Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound   Target Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound

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Query: EC:3.6.1.3 (ATPase)
65,361 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Competitive rhythmic sportive gymnastics have been accused of promoting an unphysiologic weight reduction which may progress to manifest anorexia nervosa. In this study, eight young female gymnasts who represented Norway in the European Championships in Rhythmic Sportive Gymnastics 1982 were examined for evidence of malnutrition. Ten girls, matched for age and height, served as controls. The examination included registration of anthropometric data (height, weight, and body-mass index), motor and sensory neurography and biopsies of the vastus lateralis muscle with exact measurements of muscle fibre areas on sections stained for myofibrillar ATPase activity. The mean body weight of the gymnasts did not differ from that of the control group or of a large series of age matched Norwegian females. This finding excludes the possibility of general malnutrition among the examined gymnasts. Muscle fibres of both types 1 and 2 were found to be smaller in the gymnasts than in the controls, with values of 3,404 microns2 vs 3,811 microns2 for type-1 fibres and 2,985 microns2 vs 3,942 microns2 for type-2 fibres respectively. Although contradictory to most previous reports, this finding suggests that the reduction in fibre size among the gymnasts might be an effect of physical training. There were some differences in neurographic parameters between the groups, but the mean values were all within normal ranges. The motor nerve conduction velocity in the proximal segments of the median and ulnar nerves was significantly slower in the gymnasts and, as a possible consequence of smaller muscle fibres, the motor responses were generally less in this group.
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PMID:Are young female gymnasts malnourished? An anthropometric, electrophysiological, and histological study. 654 Jun 76

In vivo jejunal transport of amino acids, monosaccharides, sodium, and electrolytes were studied in rats made nephrotic with puromycin aminonucleoside (PAN) and in pair-fed controls. Studies were performed 14 days after a single intravenous dose of PAN when rats were no longer edematous, but were still hypoproteinemic. There was decreased absorption of glucose, 3-0-methyl glucose, glycine, phenylalanine, histidine, water, and sodium in the nephrotic animals but transport of fructose, lysine and potassium was similar in the nephrotic and control animals. Enzyme kinetic studies for glucose transport showed a mixed type of inhibition affecting both Vm and Km. The jejunal mucosa of nephrotic and control rats had similar ATP content and enzyme activity for lactase, sucrase, maltase and (Na-K)-ATPase and the ratios of RNA to DNA were similar in the nephrotic and control rats. No abnormality of the jejunum was detected by light or electron microscopy. The data suggest that the impairment of absorption is a result of decreased activity of jejunal membrane carrier mechanisms. The altered transport may be secondary to effects related to the metabolic consequences of nephrotic syndrome and does not appear to be related to acute purine aminonucleoside toxicity, edema or malnutrition.
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PMID:Jejunal transport in experimental nephrotic syndrome. 662 9

Diabetes mellitus is associated frequently with congestive heart failure in humans, even in the absence of associated coronary disease or hypertension. Nevertheless, the effects of the diabetic state on myocardial mechanics have not been studied. Accordingly, diabetes was induced in female Wistar rats by injection of streptozotocin (60 mg/kg). Left ventricular papillary muscles were studied 5, 10, and 30 weeks later and compared with controls. Relaxation was delayed significantly and velocity of shortening was depressed at all loads. However, the passive and active force-length curves, as well as the series elastic properties, were not altered. The changes in cardiac performance were found over a range of muscle lengths, stimulus frequencies, and bath concentrations of calcium, glucose, and norepinephrine. The duration of diabetes had no major effect on the mechanical changes observed. The possible influences of drug-induced cardiac toxicity, malnutrition, and altered thyroid hormone levels have been considered; the latter two factors could not be excluded completely from having some influence on the mechanical properties of diabetic cardiac muscle. Evidence is cited showing abnormalities in calcium uptake by sarcoplasmic reticulum and depressed actomyosin ATPase activity. Thus a cardiomyopathic state has been produced in the rat consequent to the induction of experimental diabetes mellitus. Various mechanisms for this entity have been suggested.
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PMID:Altered myocardial mechanics in diabetic rats. 743 39

Only in the duodenum and in the colon calcium is absorbed by a cellular 1,25 alpha-Vitamin D3-dependent transport mechanism. Calcium absorption is highest in the proximal large intestine, about ten times higher than in the duodenum or in the descending colon. 1,25 alpha-Vitamin D3 stimulates calcium transport by genomic (slow effect: synthesis of cytosolic calcium binding protein CabP and basolateral Ca-ATPase) and non-genomic action (rapid effect: transcaltachyia, liponomic effect at the brush border membrane). CabP-dependent translocation across the cytosol is thought to be rate limiting step of cellular calcium transport. However, only about 50% of calcium absorption is cellular mediated but the same amount of calcium convectively is absorbed by transepithelial water flow across the paracellular pathway (solvent drag effect). 1,25 alpha-Vitamin D3 not only activates cellular calcium absorption but also increases paracellular permeability for calcium by an unknown mechanism. However, essential steps in the cascade from the interaction of 1,25 alpha-Vitamin D3 with the specific receptor over the regulation of the synthesis of calcium binding and transporting proteins to the induction of cellular calcium transport are not as yet clearly understood. The exact feedback mechanism of synchronized calcium transport across the distinct subcellular compartments seems also to be resolved. Cellular calcium transport is not found in the jejunum or in the ileum, what can be explained by the absence of specific 1,25 alpha-Vitamin D3-dependent carrier systems in these segments. On the other hand calcium is secreted across the jejunum and ileum by an anomalous solvent drag effect. Hence, intestinal calcium metabolism seems to underlie an eneteroenteral circuit: 1,25 alpha-Vitamin D3-controlled cellular calcium absorption across the duodenum is followed by paracellular calcium secretion across the jejunum and ileum. The carrier in the proximal colon which works at the optimal level already under normal nutritional condition could be of physiological importance for the reclamation of unabsorbed dietary calcium and for the reabsorption of calcium that is secreted across the distal small intestine. Under certain pathophysiological conditions, i.e. malabsorption in proximal segments or malnutrition, calcium in addition may be conserved by the 1,25 alpha-Vitamin D3-sensitive carrier in the descending colon.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:[New findings on the mechanism and regulation of intestinal calcium transport]. 780 57

In 743 cases, the TCM and WM susceptible factors of senile cataract (SC) was studied by the clinical epidemiological investigation. By single factor analysis, the result showed that in WM, the susceptible factors of SC mostly related to (1) case history: coronary heart disease, old ages, smoking, multiple offsprings; (2) physical sign: short build, with coronary sulcus, higher systolic pressure, pulse pressure and average arterial pressure; (3) cardiovascular function: abnormal EKG, higher heart beat index, short microcirculatory stasis time, lower carrier viscosity of blood; (4) dysfunction of brain; (5) deficiency of pulmonary function; (6) lower RBC ATPase, higher whole blood reduction viscosity. While in TCM, it was related to (1) old aged and general asthenia, (2) deficiency of Qi, Heart, Liver or Kidney, (3) Blood Stasis. By stepwise regression analysis, the result showed that SC occurred through the combination with 13 factors of TCM and WM, including Yin Deficiency, senility index, hemorheology index, brain function, pulmonary function, blood pressure, body height, character, optical fundus, etc.
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PMID:[Investigation on traditional Chinese medicine and Western medicine susceptible factors on senile cataract]. 795 Feb 14

Common metabolic problems in northeastern Thailand include renal stone disease, distal renal tubular acidosis, hypokalemic periodic paralysis, sudden unexplained nocturnal death and malnutrition-related diabetes mellitus. There is evidence of decreased activity of Na,K-ATPase and H,K-ATPase. A preliminary study was made of the vanadium concentration in the soil and water in northeastern Thailand. The urinary and tissue vanadium concentrations were also determined in the northeastern villagers. The soil was found to have high vanadium content. The vanadium content was also high in the urine, kidneys and lungs of the villagers. It is postulated that these metabolic problems are attributed to the inhibition of Na,K-ATPase and H,K-ATPase activity by vanadium.
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PMID:Metabolic problems in northeastern Thailand: possible role of vanadium. 839 62

Buffered propionic acid was injected s.c. into rats twice a day at 8 h intervals from the 6 to 21 days of age. Control rats received saline in the same volumes. The animals were weighed and killed by decapitation at 23 days. Whole brain and cerebral cortex were weighed and synaptic plasma membranes were prepared from cortex for the determination of Na+,K+-ATPase and Mg2+-ATPase activities. Body, whole brain and cortical weights were similar in the two groups, suggesting that propionic acid does not cause malnutrition in rats. Na+,K+-ATPase activity was significantly reduced by 30% in membranes from the propionate-treated group, whereas Mg2+-ATPase activity was not. In another set of experiments, synaptic plasma membranes were prepared from cerebral cortex of 23-day-old rats and incubated with propionic acid at final concentrations ranging from 0.1 to 2.0 mM. Na+,K+-ATPase activity, but not Mg2+-ATPase activity, was inhibited by 22-32%. Since propionic acid concentrations in plasma of chronically treated rats and of propionic acidemic children are of the same order of magnitude as those tested in vitro, the results suggest that the inhibition of Na+,K+-ATPase activity may be related to the neurological dysfunction of patients affected by propionic acidaemia.
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PMID:Inhibition of Na+,K+-ATPase from rat brain cortex by propionic acid. 966 89

To evaluate a possible role of ovarian sex hormones in the Ca2+ responsiveness of cardiac myofilament activation, the relations of pCa (-log Ca2+ molar concentration) to actomyosin adenosine triphosphatase (ATPase) activity of isolated myofibrillar preparations from 8-10 week ovariectomized (Ovx) rat hearts were compared with those from sham-operated hearts. Deficiency of ovarian sex hormones in plasma of ovariectomized rats was indirectly verified by a significant reduction in uterine weights. Body weights of the ovariectomized rats were significantly greater than those of sham-operated controls. Despite a significant increase in heart weight of 10 week ovariectomized animals, the percent of heart weight-to-body weight ratio was not different from control group. The maximum myofibrillar ATPase activity at pH 7.0 was significantly suppressed after ovariectomy in both eight and ten week groups. However, the maximum ATPase activity at pH 6.5 was significantly suppressed only in 10 week ovariectomized hearts. Surprisingly, in every condition with depressed maximum myofibrillar ATPase activity, the pCa-actomyosin ATPase relationships of ovariectomized cardiac myofilaments demonstrated a significant leftward shift in pCa50 (-log half-maximally Ca2+ activation) from those of sham-operated controls. There was, however, no change in the Hill-coefficient of these cardiac myofilaments after ovariectomy. Analysis of myofilament proteins using gel electrophoresis demonstrated neither change nor loss of any thin filament proteins. These results indicate a possible modulating effect of ovarian sex hormone deficiency on the Ca2+ responsiveness of cardiac myofilament activation by induction of myofilament Ca2+ hypersensitivity but suppression of maximum myofibrillar ATPase activity.
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PMID:Increase in calcium responsiveness of cardiac myofilament activation in ovariectomized rats. 974 96

Energy restriction (ER), without malnutrition, increases maximum life span and retards the development of a broad array of pathophysiological changes in laboratory rodents. The mechanism responsible for the retardation of aging by ER is, however, unknown. One proposed explanation is a reduction in energy expenditure (EE). Reduced EE may increase life span by decreasing the number of oxygen molecules interacting with mitochondria, thereby lowering reactive oxygen species (ROS) production. As a step toward testing this hypothesis, it is important to determine the effect of ER on EE. Several whole-body, organ, and cellular studies have measured the influence of ER on EE. In general, whole-body studies have reported an acute decrease in mass-adjusted EE that disappears with long-term ER. Organ-specific studies have shown that decreases in EE of liver and gastrointestinal tract are primarily responsible for initial reductions in EE with ER. These data, however, do not determine whether cellular EE is altered with ER. Three major processes contributing to resting EE at the cellular level are mitochondrial proton leak, Na(+)-K(+)-ATPase activity, and protein turnover. Studies suggest that proton leak and Na(+)-K(+)-ATPase activity are decreased with ER, whereas protein turnover is either unchanged or slightly increased with ER. Thus, two of the three major processes contributing to resting EE at the cellular level may be decreased with ER. Although additional cellular measurements are needed, the current results suggest that a lowering of EE could be a mechanism for the action of ER.
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PMID:Restriction of energy intake, energy expenditure, and aging. 1108 84

Metabolic myopathies are due to deficiencies of energy production involving glycogen, lipid, or mitochondrial metabolism. Deficiency of sarcoplasmic calcium-ATPase is at the origin of Brody's syndrome. Patients may present with exercise intolerance, myoglobinuria or progressive muscle weakness. The first step of diagnosis relies on the performance of in vivo metabolism investigations: forearm or bicycle ergometer exercise tests, phosphorus nuclear magnetic resonance spectroscopy. A few enzymatic defects may be directly measured on blood sampling, but muscle biopsy is necessary in most cases in order to precise the etiology of the metabolic defect through enzymatic assays. We present a description of the main metabolic myopathies with an overview of clinical and laboratory evaluation leading to diagnosis.
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PMID:[Metabolic myopathies in adulthood. Features and clues for diagnosis]. 1179 77


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