J Physiol. 2012 Feb 20. [Epub ahead of print]
Obesity and Adipokines: Effects on Sympathetic Overactivity.
Smith MM, Minson CT.
University of Oregon.
Excess body weight is a major risk factor for cardiovascular disease, increasing the risk of hypertension, hyperglycemia and dyslipidemia, recognized as the metabolic syndrome. Adipose tissue acts as an endocrine organ by producing various signaling cytokines called adipokines (including leptin, free fatty acids, tumor necrosis factor-alpha, interleukin-6, C-reactive protein, angiotensinogen and adiponectin). A chronic dysregulation of certain adipokines can can have deleterious effects on insulin signaling. 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.