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)

Diabetes produced by injection of alloxan or streptozotocin results in cardiac dysfunction in rats that is associated with lower cardiac contractile protein ATPase activity. The purpose of this investigation was to examine cardiac myosin biochemistry in the Bio-Breeding Worcester (BB/W) rat, a strain in which diabetes occurs spontaneously and closely resembles insulin-dependent diabetes in humans. Hearts from diabetic BB/W rats were studied at 1, 4, and 7 mo after the onset of diabetes and were compared with age-matched BB/W rats that were bred for resistance to diabetes. Calcium-stimulated myosin ATPase activity was significantly decreased after 4 and 7 mo of diabetes, and actin-activated myosin ATPase was significantly depressed at all time points. Differences between hearts from control and diabetic animals increased with the duration of diabetes. Closely associated with reductions in myosin ATPase activity in the diabetes was a shift in the isomyosin content from the normally predominant V1 to the V3 isoenzyme. Thus diabetes that results from genetic causes leads to depressed myosin enzymatic activity in the rat. Furthermore, since previous studies have shown that BB/W diabetic rats do not develop hypothyroidism, the present results support the view that altered thyroid function does not mediate the abnormalities in cardiac contractile proteins in diabetes.
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PMID:Abnormal cardiac biochemistry in spontaneously diabetic Bio-Breeding/Worcester rat. 293 20

One of the leading causes of mortality in diabetics is myocardial disease. In the past few years this subject has generated a significant amount of interest with the result that myocardial problems associated with diabetes are far better understood. Though originally thought to occur as a result of atherosclerosis, various studies have shown that heart disease can occur in the absence of atherosclerosis, suggesting a diabetic cardiomyopathy. Using diabetic animals, it has been possible to characterize diabetes-induced myocardial abnormalities. Diabetic rat hearts do not respond to conditions of high stress as well as controls. The functional depression is accompanied by altered cardiac enzyme systems. A decrease in myosin ATPase activity which appears to be a result of diabetes-induced hypothyroidism is seen. Also, a depression of sarcoplasmic reticular calcium ATPase, along with a depression of calcium uptake by the SR, is seen in diabetic rat hearts. Na+, K+ ATPase activity has also been shown to be depressed and the depression appears to correlate with depressed atrial contractility. High levels of circulating fats in diabetics may alter the integrity of membranes leading to altered enzyme activities. Insulin treatment has been relatively successful at reversing or preventing myocardial changes in the diabetic rat. Other treatments that have been studied include thyroid hormone treatment, since the depression of myosin ATPase can be corrected by such treatment; and carnitine treatment, as the elevation of long chain acyl carnitines (LCAC) and the resulting depression of calcium uptake in the SR can be so normalized. These treatments have not been successful at normalizing cardiac function. A combination of the two treatments normalized function only partially, suggesting that factors besides myosin ATPase and SR calcium uptake are involved. Other treatments that have been tried include vanadate, methyl palmoxirate, and choline and methionine. Vanadate treatment has proved to be encouraging in that it normalizes both function and hyperglycemia. Methyl palmoxirate, a fatty acid analog, normalized only the elevation of LCAC but did not affect function. Methionine and choline were only partially successful in preventing the functional alterations of diabetic rat hearts. The purpose of the present article is to review our understanding of diabetes-induced myocardial problems and their possible causes. Findings from our laboratory and others are described in which attempts have been made to normalize cardiac function.
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PMID:Diabetes-induced abnormalities in the myocardium. 293 41

Hyperthyroidism, and alternatively hypothyroidism, were induced in spontaneously hypertensive broad-breasted white turkeys (BBWT) to see if these conditions influenced the pattern of Ca++-activated ATPase activity and isomyosin synthesis in the cardiac muscle. Nine animals were given thyroxine 500 micrograms p.o., 9 animals propylthiouracil 150 mg p.o., 6 animals placebo p.o. All animals were treated daily from the 27th to the 33rd week of age. The ventricular myosin Ca++-activated ATPase activity was assayed in all the animals; aortic smooth-muscle myosin light chains were analysed by mono- and two-dimensional gel electrophoresis, and myosin heavy chains by proteolytic mapping. No significant difference was found between the three groups in the ventricular myosin Ca++-activated ATPase activity. As for aortic myosin, a similar peptide map of heavy chains but a different phosphorylative level of the LC1 light chain was found in the three groups of animals. It is concluded that a thyroid-hormone modulation of contractile proteins in vascular smooth muscle, but not in cardiac muscle, exists in the broad-breasted white turkey.
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PMID:Ventricular and aortic myosin in hypothyroid and hyperthyroid broad breasted white turkeys. 294 72

The effects of amiodarone on heart weight, production of 14C-CO2 from labelled glucose, myosin ATPase activity, and myosin isoenzyme patterns were determined by comparing control and amiodarone-treated male Wistar rats. Since it has been suggested that amiodarone may interfere with thyroid hormone action on the heart, similar experiments were also carried out in hypothyroid and amiodarone-plus-triiodothyronine(T3)-treated rats, and the data were compared to those obtained in amiodarone-treated rats. Amiodarone treatment for 6 weeks resulted in lower heart weight, decreased atrial production of 14C-CO2 from labelled glucose, decreased myosin Ca-ATPase activity, and preferential synthesis of V3 isomyosin. These effects were similar to those observed in hypothyroid rats but were lesser in magnitude. T3 treatment of amiodarone-treated rats reversed all the changes induced by amiodarone. Serum thyroxine (T4) was higher in amiodarone-treated than in control rats, while serum T3 was similar. Serum T3 was higher in the amiodarone-plus-T3 than in the amiodarone-treated group. These results show that 1) amiodarone-induced changes resemble hypothyroidism with respect to cardiac myosin expression and atrial CO2 production, 2) amiodarone causes hypothyroid-like changes despite normal serum T3 and increased serum T4, and 3) T3 reverses the effects of amiodarone. These data support the hypothesis that amiodarone inhibits the action of thyroid hormone on the heart.
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PMID:Effect of amiodarone on rat heart myosin isoenzymes. 295 16

Changes both in the ATPase myofibrillar profile and in the electrophoretic pattern of myosin isoforms were examined in the mouse dorsal skeletal muscle (longissimus) during postnatal development. In the newborn, only type II C and a few type I fibers were present; differentiation into type II A and II B fibers took place during the 3 weeks following birth. During the same period, a transition from three neonatal isomyosins to four adult isoforms was observed. The two phenomena were related to a marked increase in the serum thyroid hormones levels. Hypothyroidism and hyperthyroidism experiments were performed. Hypothyroidism produced by propylthiouracil treatment of pregnant females and thiourea injections of the litters was shown to induce a complete inhibition of postnatal muscular differentiation. Hyperthyroidism produced by triiodothyronine treatment of the neonate mice significantly accelerated the myosin transition and the switch in the myofibrillar pattern. Our results suggest a primordial role for thyroid hormones in directly regulating the appearance of myosin and fiber adult types and in modulating directly or indirectly the disappearance of the neonatal types.
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PMID:Regulation by thyroid hormones of terminal differentiation in the skeletal dorsal muscle. I. Neonate mouse. 295 61

The effects of hypothyroidism on structural and functional properties of the actomyosin-ATPase complex of rat fast-twitch gastrocnemius muscle were examined and related to energetic and mechanical parameters. Hypothyroidism resulted in the appearance of a small band of the myosin heavy chain subunit of the slow form (MHCs) 8% of total MHC) which was absent in the euthyroid group. This observation corresponded with lower activities of myofibrillar ATPase (-14%) and Ca-activated myosin ATPase (-9%) in the hypothyroid group, although these changes were not significant. No effect of hypothyroidism on the Ca2+-sensitivity of the myofibrillar-ATPase activity was observed and tetanic force was not changed. Twitch force, however, was significantly increased by hypothyroidism. The degree of myosin P-light chain phosphorylation (percentage of total amount of P-light chain) determined after 5 and 10 s of tetanic stimulation (130 Hz, 35 degrees C), respectively, proved to be significantly lower in the hypothyroid group (5 s: 57%; 10 s: 61%) vs the euthyroid group (5 s: 79%; 10 s: 82%). There was no difference in P-light chain phosphorylation at rest between eu- and hypothyroids. The results suggest that a decreased actomyosin-ATPase activity can only in part contribute to the 30% lower energy turnover during force development found for fast-twitch skeletal muscle of hypothyroid rats. Moreover, the increase in twitch force by hypothyroidism cannot be explained by a change in myosin P-light chain phosphorylation. Isometric twitch tension potentiation after a 2 s tetanus and during low-frequency repetitive stimulation was reduced (up to -60%) in muscles of hypothyroid rats, which may well be related to the lower extent of P-light chain phosphorylation in hypothyroids.
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PMID:Structural and functional aspects of the actomyosin complex from fast-twitch muscle of euthyroid and hypothyroid rats. 296 Sep 52

Cardiac muscle function and biochemistry were examined after long-term amiodarone administration in the rabbit (20 mg/kg/day for 28 days). Isolated cardiac muscle preparations were obtained from control and amiodarone-treated rabbits, and were studied in vitro. Amiodarone treatment did not alter the magnitude of force development in isolated atrial and papillary muscle preparations, but depressed the rate of force development (dF/dt). The muscle preparations responded similarly to inotropic and chronotropic stimulation with isoproterenol, histamine, and tyramine, although the intrinsic rate of right atrial preparations from the drug-treated animals was reduced. Na+-K+ ATPase activity in crude ventricular homogenates was increased in the amiodarone-treated group. Mitochondrial respiratory function in amiodarone-treated left ventricular tissue was depressed for glutamate, malate, and glutamate + malate. The reduction in respiratory function occurred without uncoupling oxidative phosphorylation or altering respiratory function for succinate. The pharmacologic effects of amiodarone observed in the present study were not observed with the simultaneous administration of triiodothyronine (5 micrograms/day). No difference in ATP-dependent calcium uptake or in calcium-dependent ATPase activity were observed in sarcoplasmic reticulum preparations from control, amiodarone, and amiodarone + T3 groups. The pharmacologic effects of amiodarone in rabbit hearts resemble those previously reported with hypothyroidism and are not observed after triiodothyronine administration.
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PMID:Changes in cardiac muscle function and biochemistry produced by long-term amiodarone and amiodarone + triiodothyronine administration in the rabbit. 296 Sep 89

Studies were conducted to analyze the effect of the thyroid hormone on ventricular myosin during ontogenesis of mice, rats and rabbits. Hypothyroidism was induced in mice and rats by administering propylthiouracyl in drinking water. Rabbits were made hyperthyroid by chronic administration of thyroxine. The change in the thyroid state of rats and rabbits influenced young and adult animals differently depending on whether V1 or V3 was the major ventricular isomyosin form present. Measurements of Ca2+-ATPase activity of myosins from young and old control animals and from animals with changed thyroid state showed that hypothyroidism in rats is associated with a greater decrease of myosin ATPase in young rats which contain V1 isomyosin only, when compared with old rats which contain a preponderance of V3 isomyosin and less of the V1 form. In rabbits, ATPase activity of ventricular myosin was more elevated after thyroxine administration in adult rabbits, which contain V3 isomyosin only, than in young rabbits in which myosin consists of V1 and V3 isomyosins. Ventricular myosins of young and adult mice did not differ in their ATPase activity and the treatment of mice with propylthiouracyl had only slight effect on myosin ATPase. It can be concluded based on these results that the hypothesis concerning hypothyroidism inducing transformation of V1 into V3 isomyosin does not hold generally.
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PMID:Ventricular myosin from young and adult animals with respect to the thyroid state. 296 48

Thyroid hormone is known to modulate cell membrane sodium/potassium adenosine triphosphatase (Na/K-ATPase). To determine whether the activity of this enzyme differed in patients with nonthyroidal illness with low levels of circulating thyroid hormones and patients with documented clinical hypothyroidism, we measured Na/K-ATPase activity in red blood cells from patients with hypo- and hyperthyroidism, patients with nonthyroid disease with and without reduced circulating levels of thyroid hormone, and normal subjects. We also assessed whether the activity of this enzyme reflects decreased thyroid hormone action at the cellular level in patients with nonthyroidal illness. Hyperthyroidism was associated with decreased and hypothyroidism with increased erythrocyte Na/K-ATPase activity [142 +/- 24 (+/- SE) and 371 +/- 37 nmol Pi/mg X h; P less than 0.05 and P less than 0.01 compared to normal]. Enzyme activity in cells from patients with nonthyroidal illness and low levels of circulating T3 was significantly higher than that in cells from normal subjects (289 +/- 11 vs. 223 +/- 16 nmol Pi/mg X h; P less than 0.01), but was not significantly different from that in cells from hypothyroid patients. Red cell Na/K-ATPase activity in patients with nonthyroidal illness and normal thyroid function tests (185 +/- 38 nmol Pi/mg X h was indistinguishable from normal values. These data confirm that hyperthyroid patients have decreased red cell Na/K-ATPase activity and provide direct evidence that erythrocyte ATPase activity is increased in hypothyroid patients. The change in enzyme activity in patients with nonthyroidal illness and decreased circulating T3 levels was comparable to that in hypothyroidism. These results suggest that since red cell Na/K-ATPase activity does not distinguish between ill patients with low thyroid function tests and those with hypothyroidism, tissue hypothyroidism may exist in the former group of patients.
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PMID:Erythrocyte sodium/potassium adenosine triphosphatase in thyroid disease and nonthyroidal illness. 298 90

The effect of thyroid status on the postnatal development of the two molecular forms of Na+,K+-ATPase, distinguished kinetically on the basis of their ouabain sensitivity, was examined in rat brain. Hypothyroidism induced by PTU from day 1 postnatally significantly reduced the Na+,K+-ATPase activity in cerebellum (22-30 days) but not forebrain, whereas hyperthyroidism (T4 treatment from day 1) had no effect. The hypothyroidism-induced reduction in cerebellum was reflected by a 20-45% reduction in the activity of the alpha(+) form of Na+,K+-ATPase (high ouabain affinity) against control brains compared to a 60-70% reduction in the activity of the alpha form (low ouabain affinity). These results show that neonatally induced hypothyroidism leads to a selectively greater impairment of the ontogenesis of the activity of cerebellar alpha form of Na+,K+-ATPase. This may possibly reflect a retarded development of a selective cerebellar cell population containing predominantly the alpha form of the enzyme.
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PMID:Effect of thyroid status on the development of the different molecular forms of Na+,K+-ATPase in rat brain. 298 30


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