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)

Ca2+ pump activity of skeletal muscle microsomes containing fragments of sarcoplasmic reticulum was examined in rats 8 wk after the induction of chronic diabetes by an intravenous injection of streptozotocin (65 mg/kg). In comparison with the control values, both ATP-dependent Ca2+ uptake and Ca2+-stimulated ATPase activities were increased in the microsomal fraction from diabetic rats. These changes were seen as early as 7 days after streptozotocin injection and were apparent at various times of incubation (1-10 min) as well as at different concentrations of free Ca2+ (10(-7)-5 X 10(-5) M Ca2+). Insulin administration to diabetic animals for 2 wk reversed Ca2+ uptake and ATPase activities to control levels. The increase in microsomal ATPase activity of the diabetic preparation due to cAMP-dependent protein kinase or calmodulin was greater than in the control microsomes and the depression by a specific inhibitor of protein kinase, but not of calmodulin, was greater in diabetic muscle. The enhanced Ca2+ pump activity was associated with altered phospholipid composition and protein profile of the diabetic preparations. The rate of Ca2+ release from microsomal vesicles was unaffected by the diabetic condition. Isometric contractile force development as well as positive dF/dt and negative dF/dt of the skeletal muscle from diabetic animals were higher at different pulse strengths (0.5-100 V) and at different Ca2+ concentrations (0.25-2.5 mM). These results suggest that diabetes is associated with enhanced sarcoplasmic reticular Ca2+ pump activity, and this may account for the hyperfunction of skeletal muscle in this disease.
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PMID:Calcium pump activity of sarcoplasmic reticulum in diabetic rat skeletal muscle. 243 Apr 66

Acute reversible diabetic nerve dysfunction has been associated with a reversible myo-inositol-related (Na+ + K+)-ATPase defect, while poorly reversible chronic nerve dysfunction correlates with progressive axoglial dysjunction of peripheral nerve. The causal relationships between biochemical and neuroanatomical abnormalities and those of nodal membrane function are not known. Nodal clamp examinations were carried out in the sciatic nerve of diabetic BB-rats to elucidate the events underlying diabetic nerve dysfunctions and how these relate to metabolic and structural defects of diabetic nerve. With increasing duration of diabetes, there was a progressive decline in nodal action potentials attributable to decreased Na+ permeability and a decrease in the membranous Na+ gradient. Vigorous insulin therapy in short-term (6-week) diabetic BB-rats normalized the Na+-permeability defect and the membranous Na+ gradient. These defects did not reverse in long-term (24-week) diabetic animals subjected to the same treatment. This poorly reversible nodal dysfunction accounts for the not readily reversible conduction defect in chronic diabetes and is probably directly related to irreversible axoglial dysjunction.
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PMID:Reversible and irreversible nodal dysfunction in diabetic neuropathy. 243 93

Sarcolemmal Ca2+-dependent ATPase activity and the mechanical response to calcium and verapamil were studied in myocardium from normal rats and those with diabetes induced by streptozotocin. Sarcolemmal Ca2+-ATPase activity was increased in diabetic animals, depending on the duration of the diabetes. Both the maximal velocity and the affinity were greater in hearts of diabetic rats compared with normal controls. In insulin treated diabetic hearts the affinity of the enzyme for calcium decreased but the maximal velocity was not modified. The enzyme activity was stimulated maximally by millimolar concentrations of calcium and inhibited by lanthanum chloride. Calcium induced a concentration dependent increase in dF/dt in normal and diabetic hearts, but in diabetes the dose-response curve to calcium chloride was shifted to the left. Verapamil depressed the dF/dt in a concentration dependent manner in normal and diabetic hearts; but the drug was more effective in diabetic than in normal rats. These results suggest that an increase in sarcolemmal Ca2+-ATPase activity may be of critical importance in the hypersensitivity of diabetic heart in the presence of low extracellular calcium and calcium blockade.
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PMID:Hypersensitivity to calcium associated with an increased sarcolemmal Ca2+-ATPase activity in diabetic rat heart. 245 76

The incorporation of [32P]orthophosphate into phospholipids and proteins of sciatic nerve from genetically diabetic (db/db) and littermate control (db/m) C57BL/KsJ mice was studied. Nerves from animals of ages 12, 16, 22, 26, and 38 wk were incubated in vitro. Among phospholipids, the uptake of isotope into phosphatidic acid was higher at nearly all ages examined. Phosphorylation of several proteins, including the major myelin glycoprotein, P0, and the small myelin basic proteins Pr + P2, was significantly enhanced in nerves from both 12- and 38-wk-old diabetic mice. The altered pattern of protein phosphorylation, but not that of phospholipid metabolism, was similar to changes observed in sciatic nerve from streptozocin-induced diabetic rats. The relationship of the results to reported levels of myo-inositol, sorbitol, and Na+-K+-ATPase activity and to functional abnormalities in nerves of db/db mice is discussed. The findings suggest that caution should be exercised in reaching conclusions concerning which biochemical alterations observed in different animal models of diabetic neuropathy are invariably associated with the development of this disorder.
Diabetes 1988 Dec
PMID:Phospholipid metabolism and protein phosphorylation in sciatic nerve from genetically diabetic (db/db) mouse. 246 25

Cell line IgSV195, derived from a pancreatic tumor that arose in an SV40 T-antigen transgenic mouse, retains certain morphological and physiological characteristics of pancreatic beta-cells throughout in vitro and in vivo passage. Insulin secretion is stimulated by exposure of these cells to fetal bovine serum and a combination of 3-isobutyl-1-methylxanthine and glutamine but not by concentrations of glucose in the physiological range. Insulin processing appears to be intact. Neither class I nor class II major histocompatibility complex (MHC) antigens are routinely expressed at the cell surface; however, MHC class I--but not class II--encoded gene products are detected after treatment with recombinant interferon-gamma (IFN-gamma) alone or in combination with tumor necrosis factor. Cytolysis of IgSV195 cells by SV40 T-antigen-specific H-2b-restricted lymphocytes is similarly dependent on IFN-gamma pretreatment. These results emphasize that SV40 T-antigen transgenic mice are likely sources of cell lines that retain their differentiated function in vitro. The IgSV195 cell line provides an accessible model in which to investigate the control of gene expression and function of pancreatic beta-cells.
Diabetes 1989 Aug
PMID:Functional pancreatic beta-cell line from SV40 T-antigen transgenic mouse. 250 59

1. The effects of a six week period of streptozotocin-induced diabetes on tissue catecholamines and on in vivo noradrenaline turnover were assessed in rats. 2. Noradrenaline concentrations measured in heart ventricle, terminal ileum, vas deferens, spleen and adrenal tissue from the diabetic rats were all found to be elevated compared to those found in control rat tissues. The adrenaline contents of the adrenal glands were also raised in these animals. 3. Noradrenaline turnover in heart ventricle, terminal ileum and vas deferens was estimated from the decline in tissue content of the amine following inhibition of its synthesis with alpha-methyl-p-tyrosine. Turnover was found to be increased in all three tissues. 4. The involvement of the polyol pathway in the above changes was investigated by examining the effects of continuous treatment with an aldose reductase inhibitor, Statil (ICI 128436) or dietary myo-inositol supplementation. Either treatment was found to prevent or reduce the increases in tissue noradrenaline and in its turnover. Myo-inositol treatment also partially prevented the rise in adrenal adrenaline. 5. It is concluded that the elevation of tissue catecholamines and of noradrenaline turnover by diabetes was related to myo-inositol depletion secondary to excessive sorbitol synthesis. Possible mechanisms for the observed increase in noradrenaline turnover could involve Na+, K+-ATPase depression.
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PMID:Tissue noradrenaline and the polyol pathway in experimentally diabetic rats. 250 23

The effect of a dietary supplement of an aldose reductase inhibitor (ponalrestat) or of myo-inositol on sodium transport into the rat brain and on concentrations of saccharide and polyols in cortical brain tissue and sciatic nerve was investigated in control rats and in streptozotocin-diabetic rats after a diabetes duration of 2 weeks. In untreated diabetes, the neocortical blood-brain barrier permeability for sodium decreased by 28% (3.4 +/- 0.4 vs 4.7 +/- 1.6 x 10(-5) ml/s g, mean +/- SD) as compared to controls. Levels of glucose, sorbitol and fructose increased in brain as well as in nerve tissues, whereas myo-inositol depletion was not demonstrable. Ponalrestat treatment of diabetic animals had no effect upon the decreased neocortical blood-brain barrier permeability to sodium (3.5 +/- 0.9 vs 4.7 +/- 1.1 x 10(-5) ml/s g) despite normalization of brain and nerve content of sorbitol and fructose. Myo-inositol supplementation of diabetic rats normalized sodium passage into the brain (4.2 +/- 1.1 vs 4.4 +/- 0.5 x 10(-5) ml/s g). Brain concentrations of monosaccharides and polyols were normalized as compared to the myo-inositol treated control group and nerve concentrations of glucose, sorbitol, and fructose were significantly increased. Myo-inositol treatment leads to a normalization of blood-brain barrier permeability; it is suggested that myo-inositol exerts a restituting effect upon Na+/K+-ATPase activity of the cerebral endothelial cells.
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PMID:Myo-inositol normalizes decreased sodium permeability of the blood-brain barrier in streptozotocin diabetes. 252 78

Experimental diabetes results in a reduction of the sarcoplasmic reticulum (SR) Ca2+-stimulated ATPase activity and a redirection of myosin isoenzymes from V1 to V3. Similar, but less pronounced, changes were induced by subjecting rats to intermittent fasting for 6 weeks. Low amounts of sucrose (0.8%) in the drinking water prevented the subcellular changes in fasted rats; however, sucrose neither affected the levels of plasma thyroid hormones nor normalized the reduced body weight. Plasma glucose was lowered without any changes in plasma insulin in the fasted rats receiving sucrose; this suggested an enhanced peripheral glucose utilization. Thus, the signals in the diabetic heart leading to changes in SR and myosin can be mimicked by intermittent fasting and seem to be linked to a shift in fuel utilization by the myocytes.
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PMID:Diabetes-like action of intermittent fasting on sarcoplasmic reticulum Ca2+-pump ATPase and myosin isoenzymes can be prevented by sucrose. 252 55

31P NMR was used to study the erythrocytes of three patients who exhibited a familial multisystem disease characterized by fatty liver, diabetes and nonspherocytic hemolytic anemia of unknown etiology. 31P NMR measurements disclosed an abnormally high level of intracellular inorganic phosphate (Pi) and an abnormally low level of ATP in the erythrocytes 6 h after blood withdrawal from proband (I-1). This finding suggested that ATP was markedly decreased in the red cells of this proband, as compared with those of normal subjects. Time-dependent changes of 31P NMR spectra of the erythrocytes from the two daughters (II-1, II-2) of the proband demonstrated clearly an enhanced decomposition of ATP with a concomitant increment of Pi. Several ATP-consuming enzymes in erythrocytes, such as those in the Embden-Meyerhof system, pentose phosphate pathway enzymes, Na+, K(+)-ATPase and Ca2+, Mg2(+)-ATPase, were within normal limits of activity, but Mg2(+)-ATPase was drastically above the normal limit. The Mg2(+)-ATPase activity was 3 times higher in the red cell membranes of these patients than in those from normal subjects.
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PMID:An interesting syndrome of hemolytic anemia, degeneration of the liver and diabetes associated with a high red cell Mg-ATPase, detected by 31P NMR spectroscopy. 253 4

Low sodium and potassium adenosine triphosphatase (ATPase) activity has been proposed as a mechanism behind diabetic neuropathy. In this study the platelet ATPase activity and platelet noradrenaline efflux rate were determined in 47 insulin-dependent diabetes mellitus (IDDM) patients and 20 controls. Ulnar motor conduction velocities, tested in a subgroup, were lower in patients than in controls (52.7 +/- 1.3 m s-1 vs. 61.3 +/- 1.4 m s-1; P less than 0.001). Platelet ATPase activity tended to be increased in the patients compared with the controls (29.9 +/- 1.0 x 10(-3) min-1 vs. 26.9 +/- 1.1 x 10(-3) min-1; NS). In ulnar nerve function tested subjects, ATPase activity was higher in patients than in controls (31.2 +/- 1.7 x 10(-3) min-3 vs. 25.9 +/- 1.3 x 10(-3) min-1; P less than 0.01). The platelet noradrenaline efflux rate tended to be higher in patients with lower brake indices, a sign of autonomic neuropathy, than in controls (29.0 +/- 3.0 x 10(-3) min-1 vs. 21.2 +/- 0.9 x 10(-3) min-1; P less than 0.05). The platelet ATPase activity was not decreased in IDDM patients, however, a connection between diabetic autonomic neuropathy and platelet transmittor leakage was indicated.
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PMID:Platelet sodium and potassium ATPase [corrected] activity and noradrenaline efflux rate in relation to autonomic and peripheral nerve function in insulin-dependent diabetic patients. 253 27


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