Perturbed autonomic nervous system function in metabolic syndrome

Neuromolecular Med. 2008;10(3):169-78. doi: 10.1007/s12017-008-8022-5. Epub 2008 Jan 26.

Abstract

The metabolic syndrome is characterized by the clustering of various common metabolic abnormalities in an individual and it is associated with increased risk for the development of type 2 diabetes and cardiovascular diseases. Its prevalence in the general population is approximately 25%. Central fat accumulation and insulin resistance are considered as the common denominators of the abnormalities of the metabolic syndrome. Subjects with metabolic syndrome have autonomic nervous system dysfunction characterized by predominance of the sympathetic nervous system in many organs, i.e. heart, kidneys, vasculature, adipose tissue, and muscles. Sympathetic nervous system activation in metabolic syndrome is detected as increased heart rate and blood pressure, diminished heart rate variability, baroreceptor dysfunction, enhanced lipolysis in visceral fat, increased muscle sympathetic nerve activity, and high urine or plasma catecholamine concentrations as well as turnover rates. The augmented sympathetic activity in individuals with metabolic syndrome worsens prognosis of this high-risk population. The mechanisms linking metabolic syndrome with sympathetic activation are complex and not clearly understood. Whether sympathetic overactivity is involved in the development of the metabolic syndrome or is a consequence of it remains to be elucidated since data from prospective studies are missing. Intervention studies have demonstrated that the autonomic disturbances of the metabolic syndrome may be reversible.

Publication types

  • Review

MeSH terms

  • Autonomic Nervous System / physiopathology*
  • Diabetes Mellitus / metabolism
  • Diabetes Mellitus / physiopathology
  • Dyslipidemias / physiopathology
  • Humans
  • Hypertension / physiopathology
  • Insulin Resistance / physiology
  • Metabolic Syndrome / metabolism
  • Metabolic Syndrome / physiopathology*
  • Obesity / physiopathology