ouabain/obesity

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The effect of diet on ouabain binding to erythrocytes from obese subjects.

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Ouabain binding to erythrocyte membranes is increased in obese subjects. Three study groups are compared: 14 reference subjects, 102 +/- 16% of ideal weight; 9 obese on unrestricted diets, 207 +/- 16% of ideal weight; 11 obese on restricted diets, 202 +/- 35% of ideal weight. A reproducible (CV =

Erythrocyte ouabain binding and intracellular Na+ in normotensive obese women and obese women receiving medication for hypertension.

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People with "primary obesity" may be hypertensive because they have lost their ability to compensate for the effect of low Na+-K+-ATPase levels on blood pressure. In obese patients receiving hypertensive medication (n = 13), but not in normotensive nonmedicated patients (n = 42), diastolic blood

Spectrophotometric assay of renal ouabain-resistant Na(+)-ATPase and its regulation by leptin and dietary-induced obesity.

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Apart from Na(+),K(+)-ATPase, a second sodium pump, Na(+)-stimulated, K(+)-independent ATPase (Na(+)-ATPase) is expressed in proximal convoluted tubule of the mammalian kidney. The aim of this study was to develop a method of Na(+)-ATPase assay based on the method previously used by us to measure

Erythrocyte sodium content, sodium transport, ouabain binding capacity and Na+, K+-ATPase activity in lean and obese subjects.

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Erythrocyte sodium content, sodium transport (ouabain-sensitive efflux rate of sodium, and ouabain-sensitive efflux rate constant of sodium) 3H ouabain binding capacity and sodium-potassium-activated ouabain-sensitive adenosine triphosphatase (Na+-K+-ATPase) activity were measured in 18 lean

Regulation of renal ouabain-resistant Na+-ATPase by leptin, nitric oxide, reactive oxygen species, and cyclic nucleotides: implications for obesity-associated hypertension.

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This study examined the effect of leptin on renal ouabain-resistant Na(+)-ATPase, which drives the reabsorption of about 10% of sodium transported in the proximal tubule. Chronic leptin administration (0.25 mg/kg s.c. twice daily for seven days) increased Na(+)-ATPase activity by 62.9%. This effect

Evaluation of ouabain-insensitive red blood cell cation transport in obese children.

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Inhibition of insulin receptors by vanadate and ouabain.

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Insulin binding studies were performed, using cells from 5 non-obese, non-diabetic subjects, on four separate days: 2 were paired control studies to demonstrate precision, and 2 other sets were binding studies in which one incubation solution was a control and the other contained either vanadate,

Definition, measurement, and classification of the syndromes of obesity.

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The definition and risks of obesity have been reviewed and a nomogram provided for reference. Organization of information about the syndromes of obesity has been approached from several points of view. An anatomic classification has been developed, in which generalized and localized forms of fat

Human leptin administered intraperitoneally stimulates natriuresis and decreases renal medullary Na+, K+-ATPase activity in the rat -- impaired effect in dietary-induced obesity.

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BACKGROUND Leptin, produced by adipose tissue, apart from regulating food intake and energy expenditure, also has natriuretic activity. In this study we examined the effect of leptin on renal Na+, K+-ATPase responsible for active tubular sodium reabsorption, and compared the renal effects of leptin

Functionally abnormal Na+-K+ pump in erythrocytes of a morbidly obese patient.

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The Na(+)-K(+) pump in the erythrocytes of a mordibly obese patient shows a unique constellation of functional abnormalities. The number of pump units, measured by [(3)H]ouabain binding to intact cells, as well as the enzymatic activity of the (Na(+)-K(+))-dependent ATPase in erythrocyte membranes

Hyperphagia and obesity in Na,K-ATPase alpha2 subunit-defective mice.

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OBJECTIVE The Na,K-ATPase alpha2 subunit gene (Atp1a2) is expressed in the brain, skeletal muscles, heart, and adipocytes. Specific function of the alpha2 subunit, such as involvement in differentiation and function of adipocytes, has not been addressed. The aim of this study was to examine whether

Serum insulin, insulin sensitivity, and erythrocyte sodium metabolism in normotensive and essential hypertensive subjects with and without overweight.

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Increased insulin circulating levels and perturbations of intracellular sodium metabolism have been reported in essential hypertensive patients, leading to postulate their involvement in the pathophysiology of the disease. In-vitro studies have shown that insulin modulates the activity of some

Platelet sodium kinetics, blood pressure and serum urate: aberrations in non-obese men at risk for type 2 diabetes mellitus.

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The rate constants for the ouabain- and frusemide-sensitive 22Na+ efflux, the number of [3H]ouabain binding sites and the effect of plasma on [3H]ouabain binding were determined in platelets, as were blood pressure (BP) and serum urate concentrations, in 35 normoglycaemic men with family histories

The effect of oral glucose on the leucocyte sodium pump in normal and obese subjects.

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The effect of oral glucose (40 g/m2 body surface area) on the leucocyte 22Na efflux rate constants (ERC) was studied in 13 normal weight and 10 obese subjects. The ouabain-sensitive 22Na ERC was higher in leucocytes isolated from fasting obese subjects (median [range] for obese 2.77 [2.33-3.11] vs

Na+,K+-ATPase enzyme units in lean and obese (ob/ob) thyroxine-injected mice.

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The possible involvement of Na+,K+-ATPase in the etiology of obesity in the obese (ob/ob) mouse was explored. The number of Na+,K+-ATPase enzyme units in skeletal muscle, liver, and kidneys from 4- and 8-wk-old obese and lean mice was estimated from saturable [3H]ouabain binding to particulate

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