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Erschienen in: NeuroMolecular Medicine 3/2008

01.09.2008 | Original Paper

Perturbed Autonomic Nervous System Function in Metabolic Syndrome

verfasst von: Nicholas Tentolouris, Georgia Argyrakopoulou, Nicholas Katsilambros

Erschienen in: NeuroMolecular Medicine | Ausgabe 3/2008

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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.
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Metadaten
Titel
Perturbed Autonomic Nervous System Function in Metabolic Syndrome
verfasst von
Nicholas Tentolouris
Georgia Argyrakopoulou
Nicholas Katsilambros
Publikationsdatum
01.09.2008
Verlag
Humana Press Inc
Erschienen in
NeuroMolecular Medicine / Ausgabe 3/2008
Print ISSN: 1535-1084
Elektronische ISSN: 1559-1174
DOI
https://doi.org/10.1007/s12017-008-8022-5

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