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Página 1 a partir de 1034 resultados
Attenuation of hyperinsulinemia by NN414, a SUR1/Kir6.2 selective K-adenosine triphosphate channel opener, improves glucose tolerance and lipid profile in obese Zucker rats.
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Chronic attenuation of hyperinsulinemia by diazoxide (DZ), a K-adenosine triphosphate (ATP) channel opener and an inhibitor of glucose-mediated insulin secretion, improved glucose tolerance and lipid profile and decreased the rate of weight gain in obese Zucker rats. To determine whether suppression
Differences in the expression of the adenosine A1 receptor in adipose tissue of obese black and white women.
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BACKGROUND
African-American women (AAW) lose less weight and at a slower rate than Caucasian women (CAW) under the same weight-loss regimens. A potential cause of this finding is inhibition of lipolysis.
OBJECTIVE
Because alpha-2 and adenosine receptors are directly involved in inhibition of
Long-term treatment with the beta-3 adrenoceptor agonist, mirabegron ameliorates detrusor overactivity and restores cyclic adenosine monophosphate (cAMP) levels in obese mice.
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OBJECTIVE
To evaluate the effects of the beta-3 adrenoceptor agonist, mirabegron in a mouse model of detrusor overactivity induced by obesity.
METHODS
C57BL/6 male mice were fed with standard chow or high-fat diet for 12 weeks. Lean and obese mice were treated orally with mirabegron (10 mg/kg/day)
Abnormalities of sodium transport by sodium, potassium-activated adenosine triphosphatase in erythrocytes from obese children.
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1. Intracellular Na+ concentration [Na+]i and Na+ extrusion catalysed by sodium potassium-activated adenosine triphosphatase (Na+, K+-pump) were evaluated in erythrocytes from 21 obese children and 20 normal weight- and age-matched controls. 2. Obese children showed a significantly decreased Vmax.
Erythrocyte sodium-potassium-stimulated adenosine triphosphatase activity is not related to obesity.
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Altered erythrocyte sodium potassium (Na,K)-stimulated adenosine triphosphatase (ATPase) activity has been cited as having pathophysiologic significance in morbidly obese man. Previous studies have failed to consider obese patients after weight loss and, therefore, did not clarify the role of ATPase
Red cell sodium-potassium adenosine triphosphatase sites and intracellular sodium increased in obese school children.
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Principally to ascertain whether mineral metabolism is involved in weight regulation, the 40 most obese of 1,774 children, aged 10-11 years, screened for obesity were compared with 46 age-matched controls. The obese children had more 3H-Ouabain erythrocyte binding sites (p = 0.04), higher
Adenosine actions are preserved in corpus cavernosum from obese and type II diabetic db/db mouse.
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BACKGROUND
Erectile dysfunction (ED) in diabetes is associated with autonomic neuropathy and endothelial dysfunction. Whereas the nonadrenergic-noncholinergic (NANC)/neurogenic nitric oxide pathway has received great attention in diabetes-associated ED, few studies have addressed sympathetic
Abnormal A1 adenosine receptor function in genetic obesity.
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Obesity is increasingly recognized as an important health problem in developed, industrialized countries. As a large proportion of the variance in individual adiposity is based on genetic factors (1-3), recent efforts have focused on identifying genes involved in regulating the percentage of body
Overexpression of the A1 adenosine receptor in adipose tissue protects mice from obesity-related insulin resistance.
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In-vitro studies have implicated the A(1) adenosine receptor (A(1)AR) of adipocytes in inhibition of lipolysis, stimulation of lipogenesis and enhancement of the action of insulin on glucose metabolism. To determine whether any of these activities were physiologically relevant in an intact animal,
[Effect of Electroacupuncture on Adenosine Receptor Expression in White Adipose Tissue of Diet-induced Obese Mice].
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OBJECTIVE
To investigate the effects of electroacupuncture (EA) on the expression of adenosine receptor (AR) in the white adipose tissue (WAT) of diet-induced obese (DIO) mice, so as to reveal a peripheral mechanism of EA underlying improvement of body weight.
METHODS
Forty three-week-old C 57 BL/6
Adenosine accumulation causes metabolic disorders in testes and associates with lower testosterone level in obese mice.
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Overweight and obese men face numerous health problems, including type 2 diabetes, subfertility, and even infertility. However, few studies have focused on the effects of nutritional status and obesity-related regulatory signals on fertility deficiency. Our previous observations have shown that the
Cellular insulin resistance in adipocytes from obese polycystic ovary syndrome subjects involves adenosine modulation of insulin sensitivity.
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Cellular insulin resistance in polycystic ovary syndrome (PCOS) has been shown to involve a novel postbinding defect in insulin signal transduction. To find possible mechanisms for this defect, adipocytes were isolated from age- and weight-matched obese normal cycling (NC) and PCOS subjects. Insulin
Effect of glucagon infusion on blood glucose, plasma immunoreactive insulin, growth hormone and adenosine 3'5'-monophosphate in obese children.
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The behaviour of plasma glucose, immunoreactive insulin, growth hormone and adenosine 3',5'-monophosphate (cAMP) in response to glucagon infusion was investigated in obese and control children. Hyperinsulinaemia and low growth hormone levels were found in the obese group. Hyperinsulinaemia did not
The relationship between serum total sialic acid levels and adenosine deaminase activity in obesity.
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OBJECTIVE
To evaluate the relationship between serum adenosine deaminase (AD) activity and serum total sialic acid (TSA) levels in obese individuals.
METHODS
We performed this study at the Department of Chemistry, Division Biochemistry, Kahramanmaras Sutcu Imam University Arts and Science Faculty,
Decreased activity of (Ca2+ + Mg2+)-adenosine triphosphatase (ATPase) and a hormone-specific defect in insulin regulation of ATPase in kidney basolateral membranes from obese fa/fa rats.
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The plasma membrane enzyme (Ca2+ + Mg2+)-adenosine triphosphatase (ATPase) is hormonally regulated and may participate in Ca2+ signaling by removing excess Ca2+ from the cell. Therefore, observations of a hormone-specific loss of insulin stimulation of ATPase in kidney membranes from
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