The sympathetic nervous system and insulin resistance in achilles tendinopathy

2015 ◽  
Vol 19 ◽  
pp. e98
Author(s):  
J. Jewson ◽  
E. Lambert ◽  
M. Storr ◽  
G. Lambert ◽  
J. Gaida
Keyword(s):  
Insulin Resistance ◽  
Nervous System ◽  
Sympathetic Nervous System ◽  
Achilles Tendinopathy ◽  
Sympathetic Nervous

Hypertension and insulin resistance: role of sympathetic nervous system activity

1992 ◽  
Vol 263 (5) ◽  
pp. E935-E942 ◽  
Author(s):  
M. A. Supiano ◽  
R. V. Hogikyan ◽  
L. A. Morrow ◽  
F. J. Ortiz-Alonso ◽  
W. H. Herman ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Nervous System ◽  
Sympathetic Nervous System ◽  
Multiple Regression Model ◽  
Metabolic Effects ◽  
Plasma Norepinephrine ◽  
Intravenous Glucose ◽  
Arterial Blood ◽  
Sympathetic Nervous ◽  
Intravenous Glucose Tolerance Tests

he purpose of this study was to test the hypothesis that heightened sympathetic nervous system (SNS) activity contributes to the mechanism by which hypertension is associated with insulin resistance in humans. We performed frequently sampled intravenous glucose tolerance tests to determine tissue sensitivity to metabolic effects of insulin (SI) and measured plasma norepinephrine (NE) levels in 21 normotensive and 14 hypertensive Caucasian subjects. Compared with the normotensive subjects, hypertensive subjects had decreased SI (5.4 +/- 0.5 vs. 4.0 +/- 0.7 x 10(-5) x min-1 x pM-1; P = 0.03) but similar plasma NE levels (normotensive: 1.82 +/- 0.12 vs. hypertensive: 1.73 +/- 0.16 nM; P = 0.23). In a multiple regression model, only body mass index (BMI) and mean arterial blood pressure (MABP) were significant independent predictors of SI [SI = (-0.513)(BMI) + (-0.058)(MABP) + 23.6; r = 0.748; P = 0.0001]; age, plasma glucose, epinephrine, and NE level did not enter this model. As an additional test of this hypothesis, seven hypertensive subjects were restudied after 10 days of guanadrel therapy to determine whether SI would increase during suppression of SNS activity by guanadrel. Despite a significant reduction in plasma NE levels with guanadrel (baseline: 1.63 +/- 0.18 vs. guanadrel: 0.99 +/- 0.14 nM; P = 0.01), there was no significant change in SI (baseline: 2.97 +/- 0.78 vs. guanadrel: 2.41 +/- 0.54 x 10(-5).min-1 x pM-1; analysis of variance P = 0.57). We conclude that, in the Caucasian population we studied, heightened SNS activity is not essential for the insulin resistance observed in hypertensive humans.

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.

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