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Query: UMLS:C0028754 (obesity)
 124,988 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Leucocyte ouabain-sensitive 22Na+ efflux was studied in 35 normal and 12 obese subjects. This efflux rate constant was raised in the obese (2.72 +/- SEM 0.13 vs 2.31 +/- 0.08 h-1, P less than 0.006), indicating a higher activity of the sodium pump in vivo, There was a significant correlation between this efflux rate constant and fasting insulin level in both the whole population and in the normals alone (rs = 0.36, P less than 0.007, and rs = 0.40, P less than 0.009 respectively). A hyperinsulinaemic-euglycaemic clamp was performed on seven normal volunteers. After 2 h, there was a significant stimulation of the leucocyte efflux rate constant (from 2.86 +/- 0.17 to 3.33 +/- 0.18 h-1, P less than 0.01). In-vitro incubation of leucocytes with insulin produced a maximal stimulation of the Na+-K+-ATPase activity of about 35% at 2 h with half-maximal stimulation achieved at 46 mU/l. Insulin (100 mU/l) also stimulated the leucocyte ouabain-sensitive 22Na+ efflux rate constant in vitro by about 11% with or without 1 h of preincubation with the insulin. These findings may explain the hypokalaemic and sodium retaining effects of insulin in man; they may also partially explain the raised Na+ efflux rate constants in obesity.
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PMID:The leucocyte sodium pump in healthy and obese subjects: the association of insulin with its activity. 244 7

The number and activity of erythrocyte ATPase-dependent sodium-potassium pump units were increased in obese subjects (p = 0.02). No link was observed between the number or activity of the pump units and hypertension. The ouabain-insensitive rubidium (i.e. potassium) transport was not associated with relative body weight or blood pressure status. Sodium-lithium countertransport correlated significantly with obesity but not with blood pressure status. In the hypertensive patients, before or after therapy with verapamil, hydrochlorothiazide, pindolol or atenolol there were no significant differences in cation transport. We propose that the correlation between obesity and essential hypertension cannot be explained by these two cation transport systems.
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PMID:Erythrocyte cation transport in obesity, hypertension, and during antihypertensive drug therapy. 257 70

A study was made of the erythrocytic membranes in patients with stage II-III metabolic and alimentary obesity. The red blood cells may serve as model of the membranes of other cells of the internal organs, that is why their changes are likely to mirror the total impairment of the function of the cell membranes in the illness under consideration. The patients' red blood cells were characterized by high permeability, increased ATPase activity, catalase activation, reduction of the content of the thiol groups, and by the displacement of the thiol-disulfide balance towards oxidized forms. A correlation was discovered between the elevation of red blood cell permeability and red blood cell K+, Na+-ATPase activation. The changes in the thiol-disulfide balance brought about inconclusive shifts in the magnitude of permeability, in the activity of ATPase isoenzymes, and in the content of cholesterol fractions in red blood cells of patients with metabolic and alimentary obesity. The changes thus discovered are of paramount importance for understanding the pathogenesis of metabolic abnormalities associated with obesity and for rational treatment of this patients' group.
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PMID:[New data on characteristics of the chemism of erythrocytes in patients with metabolic-alimentary obesity]. 280 Apr 51

In a search for the role of long-term hypocaloric feeding on the expression of the erythrocyte Na pump in obesity, we examined three groups of subjects. Group 1 consisted of 10 obese subjects who had been under treatment for a long period of time with a very-low-calorie diet (500 kcal/d) while group 2 consisted of 10 age-, sex-, and body mass index-matched obese subjects on their usual diet; in the third group, 12 normal-weight subjects on a free diet served as controls. There was no difference between the groups in the number of erythrocyte binding sites per cell. On the contrary, the Na-K-ATPase activity was significantly lower in the obese group 1 (0.35 +/- 0.09 mumol Pi x mg protein-1 x h-1) compared to that observed in the obese group 2 (0.42 +/- 0.07, P less than .05) and in control subjects (0.45 +/- 0.06, P less than .05). Sex, duration of hypocaloric feeding, and the amount of weight loss before the study in the obese group 1 seemed not to be related to the Na pump parameters. We conclude that long-term severe hypocaloric feeding may be a factor in altered erythrocyte Na-K-ATPase in obese individuals.
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PMID:Erythrocyte Na-K-ATPase membrane activity in obese patients fed over a long-term period with a very-low-calorie diet. 282 67

A number of previous investigations in obese and normal-weight adults suggested a link between (usually) lower than normal erythrocyte Na+-K+ ATPase activity and obesity, although more recent studies have disputed this link. Developmental patterns of ATPase activity in children have not been studied. Infants of diabetic mothers show an increased incidence of macrosomia and such infants are at risk for later development of obesity. These children provide an ideal group to study the link (if any) between this enzyme and obesity, as well as changes in the level of the enzyme which may occur with age and/or the onset of obesity. The Na+-K+ ATPase levels in erythrocytes from 87 normal children and 27 infants of diabetic mothers were therefore studied by an ouabain-binding method. The study populations contained representatives of three ethnic groups (black, Caucasian and Hispanic) and individuals of normal body weight, as well as overweight and obese individuals. The ATPase activities were not correlated with body weight, sex, or age, nor was umbilical cord red cell ATPase correlated with birthweight. Several children who are being followed have shown considerable variation in percentage ideal body weight (IBW); however their ATPase levels have remained unchanged. There were, however, significant differences among the ethnic groups, with Caucasians having the highest values (0.443 +/- 0.012 pmol ouabain bound/10(9) cells). These data demonstrate the importance of matching study groups by race when investigating factors affecting this enzyme. The differences among the ethnic groups suggest a genetic component in the determination of the activity of this enzyme. This link was further investigated in 14 families and revealed considerable heterogeneity within a given ethnic group, with family members generally having similar enzyme activities, thus supporting a genetic basis for the different enzyme levels. Thus erythrocyte Na+-K+ ATPase in childhood is primarily regulated by genetic factors which are generally independent of body weight.
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PMID:Erythrocyte Na+-K+ ATPase activity in childhood: regulation by genetic factors independent of body weight. 283 Nov 62

A number of erythrocyte Na-K ATPase units were measured in 22 patients with hyperthyroid Graves' disease, 3 with primary hypothyroidism, 3 with simple obesity, 13 with chronic renal failure on hemodialysis, and 20 normal controls, using ouabain binding assay as described by DeLuise et al. The number of Na-K ATPase units, derived by maximal binding of 3H-ouabain, was decreased in patients with simple obesity (Mean +/- SD, 0.26 +/- 0.07 pmol/10(9) RBC), as compared with that in normal controls (0.39 +/- 0.10), and a significant negative correlation between the number of the binding sites and the ratio of the measured body weight to the optimal body weight calculated by the modified Broca's method was observed in normal controls and patients with obesity (r = -0.51, p less than 0.05). The results agreed closely with that reported by DeLuise et al and provided validation of our estimates of the erythrocyte Na-K pump units. The maximal 3H-ouabain binding was significantly diminished in patients with hyperthyroid Graves' disease (0.28 +/- 0.07) when compared with that in normal controls, while the bindings were significantly elevated in patients with hypothyroidism (0.91 +/- 0.26). These results were in disagreement with those previously reported by animal studies where Na-K ATPase was found to be stimulated by thyroid hormones. It might be possible to partly explain this discrepancy by the degradation of Na-K ATPase in erythrocytes in addition to the apparent differences between erythrocytes and the other tissues and by the length of time that the tissue was exposed to the action of the hormones. Therefore, erythrocyte from normal controls and patients with hyperthyroid Graves' disease were divided into low and high density portions by a discontinuous 'percoll' density gradient centrifugation, and the bindings of the erythrocytes in two portions were separately measured. The bindings of erythrocyte in the higher density portion, representing relatively old-aged erythrocyte, were diminished to 92 +/- 19% of the bindings of the original whole erythrocytes in normal controls. An even more marked reduction of the maximal bindings of 3H-ouabain in old-aged erythrocytes was observed in patients with hyperthyroid Graves' disease (72 +/- 26%). Moreover, this % reduction based on aging related significantly to serum T4 concentrations in those patients (r = 0.85, p less than 0.05). These findings suggest that the number of erythrocyte Na-K ATPase units may reflect the overall peripheral metabolic state, regulated by thyroid hormone-dependent thermogenesis.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:[Clinical studies on assay for Na-K ATPase in human blood cells. I. Erythrocyte Na-K ATPase assay in patients with thyroid dysfunction and in those with chronic renal failure]. 284 3

The number of Na-K pump units, the Na-K-ATPase activity, the K transport turnover rate per pump unit and the intracellular Na and K concentrations were measured in the erythrocytes of 56 obese patients and 20 normal subjects. No differences were found between the two groups. In obese patients, we failed to observe any influence of dietary habits, age of onset, or family history of obesity on the Na pump status. On the other hand, we found that the number of pump units was not a close reflection of the membrane cation transport and in some patients with an abnormally high number of pump units, an inappropriately low Na-K-ATPase activity was observed. We also identified two small groups of obese patients with, respectively, abnormally high or low K transport turnover rate per pump unit. Our study seems to support the hypothesis that abnormalities in the erythrocyte Na-K pump system are not usual in the obese population but are probably present only in a limited number of selected patients.
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PMID:Heterogeneity of the erythrocyte Na-K pump status in human obesity. 299 83

Ion metabolism in obesity-associated hypertension is reviewed. A hypothesis is presented which proposes that ion imbalances in obesity may play an etiological role in obesity-associated diabetes mellitus as well. It is suggested that the rise in intracellular calcium--secondary to reduced sodium, potassium-activated adenosine triphosphatase (Na,K-ATPase) activity--may aid in the development of increased vascular tone and decreased glucose tolerance.
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PMID:Hypertension and diabetes in obesity: a review and new ideas on the contributing role of ions. 301 58

The methodological aspects of (Na+, K+)-ATPase-dependent uptake of 86Rb, a potassium analog, were examined on human lymphocytes isolated from peripheral blood. The study of the time-course, the kinetic parameters, i.e., maximum velocity (Vmax) and Michaelis constant (Km) and the ouabain inhibition curve of 86Rb+ uptake confirm that circulating lymphocytes represent a suitable model for the study of (Na+,K+)-ATPase in human diseases. An application to human obesity is reported: the results indicate that 86Rb+ uptake on circulating lymphocytes is similar in obese and non-obese subjects. Therefore, (Na+,K+)-ATPase does not seem to be involved in the pathogenesis of human obesity.
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PMID:Effects of sodium and potassium adenosine-triphosphatase on circulating lymphocytes: an approach to human obesity. 303 8

Ouabain-sensitive 86Rb influx and [3H] ouabain binding capacity were investigated in the leucocytes of 17 obese patients and 15 control subjects. Both were significantly increased in the obese when compared with controls. Following dietary restriction and a 4% to 5% weight reduction in the obese over 2 weeks, [3H] ouabain binding and ouabain-sensitive 86Rb influx (a model for K+ influx) decreased to levels similar to those in controls. This shows that the number of Na-K ATPase sites on leucocyte membranes of the obese are significantly increased and that this is associated with accelerated 86Rb transport. Since both of these indices decreased following 4% to 5% reduction in body weight while the patients were still obese, increased Na-K ATPase is neither a marker of nor cardinal to the pathogenesis of obesity. We conclude that (1) increase in Na-K ATPase units and 86Rb influx are not characteristic of obesity itself and (2) dietary restriction over the short-term with limited weight reduction restores Na-K ATPase units and 86Rb influx to normal.
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PMID:Increased leucocyte Na-K ATPase in obesity: reversal following weight loss. 304 Nov 76


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