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)

A significant increase of the (Na+ + K+)-activated ATPase was found in mucosal homogenates of rat small intestine under conditions of alloxan and streptozotocin diabetes. From studies with isolated plasma membranes it has been shown that the activity changes were caused by that part of the (Na+ + K+)-activated ATPase only which is localized in the basolateral plasma membranes, whereas the enzyme activity in the brush border region remains unchanged. In connection with the enhanced capacity of ion, nonelectrolyte and water absorption in experimental diabetes, our findings support a concept of intestinal transport mechanism which suggest that the basolateral part of the (Na+ + K+)-activated ATPase is responsible for metabolic energy supply. The luminal part of the enzyme may be involved in regulation of passive Na+ influx.
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PMID:[Increase of (Na+ + K+)-activated ATPase activity of basolateral plasma membranes from intestinal mucosa of diabetic rats]. 630 25

Male Sprague-Dawley rats made diabetic with alloxan (37.5 mg/kg) or streptozotocin (65 mg/kg) were killed after 3-6 weeks of disease; renal tissues were studied for phospholipid content and for fatty acid composition of the phospholipids. No consistent change was noted in total phospholipid content nor in the proportion of various phospholipids in diabetics. However, diabetic animals showed a consistent reduction of arachidonic acid content in phosphatidylcholine (PC) and phosphatidylethanolamine in whole renal cortex, plasma membranes purified from renal cortex, and in isolated glomeruli. Associated with the fall in arachidonic acid was a rise in linoleic acid in the samples studied. Insulin therapy returned the fatty acid profiles to normal. These results are similar to patterns observed in other diabetic tissues and suggest that diabetes is associated with generalized changes in cell membranes. That these structural changes may have functional significance is suggested by demonstrated alterations in the temperature-dependence of adenylate cyclase in renal plasma membranes of diabetic animals. Adenylate cyclase is thought to be intimately associated with PC in plasma membranes, a phospholipid showing significant changes in fatty acid content in diabetes (unsaturation index 165 +/- 2 for normals, 147 +/- 5 for diabetics). Na+,K+-ATPase which is thought to be primarily associated in vivo with phosphatidylinositol (PI), shows no change in apparent energy of activation in diabetes. The fatty acid content of PI is minimally altered in diabetes, and the unsaturation index is unchanged.
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PMID:Changes in renal phospholipid fatty acids in diabetes mellitus: correlation with changes in adenylate cyclase activity. 631 7

Mg-independent Ca-ATPase activity was measured in secretory granules, mitochondria and microsomes from albino mouse islets and in secretory granules from noninbred ob/ob mouse islets. The enzyme existed in a high-affinity (Km for Ca2+ approx. 10(-7) M) and a low-affinity (Km approx. 10(-5) M) form. In all subfractions the high-affinity Ca-ATPase was inhibited by cyclic AMP, caffeine and Na+. Alloxan stimulated the microsomal Ca-ATPase by 25%, but had no effect on Ca-ATPase activity in granules and mitochondria. Glucose and glucose metabolites had no effect on Ca-ATPase in the secretory granule fraction from ob/ob mouse islets, whereas NADH inhibited the enzymes by 35%. The secretory granule Ca-ATPase was also inhibited by pCMBS (43%), chlorpromazin (87%) and ruthenium red (23%). 45Ca uptake was studied in secretory granules isolated from ob/ob mouse islets. The uptake was accelerated by addition of ATP, the maximum effect being found at 1 to 2 mM ATP. Omission of MgCl2 decreased the uptake by 25%. 45Ca uptake was abolished in the presence of pCMBS and chlorpromazine, whereas caffeine had no effect. The importance of Ca-ATPase in 45Ca transport and regulation of insulin release is discussed.
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PMID:Ca-ATPases in pancreatic islets. 645 Jan 52

Thirty rats were treated with methylprednisolone, 30 rats were treated with alloxan, and 30 control rats were treated with saline alone. The levels of fasting serum insulin and blood glucose and of plasma GIP before and after duodenal instillation of glucose or amino acids were measured using an acute rat preparation that enabled multiple blood samplings from the portal vein. Treatment of the rats with methylprednisolone was followed by increased fasting levels of serum insulin, blood glucose, and plasma GIP and by an augmented GIP release in response to duodenal glucose and amino acids as compared with normal controls. Similarly, treatment with alloxan was followed by decreased fasting levels of serum insulin, by increased fasting levels of blood glucose and plasma GIP, and by an increased GIP release in response to duodenal glucose and amino acids. The augmented GIP release in response to duodenal instillation of glucose and amino acids both in methylprednisolone-treated rats and in alloxan-treated rats may be explained by an increased absorption of these nutrients owing to an increased Na+ K+ ATPase activity in the intestinal mucosa of corticosteroid- and alloxan-treated rats. The elevated fasting GIP levels, on the other hand, are difficult to explain.
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PMID:Augmented release of gastric inhibitory polypeptide into the portal vein in response to intraduodenal glucose and amino acids in anesthetized rats treated with methylprednisolone or alloxan. 675 5

Isolated working hearts from diabetic rats have a decreased ability to respond to increasing preload or afterload. The ability of cardiac sarcoplasmic reticulum to transport Ca2+ was examined in diabetic rats. Hearts were obtained from female Wistar rats 120 days or 7 days after the induction of diabetes by a single I.V. injection of either alloxan (65 mg/kg) or streptozotocin (60 mg/kg). At all Ca2+ concentrations tested (0.2-5.0 microM free Ca2+) cardiac sarcoplasmic reticulum from 120-day diabetic rats showed a significant decrease in the rate of ATP-dependent tris-oxalate facilitated Ca2+ transport (62-73% of control). This was accompanied by a decrease in Ca2+ ATPase activity. The levels of long chain acylcarnitines associated with the microsomal sarcoplasmic reticulum preparation from 120-day diabetic rats were significantly higher than those present in sarcoplasmic reticulum from control rats. Palmitylcarnitine, the most abundant of the long chain acylcarnitines, in concentrations less than 7 microM was found to be a potent time-dependent inhibitor of Ca2+ transport in both control and diabetic rat sarcoplasmic reticulum preparations; inhibition of Ca2+ transport was found to be more marked in the control preparations. This would indicate that a degree of inhibition produced by the high endogenous levels of palmitylcarnitine may already be present in the diabetic rat preparations. Cardiac sarcoplasmic reticulum prepared from acutely diabetic rats (7 days) did not show any decrease in Ca2+ transport ability. Levels of long chain acylcarnitines associated with the microsomal preparation enriched in sarcoplasmic reticulum were also unchanged. These findings suggest that the alteration in heart function in 120-day diabetic rats may be due to the buildup of cellular long chain acylcarnitines which inhibit sarcoplasmic reticulum Ca2+ transport. The absence of any change in Ca2+-transport activity or levels of long chain acylcarnitines at 7 days suggests that the alterations seen in 120-day diabetic rats must be of gradual onset.
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PMID:The effect of alloxan- and streptozotocin-induced diabetes on calcium transport in rat cardiac sarcoplasmic reticulum. The possible involvement of long chain acylcarnitines. 688 99

The effect of alloxan-induced diabetes was studied on the activity of Na+, K(+)-ATPase enzyme which is involved in numerous reactions in the metabolism of the synaptic region, Na+, K(+)-ATPase activity was examined in brain areas such as septum, amygdala, thalamus, hippocampus, pons and medulla, and in hypothalamic areas such as medial preoptic and median eminence-arcuate region. In all these areas studied, diabetes caused a decrease in the activity of Na+, K(+)-ATPase, whereas, insulin administration reversed this effect. The present results may indicate the possible involvement of Na+, K(+)-ATPase in neuropathophysiology of diabetes.
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PMID:Effect of alloxan-induced diabetes on Na+, K(+)-ATPase activity from discrete areas of the rat brain. 786 5

The effects of melatonin treatment on cardiac sarcolemmal membrane function were investigated in alloxan-injected rats. Ca(2+)-stimulated adenosine-triphosphatase (ATPase, Ca2+ pump) and Mg(2+)-ATPase activities were depressed significantly in sarcolemmal preparations from alloxan-injected rats compared with levels in control rats. These deficits were observed 2 days after alloxan injection, and they were accompanied by an increase in the density of voltage-sensitive calcium channels, as measured by the [3H]nitrendipine-binding assay. In a dose-dependent manner, treatment of rats with melatonin before alloxan injection significantly overcame the suppression of Ca(2+)-stimulated ATPase in cardiac sarcolemma. Melatonin (1, 5, and 10 mg/kg) overcame Ca(2+)-stimulated ATPase suppression by 13, 35, and 70%, respectively. In addition, melatonin at a dose of 10 mg/kg also prevented the suppression of the Mg(2+)-ATPase by 31%. The number of [3H]nitrendipine-binding sites was not influenced by melatonin. The patent Na(+)-K(+)-ATPase and ouabain-sensitive Na(+)-K(+)-ATPase activities were not different between the control and experimental groups. The results indicate that Ca2+ pump activity is suppressed by acute alloxan treatment, whereas the density of voltage-sensitive calcium channels is increased. These changes may be a consequence of alloxan toxicity to the cardiac sarcolemma. Melatonin, likely because of its antioxidant capacity, exerts a protective effect on heart sarcolemmal membrane function in alloxan-injected rats.
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PMID:Melatonin prevents the suppression of cardiac Ca(2+)-stimulated ATPase activity induced by alloxan. 804 13

The present study reports in vitro inhibition of the activities of enzymes Na(+)-K(+)-ATPase and succinate dehydrogenase by alloxan in brain and liver homogenates of Swiss mice. The Vmax of both the enzymes was reduced in presence of alloxan without any substantial alteration in Km for substrate. Lineweaver Burk's plots showed higher 1/Vmax for alloxan treated samples and convergence of both slopes to intercept-1/Km. The observations pointed to non-competitive type inhibition of the enzymes by alloxan. This may be due to the modification of essential--SH groups present within/adjacent to substrate binding sites by alloxan.
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PMID:In vitro effect of alloxan on Na(+)-K(+)-ATPase and succinate dehydrogenase activities in brain and liver of mice. 822 47

This study addresses the question of whether a decrease in basal Na+ pump [Na(+)-K(+)-adenosinetriphosphatase (ATPase)] activity occurs in the carotid artery of an alloxan-diabetic rabbit and, if so, whether it is associated with altered 86Rb+ uptake and contractile response to ouabain and K(+)-free solution. Ouabain-sensitive 86Rb+ uptake, an index of Na+ pump activity, was diminished approximately 50% in carotid arteries from diabetic rabbits. Concurrent with this, contractions induced by incubating the carotid arteries in a K(+)-free solution (in the absence of phentolamine) were significantly larger in the diabetic group. Readdition of K+ (1 mM) to arteries contracted with the K(+)-free solution caused relaxations that were slower to occur and of lesser magnitude in diabetic than in control rabbits. In contrast to the contractions caused by the K(+)-free medium, contractions caused by incubation with ouabain (1 mM) in the presence of phentolamine were significantly smaller in the diabetic group. Treatment of diabetic rabbits with an aldose reductase inhibitor, zopolrestat, at both high and low doses restored the alterations in vascular reactivity toward normal. The results indicate that the Na+ pump activity is diminished in the carotid artery of diabetic rabbit, and this is associated with abnormal vascular responsiveness and increased polyol pathway flux.
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PMID:Reduced Na(+)-K+ pump activity in diabetic rabbit carotid artery: reversal by aldose reductase inhibition. 823 5

The activities of two enzymes viz: Na(+)-K(+)-ATPase and succinic dehydrogenase (SDH) in brain and liver of alloxan diabetic Swiss albino mice are reported. Alloxan diabetes caused significant decrease in the activity of Na(+)-K(+)-ATPase reflecting reduced glucose transport across the cell membrane. On the contrary, the observed enhanced activity of the enzyme SDH is attributed to increased supply of TCA cycle substrates from accelerated oxidation of fatty acids.
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PMID:Alloxan diabetes in Swiss mice: activity of Na(+)-K(+)-ATPase and succinic dehydrogenase. 855 Jan 24


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