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

Possible involvement of an endogenous digitalislike substance (EDLS) in blood pressure regulation was investigated using a Japanese population. Mean arterial pressure (MAP) significantly correlated with urinary excretion of the EDLS, age, and the obesity index. The plasma EDLS correlated with urinary EDLS. Urinary EDLS excretion well correlated with the inhibitory activity on Na+,K+-ATPase, and also with the urinary excretion of NaCl. Obesity index correlated with the Na+,K+-ATPase inhibition and arterial pressure. Although plasma content of atrial natriuretic polypeptide correlated with the urinary Na+,K+-ATPase inhibition, it did not correlate with the rest of all parameters. Plasma vasopressin level did not correlate with these parameters either. These results clearly indicate that the circulating EDLS (ie, Na+,K+-ATPase inhibitor) is implicated in the hypertension associated with an excess intake of sodium, aging and obesity.
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PMID:Endogenous digitalislike substance in an adult population in Japan. 341 95

The purpose of this study was to determine if the metabolic response to obesity and to pair feeding of obese Zucker rats to lean Zucker rats was similar across skeletal muscles. Oxidation of glucose, palmitate and isoleucine was studied in muscle strips in vitro using appropriate 14- carbon substrates as tracers. The plantaris muscle was subjected to histochemical analyses using an alkaline actomyosin ATPase, NADH-tetrazolium reductase and an oil red 0 stain. Soleus muscles from both ad libitum and pair fed obese rats oxidized less glucose to CO2, but released similar amounts of lactate when compared to the soleus muscles of lean rats. Oxidation of glucose was similar in the extensor digitorum longus (EDL) muscle of ad libitum fed obese rats, but lower when pair fed to the intake of lean rats. No differences were apparent in palmitate oxidation to CO2 or in incorporation into lipid (both soleus and EDL muscles), except in the EDL muscle of pair-fed obese rats which exhibited a higher rate for palmitate metabolism when compared with lean rats. Isoleucine oxidation to CO2 was higher in the EDL and plantaris muscles, but similar in the soleus muscle of ad libitum-fed obese rats when compared with lean rats. The magnitude of the difference in isoleucine oxidation was similar when the obese rats were pair fed. No differences in the percentage of plantaris muscle fibers sensitive to alkaline ATPase staining were observed. The plantaris muscle of obese rats, contained a higher proportion of oxidative fibers. These results indicate the great risk in generalizing about metabolic activity of the whole skeletal muscle mass based on observations made on one, or even two, distinct muscles in this animal model. Also, pair feeding of obese to lean Zucker rats did not result in uniform changes in metabolism between muscles of the obese rats.
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PMID:Metabolic characteristics of skeletal muscle from lean and obese Zucker rats. 345 May 49

Studies on erythrocyte sodium pump activity in obesity have yielded conflicting results probably because the erythrocyte is an atypical cell, and it may not reflect ATPase activity of other cells in the body. This study was undertaken to establish a reproducible procedure to measure sodium transport in human diploid fibroblasts, and apply this method to explore any differences in the cells from obese and nonobese humans. Cell cultures were established from 12 nonobese (body mass index (BMI) = wt in kg/height in m2 (Khosla and Lowe, Br J Prev Soc Med 1967; 21: 122-128); less than 27 kg/m2) and 10 obese (BMI) greater than 35 kg/m2) subjects. Triplicate measurements of sodium efflux rate constant were made with and without ouabain (1 mmol/l) to determine the total, active (ouabain-sensitive) and passive (ouabain-insensitive) components. Reproducible results were obtained as suggested by a coefficient of variation (CV) of less 10% on successive experiments on the same cell-line, and 11 and 15% of the active sodium efflux rate constant measured in fibroblasts from nonobese and obese subjects, respectively. The active sodium efflux rate constant in fibroblasts from nonobese (0.202 +/- 0.023 (SD)) was not significantly different from that obtained in the cells from obese subjects (0.21 +/- 0.030; p greater than 0.10). These results suggest that there is no intrinsic differences in basal sodium pump activity in fibroblasts related to obesity.
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PMID:A reproducible procedure for measuring sodium transport in cultured human fibroblasts from normal and obese donors. 407 28

In an attempt to resolve the prevailing confusion about erythrocyte sodium pump activity in obesity, we measured sodium-potassium-ATPase, ouabain-inhibitable (active) sodium efflux rate constant and intracellular sodium concentration in erythrocytes from 107 non-obese and obese subjects, with a body-mass index ranging from 17 to 54 kg X m-2. All the three independently measured variables were not significantly different between the two groups and no correlations were found between these three indices and body-mass index. The expression of ATPase activity in units of membrane protein allowed our previous data to be compared with this study and other reports. Our studies and most of the published reports suggest that there is no difference in erythrocyte sodium-potassium-ATPase and sodium transport between the vast majority of obese and non-obese subjects, but there is a subgroup of obese subjects (about 5%) with abnormally high erythrocyte sodium pump activity. The variable treatment of data from this subgroup and the small numbers of obese subjects studied by various investigators are largely responsible for the conflicting results about erythrocyte sodium pump activity.
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PMID:Erythrocyte sodium pump activity in human obesity. 609 47

To determine whether muscle sodium-potassium-ATPase activity, an expression of energy turnover, is increased in obesity, we studied a group of nine non-obese and seven obese subjects undergoing elective cholecystectomy. The muscle ATPase activity was 87 per cent higher (p less than 0.001) in obese subjects compared with non-obese subjects. The increase in the ATPase activity positively correlated with both the body mass index (r = 0.81) and excess body weight (r = 0.75). No relationship was found between erythrocyte and muscle sodium-potassium-ATPase activities (r = 0.25). These findings demonstrate an increased ATPase activity in skeletal muscle obtained from obese subjects and that the erythrocyte is an inaccurate marker of this enzyme with respect to other body tissue.
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PMID:Elevated skeletal muscle sodium-potassium-ATPase in human obesity. 609 48

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 subjects and 25 obese subjects. The mean erythrocyte sodium content, sodium transport and ouabain binding capacity of obese subjects were the same as in lean subjects. There was no relationship between obesity index (wt/ht2) and sodium transport. We conclude that erythrocyte sodium transport in most obese patients is normal.
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PMID:Erythrocyte sodium content, sodium transport, ouabain binding capacity and Na+, K+-ATPase activity in lean and obese subjects. 609 24

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 pressure was inversely correlated with erythrocyte ouabain binding (P less than 0.02) and directly correlated with intracellular Na+ concentration (P less than 0.01). Moreover, there was a stronger inverse relationship between ouabain binding and intracellular Na+ in patients receiving medication for hypertension (P less than 0.01) than in normotensive patients (P less than 0.05). These data suggest that patients receiving hypertensive medication may be less able to compensate than normotensive patients, (a) for the potential effect of Na+-K+-ATPase levels on intracellular Na+ and (b) for the potential effect of intracellular Na+ concentration on diastolic blood pressure. We propose that obese people with low levels of ouabain binding (primary obesity) may have an increased risk of developing hypertension if their compensatory mechanisms fail.
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PMID:Erythrocyte ouabain binding and intracellular Na+ in normotensive obese women and obese women receiving medication for hypertension. 609 20

In order to study cation transport in vivo the changes in plasma and red cell rubidium concentrations were measured following an oral load of rubidium chloride. Eight patients receiving short-term digoxin therapy, 10 patients with chronic renal failure and 22 patients with untreated essential hypertension were studied, and the findings were compared with those in healthy control subjects matched for age, sex, race, obesity index, and plasma and red cell potassium concentrations. In patients receiving short-term digoxin therapy, and in patients with chronic renal failure, the increases in plasma rubidium concentrations after the oral load of rubidium chloride were significantly enhanced and the increases in red cell rubidium concentrations were significantly attenuated. These findings are consistent with a generalized reduction in Na+, K+-ATPase activity in vivo. In contrast, in patients with untreated essential hypertension the increases in both plasma and red cell rubidium concentrations following the oral load were significantly enhanced. These data do not support the hypothesis that essential hypertension is associated with reduced Na+, K+-ATPase activity in vivo, at least in the red cell.
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PMID:An in vivo study of cation transport in essential hypertension. 610 Jul 48

Concentrations of Na+,K+-ATPase enzyme units are lower in skeletal muscle and liver of adult obese (ob/ob) mice than in their lean counterparts. The present studies were designed to provide information on functional correlates of Na+,K+-ATPase in ob/ob mice. Obese mice had lower potassium (K+) content in muscle and liver and higher sodium (Na+) content in muscle and liver and higher sodium (Na+) content in muscle than lean counterparts. The calculated intracellular Na+/K+ ratio in muscle of obese mice was approximately twice as high as in muscle of lean mice. Oxygen consumption was measured in mice maintained at 14 degrees, 25 degrees, or 33 degrees for 40 min and injected with 0.3 or 0.9 microgram ouabain per g body weight. Ouabain, a specific inhibitor of Na+,K+-ATPase, decreased oxygen consumption less in obese mice (12%--25%) than in lean mice (19%--38%). These results suggest that Na+ pump activity may be reduced in obese mice.
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PMID:Functional correlates of Na+,K+-ATPase in lean and obese (ob/ob) mice. 626 98

1 The sympathetic noradrenergic activation of brown adipose tissue and the biochemical mechanisms involved in diet-induced thermogenesis were studied in rats. 2 A close correlation was found between brown adipose tissue Na+, K+-adenosinetriphosphatase (Na+, K+-ATPase) activity in vitro and in vivo measurements of resting oxygen consumption (VO2). The effects of noradrenaline on in vitro NA+, K+-ATPase activity in brown adipose tissue and in vivo VO2 could be mimicked by a variety of agents. These included beta-adrenoceptor agonists and agents known to induce the release of noradrenaline or inhibit the noradrenaline uptake process. The pharmacological evidence suggests that dopaminergic mechanisms may also be involved in the control of thermogenesis. 3 Amphetamine did not increase VO2 in rats without causing associated increases in locomotor activity. Ciclazindol at doses of 3-30 mg/kg intraperitoneally increased VO2 but did not appear to increase locomotor activity or evoke any other signs of CNS stimulation including lengthening of time to sleep onset or stereotypy. Separation of metabolic and CNS effects occurred only at the lowest dose of mazindol used (0.3 mg/kg i.p.). These results are probably a reflection of (a) the relative abilities of these drugs to inhibit brain and brown adipose noradrenaline uptake processes and (b) the relatively high accumulation of ciclazindol in brown adipose. 4 Of the drugs tested, only ciclazindol was a more potent inhibitor of the noradrenaline uptake system in brown adipose tissue (BAT) than in brain. Kinetic analysis also revealed that the actions of ciclazindol on the NA uptake system and Na+, K+-ATPase in BAT differed from those of mazindol. 5 These findings suggest that ciclazindol may produce an energy wasting effect in rodents without causing overt CNS stimulation; the implications of these findings in terms of human obesity are discussed.
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PMID:Sympathetic mechanisms in diet-induced thermogenesis: modification by ciclazindol and anorectic drugs. 627 18


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