Role of Sympathetic Nervous System in the Metabolic Syndrome and Sleep Apnea

2015 ◽  
pp. 165-175 ◽  
Author(s):  
Gino Seravalle ◽  
Guido Grassi
Keyword(s):  
Metabolic Syndrome ◽  
Nervous System ◽  
Sleep Apnea ◽  
Sympathetic Nervous System ◽  
The Metabolic Syndrome ◽  
Sympathetic Nervous

scholarly journals Obesity-Related Metabolic Syndrome: Mechanisms of Sympathetic Overactivity

2013 ◽  
Vol 2013 ◽  
pp. 1-12 ◽  
Author(s):  
Maria Paola Canale ◽  
Simone Manca di Villahermosa ◽  
Giuliana Martino ◽  
Valentina Rovella ◽  
Annalisa Noce ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Metabolic Syndrome ◽  
Nervous System ◽  
Sympathetic Nervous System ◽  
Sympathetic Overactivity ◽  
Area Of Interest ◽  
The Metabolic Syndrome ◽  
Sympathetic Nervous ◽  
Permissive Role

The prevalence of the metabolic syndrome has increased worldwide over the past few years. Sympathetic nervous system overactivity is a key mechanism leading to hypertension in patients with the metabolic syndrome. Sympathetic activation can be triggered by reflex mechanisms as arterial baroreceptor impairment, by metabolic factors as insulin resistance, and by dysregulated adipokine production and secretion from visceral fat with a mainly permissive role of leptin and antagonist role of adiponectin. Chronic sympathetic nervous system overactivity contributes to a further decline of insulin sensitivity and creates a vicious circle that may contribute to the development of hypertension and of the metabolic syndrome and favor cardiovascular and kidney disease. Selective renal denervation is an emerging area of interest in the clinical management of obesity-related hypertension. This review focuses on current understanding of some mechanisms through which sympathetic overactivity may be interlaced to the metabolic syndrome, with particular regard to the role of insulin resistance and of some adipokines.

scholarly journals Relevance of Sympathetic Nervous System Activation in Obesity and Metabolic Syndrome

2015 ◽  
Vol 2015 ◽  
pp. 1-11 ◽  
Author(s):  
Alicia A. Thorp ◽  
Markus P. Schlaich
Keyword(s):  
Metabolic Syndrome ◽  
Nervous System ◽  
Sympathetic Nervous System ◽  
Metabolic Control ◽  
Energy Homeostasis ◽  
Metabolic Effects ◽  
Metabolic Abnormalities ◽  
Sympathetic Overactivity ◽  
The Metabolic Syndrome ◽  
Sympathetic Nervous

Sympathetic tone is well recognised as being implicit in cardiovascular control. It is less readily acknowledged that activation of the sympathetic nervous system is integral in energy homeostasis and can exert profound metabolic effects. Accumulating data from animal and human studies suggest that central sympathetic overactivity plays a pivotal role in the aetiology and complications of several metabolic conditions that can cluster to form the Metabolic Syndrome (MetS). Given the known augmented risk for type 2 diabetes, cardiovascular disease, and premature mortality associated with the MetS understanding the complex pathways underlying the metabolic derangements involved has become a priority. Many factors have been proposed to contribute to increased sympathetic nerve activity in metabolic abnormalities including obesity, impaired baroreflex sensitivity, hyperinsulinemia, and elevated adipokine levels. Furthermore there is mounting evidence to suggest that chronic sympathetic overactivity can potentiate two of the key metabolic alterations of the MetS, central obesity and insulin resistance. This review will discuss the regulatory role of the sympathetic nervous system in metabolic control and the proposed pathophysiology linking sympathetic overactivity to metabolic abnormalities. Pharmacological and device-based approaches that target central sympathetic drive will also be discussed as possible therapeutic options to improve metabolic control in at-risk patient cohorts.

scholarly journals The metabolic syndrome in mice overexpressing neuropeptide Y in noradrenergic neurons

2017 ◽  
Vol 234 (1) ◽  
pp. 57-72 ◽  
Author(s):  
Liisa Ailanen ◽  
Suvi T Ruohonen ◽  
Laura H Vähätalo ◽  
Katja Tuomainen ◽  
Kim Eerola ◽  
...  
Keyword(s):  
Metabolic Syndrome ◽  
Nervous System ◽  
Fatty Acid ◽  
Glucose Metabolism ◽  
Sympathetic Nervous System ◽  
Chronic Treatment ◽  
Noradrenergic Neurons ◽  
Y1 Receptor ◽  
The Metabolic Syndrome ◽  
Sympathetic Nervous

A gain-of-function polymorphism in human neuropeptide Y (NPY) gene (rs16139) associates with metabolic disorders and earlier onset of type 2 diabetes (T2D). Similarly, mice overexpressing NPY in noradrenergic neurons (OE-NPYDBH) display obesity and impaired glucose metabolism. In this study, the metabolic syndrome-like phenotype was characterized and mechanisms of impaired hepatic fatty acid, cholesterol and glucose metabolism in pre-obese (2-month-old) and obese (4–7-month-old) OE-NPYDBH mice were elucidated. Susceptibility to T2D was assessed by subjecting mice to high caloric diet combined with low-dose streptozotocin. Contribution of hepatic Y1-receptor to the phenotype was studied using chronic treatment with an Y1-receptor antagonist, BIBO3304. Obese OE-NPYDBH mice displayed hepatosteatosis and hypercholesterolemia preceded by decreased fatty acid oxidation and accelerated cholesterol synthesis. Hyperinsulinemia in early obese state inhibited pyruvate- and glucose-induced hyperglycemia, and deterioration of glucose metabolism of OE-NPYDBH mice developed with aging. Furthermore, streptozotocin induced T2D only in OE-NPYDBH mice. Hepatic inflammation was not morphologically visible, but upregulated hepatic anti-inflammatory pathways and increased 8-isoprostane combined with increased serum resistin and decreased interleukin 10 pointed to increased NPY-induced oxidative stress that may predispose OE-NPYDBH mice to insulin resistance. Chronic treatment with BIBO3304 did not improve the metabolic status of OE-NPYDBH mice. Instead, downregulation of beta-1-adrenoceptors suggests indirect actions of NPY via inhibition of sympathetic nervous system. In conclusion, changes in hepatic fatty acid, cholesterol and glucose metabolism favoring energy storage contribute to the development of NPY-induced metabolic syndrome, and the effect is likely mediated by changes in sympathetic nervous system activity.

scholarly journals The metabolic syndrome — a neuroendocrine disorder?

2000 ◽  
Vol 83 (S1) ◽  
pp. S49-S57 ◽  
Author(s):  
Per Björntorp ◽  
Roland Rosmond
Keyword(s):  
Insulin Resistance ◽  
Metabolic Syndrome ◽  
Nervous System ◽  
Sympathetic Nervous System ◽  
Hpa Axis ◽  
Leptin Receptor ◽  
Psychiatric Disease ◽  
Cortisol Secretion ◽  
The Metabolic Syndrome ◽  
Sympathetic Nervous

Central obesity is a powerful predictor for disease. By utilizing salivary cortisol measurements throughout the day, it has now been possible to show on a population basis that perceived stress-related cortisol secretion frequently is elevated in this condition. This is followed by insulin resistance, central accumulation of body fat, dyslipidaemia and hypertension (the metabolic syndrome). Socio-economic and psychosocial handicaps are probably central inducers of hyperactivity of the hypothalamic–pituitary adrenal (HPA) axis. Alcohol, smoking and traits of psychiatric disease are also involved. In a minor part of the population a dysregulated, depressed function of the HPA axis is present, associated with low secretion of sex steroid and growth hormones, and increased activity of the sympathetic nervous system. This condition is followed by consistent abnormalities indicating the metabolic syndrome. Such ‘burned-out’ function of the HPA axis has previously been seen in subjects exposed to environmental stress of long duration. The feedback control of the HPA axis by central glucocorticoid receptors (GR) seems inefficient, associated with a polymorphism in the 5′ end of the GR gene locus. Homozygotes constitute about 14 % of Swedish men (women to be examined). Such men have a poorly controlled cortisol secretion, abdominal obesity, insulin resistance and hypertension. Furthermore, polymorphisms have been identified in the regulatory domain of the GR gene that are associated with elevated cortisol secretion; polymorphisms in dopamine and leptin receptor genes are associated with sympathetic nervous system activity, with elevated and low blood pressure, respectively. These results suggest a complex neuroendocrine background to the metabolic syndrome, where the kinetics of the regulation of the HPA axis play a central role.

scholarly journals Disorders of Sleep and Aggression Trait in Women Associated: What Underlies Staying “Woke”?

2019 ◽  
Vol 1 (1) ◽  
Author(s):  
Hobgood DK
Keyword(s):  
Nervous System ◽  
Sleep Apnea ◽  
Sympathetic Nervous System ◽  
Dopamine System ◽  
Patient Falls ◽  
Online Test ◽  
Sympathetic Nervous ◽  
Sleep Centers ◽  
The Brain

Narcolepsy is a sleep disorder where the patient falls asleep unwillingly. It is thought to be related to hyper functioning central sleep centers in the brain. Sleep apnea is a disorder of breathing disruption during sleep. Genes of the dopamine system have been implicated with high dopamine: norepinephrine ratio. Since dopamine has also been associated with personality traits, the hypothesis we studied herein was that patients with narcolepsy and sleep apnea would score low in catecholamine settings causing aggression trait. We found that narcolepsy and sleep apnea diagnoses showed significantly lower aggression trait using an online test. The conclusion is that narcolepsy and sleep apnea patients are not aggressive in personality, and since aggressiveness is related to sympathetic nervous system activity, this would be predictable given the role of sympathetic nervous system in wakefulness.

The sympathetic nervous system and the metabolic syndrome

2007 ◽  
Vol 25 (5) ◽  
pp. 909-920 ◽  
Author(s):  
Giuseppe Mancia ◽  
Pascal Bousquet ◽  
Jean Luc Elghozi ◽  
Murray Esler ◽  
Guido Grassi ◽  
...  
Keyword(s):  
Metabolic Syndrome ◽  
Nervous System ◽  
Sympathetic Nervous System ◽  
The Metabolic Syndrome ◽  
Sympathetic Nervous

Thyroid hormone-catecholamine interrelationships during exposure to cold

1981 ◽  
Vol 97 (1) ◽  
pp. 91-97 ◽  
Author(s):  
H. Storm ◽  
C. van Hardeveld ◽  
A. A. H. Kassenaar
Keyword(s):  
Nervous System ◽  
Plasma Concentration ◽  
Thyroid Hormone ◽  
Sympathetic Nervous System ◽  
Plasma Levels ◽  
Surgical Procedure ◽  
Exposure To Cold ◽  
Basal Plasma ◽  
Sympathetic Nervous

Abstract. Basal plasma levels for adrenalin (A), noradrenalin (NA), l-triiodothyronine (T3), and l-thyroxine (T4) were determined in rats with a chronically inserted catheter. The experiments described in this report were started 3 days after the surgical procedure when T3 and T4 levels had returned to normal. Basal levels for the catecholamines were reached already 4 h after the operation. The T3/T4 ratio in plasma was significantly increased after 3, 7, and 14 days in rats kept at 4°C and the same holds for the iodide in the 24-h urine after 7 and 14 days at 4°C. The venous NA plasma concentration was increased 6- to 12-fold during the same period of exposure to cold, whereas the A concentration remained at the basal level. During infusion of NA at 23°C the T3/T4 ratio in plasma was significantly increased after 7 days compared to pair-fed controls, and the same holds for the iodide excretion in the 24-h urine. This paper presents further evidence for a role of the sympathetic nervous system on T4 metabolism in rats at resting conditions.

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