Sayfa 1 itibaren 1036 Sonuçlar
Both asthma and obesity are large and growing public health issues. Mounting evidence now implicates obesity as a major risk factor for asthma, thus linking these 2 major epidemics. Moreover, both in human subjects and in mice, obesity appears to predispose toward airway hyperresponsiveness. This
Leptin has received extensive attention as an endogenously produced satiety factor. Although once considered to be solely derived from adipose tissue, it is now apparent that leptin can be produced by various tissues including those comprising the cardiovascular system such as blood vessels and
BACKGROUND
The asthma-obesity syndrome represents a major public health concern that disproportionately contributes to asthma severity and induces insensitivity to therapy. To date, no study has shown an intrinsic difference between human airway smooth muscle (HASM) cells derived from non-obese
The simultaneous rise in the prevalence of asthma and obesity has prompted epidemiologic studies that establish obesity as a risk factor for asthma. The alterations in cell signaling that explain this link are not well understood and warrant investigation so that therapies that target this asthma
This review concerns the influence of leptin on vascular smooth muscle cells (VSMC). VSMC express different isoforms of the leptin receptor (Ob-R) able to activate a wide range of intracellular signalling pathways, mediating many relevant biological actions. In particular, leptin promotes processes
Diabetic and obese subjects run a greater risk of developing atherosclerosis than the rest of the population. Several epidemiological studies suggest that hyperinsulinemia, which characterizes both obese and insulin resistant diabetic subjects, may be involved in atherosclerosis. Because insulin
OBJECTIVE
Adiponectin, an adipocyte-specific protein, stimulates nitric oxide production and may mediate associations between visceral obesity and vascular dysfunction. Adiponectin is lower in obese children but its relationship with vascular function has not been clarified in childhood. We aimed to
The action of insulin (0.1 U/ml) on the metabolism of human intestinal smooth muscle was studied in vitro. The experiments were performed on the muscle layer of human jujunum obtained from patients undergoing intestinal shunt operations because of obesity. Insulin significantly increased glucose
BACKGROUND
This investigation examined the mechanisms by which coronary perivascular adipose tissue (PVAT)-derived factors influence vasomotor tone and the PVAT proteome in lean versus obese swine.
RESULTS
Coronary arteries from Ossabaw swine were isolated for isometric tension studies. We found
The degree of arterial dilatation induced by exogenous nitrates (nitrate-mediated dilatation, NMD) has been similar in obese and normal-weight adults after single high-dose glyceryl trinitrate (GTN). We examined whether NMD is impaired in obesity by performing a GTN dose-response study, as this is a
The effect of oral vanadate treatment on isometric tension responses were examined in aortic rings isolated from obese and lean Zucker rats. Rats from both strains that were either maintained on food ad libitum or pair-fed were included to serve as controls. Higher plasma insulin and glucose levels
Obesity is associated with asthma and airway hyperresponsiveness. Leptin modulates some of the proinflammatory effects observed in obesity. The objective of this study was to determine the effects of leptin on airway smooth muscle responses. The effect of leptin (0.1-100 ng/ml) on migration (toward
Anticipatory smooth eye movements (ASEM; smooth eye movements in the direction of anticipated target motion) are elicited by cues that signal the direction of future target motion with high levels of certainty. Natural cues, however, rarely convey information with perfect certainty, and responses to
β-Adrenergic receptor (β-AR) agonists are the most common clinical bronchodilators for asthma. Obesity influences asthma severity and may impair response to β-AR agonists. Previous studies show that in obese mice, hyperinsulinemia plays a crucial role in β-AR desensitization in the heart. We