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noradrenaline/obesitat
L'enllaç es desa al porta-retalls
Pàgina 1 des de 470 resultats
3-Hydroxybutyrate inhibits noradrenaline-induced thermogenesis in lean but not in obese Zucker rats.
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OBJECTIVE
To determine the effect of 3-hydroxybutyrate (3OHB) on the thermogenic response to noradrenaline (NA) in lean and genetically obese Zucker fa/fa rats.
METHODS
Rats were infused with 18.7 nmol x kg(-1) x min(-1) of NA, supplemented, for 15 min, with 66.7 micromol x kg(-1) x min(-1) of
Noradrenaline-induced lipolysis in isolated mesenteric, omental and subcutaneous adipocytes from obese subjects.
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OBJECTIVE
The action of noradrenaline on human mesenteric, omental and subcutaneous adipocytes was compared. We also determined whether regional differences in the noradrenaline-effect were linked to variations in adrenoceptor subtype function.
METHODS
The lipolytic effects of different
Comparative effects of small intestinal glucose on blood pressure, heart rate, and noradrenaline responses in obese and healthy subjects.
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Meal consumption leads to an increase in sympathetic output to compensate for hemodynamic changes and maintain blood pressure (BP). Obesity is associated with a blunting of the sympathetic response to meal ingestion, but interpretation of studies investigating these responses is compromised by their
Acute effects of food, 2-deoxy-D-glucose and noradrenaline on metabolic rate and brown adipose tissue in normal and atropinised lean and obese (fa/fa) Zucker rats.
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1. Intragastric feeding (40 kJ) produced a 17% rise in metabolic rate in lean Zucker rats but only an 8% increase in obese (fa/fa) rats, and both of these responses were significantly reduced by beta-adrenergic blockade with propranolol (10 mg/kg, s.c.). 2. Parasympathetic blockade with atropine
Reduced in vivo phosphodiesterase-4 response to acute noradrenaline challenge in diet-induced obese rats.
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Altered sympathetic nervous activity has been linked to the development and persistence of obesity, partly relating to overfeeding. Binding of the selective, positron-emitting phosphodiesterase-4 (PDE4) inhibitor (R)-[11C]rolipram provides a direct index of the cAMP-hydrolyzing enzyme PDE4. This
Noradrenaline-mediated inhibition of inflammatory cytokines is altered in macrophages from obese Zucker rats: effect of habitual exercise.
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The obese Zucker rat (fa/fa) (ObZ) is a good animal model for Metabolic Syndrome (MS)-associated neuroendocrine and inflammatory disorders. The aim of the present investigation was to evaluate the effect of noradrenaline (NA) on the release of IL-1β, IL-6 and TNFα by macrophages from ObZ, as well as
Obese male subjects show increased resting forearm venous plasma noradrenaline concentration but decreased 24-hour sympathetic activity as evaluated by thrombocyte noradrenaline measurements.
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OBJECTIVE
To study resting forearm venous plasma noradrenaline (NA) and 24 h sympathoadrenal activity evaluated by measurements of thrombocyte NA and adrenaline (A) in obese male subjects before and after weight reduction.
METHODS
Blood samples were collected in obese subjects and in controls after
Reduced plasma noradrenaline concentrations in simple-obese and diabetic obese patients.
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1. Obesity may be associated with a decreased activity of the sympathetic nervous system and also with a deficiency of the response to stimuli activating the sympathetic nervous system. As insulin activates the sympathetic nervous system, the present study was undertaken to measure the plasma
Unimpaired thermogenic response to noradrenaline in genetic (ob/ob) and hypothalamic (MSG) obese mice.
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The thermogenic response to noradrenaline administration was investigated at 25 degrees C in two models of obese mice (genetic ob/ob obesity of the ' QEC ' strain and monosodium-glutamate-induced obesity) and in their respective lean littermates. Subcutaneous injections of a low dose of
Control of the forearm microcirculation: interactions with measures of obesity and noradrenaline kinetics.
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1. Obesity influences the responsiveness of the microcirculation; constriction is augmented probably reflecting heightened sympathetic nervous activity. 2. The responsiveness of the microcirculation in the forearm to constriction and dilation was therefore examined in 14 men and women with varying
Benidipine induces thermogenesis in brown adipose tissue by releasing endogenous noradrenaline: a possible mechanism for the anti-obesity effect of calcium antagonists.
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BACKGROUND
Anti-obesity effects of calcium antagonists such as benidipine and nifedipine have been described in rodent obesity models, but the mode of action of the calcium antagonists as anti-obesity agents has not been established.
OBJECTIVE
To examine whether the anti-obesity effects of calcium
Impaired insulin-induced attenuation of noradrenaline-mediated vasoconstriction in insulin-resistant obese Zucker rats.
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1. Insulin resistance is associated with hypertension but the underlying mechanism is unclear. We tested the hypothesis that insulin-induced vasodilatation is impaired in insulin-resistant obese Zucker rats. We studied mesenteric artery (approximately 220 microns diameter) function before the
Central noradrenaline transporter availability is linked with HPA axis responsiveness and copeptin in human obesity and non-obese controls.
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The central noradrenaline (NA) stress-response network co-mediates hypothalamic-pituitary-adrenal (HPA) axis activation and arginine-vasopressin (AVP) release. Dysregulation of these systems contributes to stress-related diseases such as human obesity, but their interrelation remains unclear. The
Modulation of noradrenaline-induced vasoconstriction in isolated perfused mesenteric arterial beds from obese Zucker rats in the presence and absence of insulin.
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The genetically obese Zucker rat (fa/fa) is an insulin-resistant animal model with early-onset severe hyperinsulinemia that eventually develops mild hypertension. Thus, it represents a model in which the effect of hyperinsulinemia - insulin resistance associated with hypertension on vascular
The sympathetic neurobiology of essential hypertension: disparate influences of obesity, stress, and noradrenaline transporter dysfunction?
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Although the importance of sympathetic nervous activation in the pathogenesis of essential hypertension is well documented, the exact pathophysiology of the sympathetic nervous dysfunction present remains to be delineated. This review details three relatively new findings of disturbed sympathetic
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