic sympathetic overactivity is also known to be present in central obesity, and recent findings demonstrate the consequence of an elevated sympathetic outflow to organs such as the heart, kidneys and blood vessels. Chronic sympathetic nervous system overactivity can also contribute to a further decline of insulin sensitivity, creating a vicious cycle that may contribute to the development of the metabolic syndrome and hypertension. The cause of this overactivity is not clear, but may be driven by certain adipokines. The purpose of this review is to summarize how obesity, notably central or visceral as observed in the metabolic syndrome, leads to adipokine expression contributing to changes in insulin sensitivity and overactivity of the sympathetic nervous system.

Association Between Glycemic Control and Morning Blood Pressure Surge With Vascular Endothelial Dysfunction in Type 2 Diabetic Patients

“…This concept is supported by data indicating that cerebral and cardiac events occur most often in the morning (3). It is possible that inadequate glycemic control (4) or the occurrence of insulin resistance (5) activate sympathetic activity, which leads to MBPS in DM patients. Furthermore, hypertensive patients with exaggerated MBPS exhibit elevated levels of macrophages, T cells, and tumor necrosis factor-a in atherosclerotic plaques obtained from the carotid artery compared with those without exaggerated MBPS, suggesting an association between MBPS and vascular injury in hypertensive patients (6).…”

Body fat, especially visceral fat, is associated with electrocardiographic measures of sympathetic activation

“…Several mechanisms could underlie these associations. Adipocytes, or macrophages invading the adipose tissue, secrete a number of adipokines (10,36). Distribution of the adipose tissue is a key determinant of this adipokine secretion.…”

“…Furthermore, visceral fat inhibits the secretion of anti-inflammatory factors (11). Some proinflammatory cytokines, such as leptin, can cross the blood-brain barrier and directly stimulate the central sympathetic nervous system in the hypothalamus (10,37). Other cytokines, for example, Creactive protein, TNF-a, plasminogen activator inhitor-1, and interleukin-6, cause a state of low-grade inflammation that can also stimulate the sympathetic nervous system (10, 13).…”

“…These cytokines either cross the blood-brain barrier and directly stimulate the central sympathetic nervous system in the hypothalamus, or induce a state of low-grade inflammation that can also stimulate the sympathetic nervous system (10).…”

The Fluctuation in the Heart Rate Variability Throughout Ovulation Induction Cycle: Is the Case Different in Polycystic Ovary Syndrome?

“…A link has been found in obese patients between insulin resistance and increased sympathetic nerve activity [24]. The negative link of the cardiac vagal tonus with insulin resistance has also been demonstrated [25,26].…”