Mediators of sympathetic activation in metabolic syndrome obesity

The metabolic syndrome represents a major public health burden because of its high prevalence in the general population and its association with cardiovascular disease and type 2 diabetes. Accumulated evidence based on biochemical, neurophysiologic, and indirect measurements of autonomic activity in...

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Bibliographic Details
Published in:Current hypertension reports 2008-12, Vol.10 (6), p.440-447
Main Authors: Straznicky, Nora E., Eikelis, Nina, Lambert, Elisabeth A., Esler, Murray D.
Format: Article
Language:English
Subjects:
Adipokines - metabolism
Cardiology
Cytokines - metabolism
Diabetes Mellitus, Type 2 - complications
Diabetes Mellitus, Type 2 - physiopathology
Family Medicine
Female
Follow-Up Studies
General Practice
Humans
Hyperinsulinism - complications
Hyperinsulinism - physiopathology
Hypertension
Insulin Resistance
Internal Medicine
Leptin - metabolism
Male
Medical research
Medicine
Medicine & Public Health
Metabolic Diseases
Metabolic Syndrome - complications
Metabolic Syndrome - physiopathology
Nephrology
Obesity
Obesity - complications
Obesity - physiopathology
Primary Care Medicine
Risk Assessment
Sensitivity and Specificity
Sleep Apnea, Obstructive - complications
Sleep Apnea, Obstructive - physiopathology
Sympathetic Nervous System - metabolism
Sympathetic Nervous System - physiology
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Summary:The metabolic syndrome represents a major public health burden because of its high prevalence in the general population and its association with cardiovascular disease and type 2 diabetes. Accumulated evidence based on biochemical, neurophysiologic, and indirect measurements of autonomic activity indicate that visceral obesity and the metabolic syndrome are associated with enhanced sympathetic neural drive and vagal impairment. The mechanisms linking metabolic syndrome with sympathetic activation are complex and not completely understood, and cause-effect relationships need further clarification from prospective trials. Components of the metabolic syndrome that may directly or indirectly enhance sympathetic drive include hyperinsulinemia, leptin, nonesterified fatty acids, proinflammatory cytokines, angiotensinogen, baroreflex impairment, and obstructive sleep apnea. β-Adrenoceptor polymorphisms have also been associated with adrenoceptor desensitization, increased adiposity, insulin resistance, and enhanced sympathetic activity. Because chronic sympathetic activation contributes to hypertension and its target-organ damage, sympatho-inhibition remains an important goal in the therapeutic management of the metabolic syndrome.
ISSN:1522-6417
1534-3111
DOI:10.1007/s11906-008-0083-1