Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: EC:1.3.5.1 (succinate dehydrogenase)
 8,177 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Riboflavin nutritional status was assessed on the basis of activity coefficients of glutathione reductase in erythrocyte hemolysates of normal and streptozotocin-diabetic rats. Activity coefficient values higher than 1.3 were regarded as evidence of riboflavin deficiency. All diabetic animals were found to be riboflavin-deficient, with activity coefficient values of 1.47-2.11. Treatment of diabetic rats with either insulin or riboflavin returned their activity coefficients to normal. Rats fed a restricted diet had normal activity coefficient values. The erythrocyte glutathione reductase activity was significantly lower in diabetic rats, and the augmentation of enzyme activity in the presence of flavin-adenine dinucleotide (FAD) was 72% compared to 16% in normal rats. Hepatic activities of glutathione reductase and succinate dehydrogenase, both FAD-containing enzymes, were significantly lower in diabetic than in normal rats. Like activity coefficient values, all enzyme activities were normalized after insulin or riboflavin treatments. These data suggest that insulin and riboflavin enhance the synthesis of erythrocyte and hepatic FAD. The results of the present study suggest that experimental diabetes causes riboflavin deficiency, which in turn decreases erythrocyte and hepatic flavoprotein enzyme activities. These changes can be corrected for by either insulin or riboflavin. The pathogenesis of riboflavin deficiency in diabetes mellitus is not clearly understood. The data of the present study provide evidence in addition to the previous findings of an increased prevalence of riboflavin deficiency in genetically diabetic KK mice.
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PMID:Riboflavin nutritional status and flavoprotein enzymes in streptozotocin-diabetic rats. 351 4

Heart mitochondria from chronically diabetic rats ('diabetic mitochondria'), in metabolic State 3, oxidized 3-hydroxybutyrate and acetoacetate at a relatively slow rate, as compared with mitochondria from normal rats ('normal mitochondria'). No significant differences were observed, however, with pyruvate or L-glutamate plus L-malate as substrates. Diabetic mitochondria also showed decreased 3-hydroxybutyrate dehydrogenase and succinyl-CoA: 3-oxoacid CoA-transferase activities, but cytochrome content and NADH-dehydrogenase, succinate dehydrogenase, cytochrome oxidase and acetoacetyl-CoA thiolase activities proved normal. The decrease of 3-hydroxybutyrate dehydrogenase activity was observed in diabetic mitochondria subjected to different disruption procedures, namely freeze-thawing, sonication or hypoosmotic treatment, between pH 7.5 and 8.5, at temperatures in the range 6-36 degrees C, and in the presence of L-cysteine. Determination of the kinetic parameters of the enzyme reaction in diabetic mitochondria revealed diminution of maximal velocity (Vmax) as its outstanding feature. The decrease in 3-hydroxybutyrate dehydrogenase in diabetic mitochondria was a slow-developing effect, which reached full expression 2-3 months after the onset of diabetes; 1 week after onset, no significant difference between enzyme activity in diabetic and normal mitochondria could be established. Insulin administration to chronically diabetic rats for 2 weeks resulted in limited recovery of enzyme activity. G.l.c. analysis of fatty acid composition and measurement of diphenylhexatriene fluorescence anisotropy failed to reveal significant differences between diabetic and normal mitochondria. The Arrhenius-plot characteristics for 3-hydroxybutyrate dehydrogenase in membranes of diabetic and normal mitochondria were similar. It is assumed that the variation of the assayed enzymes in diabetic mitochondria results from a slow adaptation to the metabolic conditions resulting from diabetes, rather than to insulin deficiency itself.
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PMID:Decreased rate of ketone-body oxidation and decreased activity of D-3-hydroxybutyrate dehydrogenase and succinyl-CoA:3-oxo-acid CoA-transferase in heart mitochondria of diabetic rats. 354 9

The contribution of muscle tissue to the increased metabolic efficiency of the obese (fa/fa) Zucker rat at 6 wk of age was examined. In vitro O2 consumption was similar in obese and nonobese soleus and extensor digitorum longus (EDL) muscles, whether the animals were fed ad libitum, fasted, or treated with triiodothyronine. No phenotypic difference in the in vitro O2 consumption was seen when the muscles were preincubated with or without exogenous insulin. Pyruvate kinase, citrate synthase, succinate dehydrogenase, and cytochrome oxidase activities were similar in the soleus and the EDL muscles of both phenotypes. Phosphofructokinase and lactate dehydrogenase activities were higher in the soleus muscles from the obese rats, whereas hexokinase activities were higher in the EDL muscles from the nonobese rats. Mitochondrial and whole muscle homogenate respiration rates were similar in both phenotypes. The soleus and EDL muscles from the obese animals weighed less than those from the nonobese, but empty carcass weights were similar. Taken together these data suggest that muscle mass, muscle O2 consumption, and muscle oxidative capacity are similar in 6-wk-old obese and nonobese rats. Therefore other tissues are probably responsible for the increased metabolic efficiency of the young obese rat.
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PMID:Oxygen consumption and oxidative capacity of muscles from young obese and nonobese Zucker rats. 609 7

The effect of different dosages of streptozotocin (STZ) on selected rat tissue enzyme activities and glycogen concentration were investigated. The rats were administered STZ intravenously at 60 (STZ-60), 80 (STZ-80), 100 (STZ-100), and 150 (STZ-150) mg/kg body weight. They were used 3 weeks postinjection. Mortality prior to kill occurred only in the STZ-100 and STZ-150 rats. All diabetic rats showed reduced growth rate, hyperglycemia, hypoinsulinemia, and hyperlipemia. Phosphofructokinase (PFK) and succinate dehydrogenase (SDH) activities were significantly reduced in the red gastrocnemius muscle of all diabetic rats, and in the white gastrocnemius and soleus of STZ-100 and STZ-150 groups. PFK activity in the heart remained unaltered, but SDH activity was below normal. Liver SDH activity was not affected by insulin deficiency. Glycogen content was markedly increased in the heart and decreased in the liver of all diabetic rats. Glycogen content in the skeletal muscle was similar to the controls, except for the lower values in the soleus of STZ-100 and STZ-150 rats. When STZ-80 and STZ-150 rats were given insulin therapy, the STZ-80 rats showed a greater response to the treatment. Despite similar levels of plasma immunoreactive insulin among all groups of diabetic rats, the STZ-100 and STZ-150 rats had higher mortality, greater loss in body weight, and alterations in enzyme activities and glycogen content in the tissues studied.
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PMID:Dosage effect of streptozotocin on rat tissue enzyme activities and glycogen concentration. 621 44

Succinate dehydrogenase activities in homogenates of rat and ob/ob mouse pancreatic islets were only 13% of the activities in homogenates of liver and were also several times lower than in homogenates of pancreatic acinar tissue. This indicates that the content of mitochondria in pancreatic islet cells is very low. The very low activity of succinate dehydrogenase is in agreement with the low mitochondrial volume in the cytoplasmic ground substance of pancreatic islet cells as observed in morphometric studies. This may represent the poor equipment of pancreatic islet cells with electron transport chains and thus provide a regulatory role for the generation of reducing equivalents and chemical energy for the regulation of insulin secretion. The activities of succinate dehydrogenase in tissue homogenates of pancreatic islets, pancreatic acinar tissue, and liver were significantly inhibited by malonate and diazoxide but not by glucose, mannoheptulose, streptozotocin, or verapamil. Tolbutamide inhibited only pancreatic islet succinate dehydrogenase significantly, providing evidence for a different behavior of pancreatic islet cell mitochondria. Therefore diazoxide and tolbutamide may affect pancreatic islet function through their effects on succinate dehydrogenase activity. The activities of alpha-glycerophosphate dehydrogenase in homogenates of pancreatic islets and liver from rats and ob/ob mice were in the same range, while activities in homogenates of pancreatic acinar tissue were lower. None of the test agents affected alpha-glycerophosphate dehydrogenase activity. Thus the results provide no support for the recent contention that alpha-glycerophosphate dehydrogenase activity may be critical for the regulation of insulin secretion.
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PMID:Characterization of succinate dehydrogenase and alpha-glycerophosphate dehydrogenase in pancreatic islets. 636 Jan 62

Rats were given a daily injection of L-epinephrine, 100 micrograms/100 g body wt, for 6 wk. The hearts of the epinephrine-treated animals were heavier (11.5%), and blood glucose and plasma insulin concentrations were lower than those of control rats. Acute responses to epinephrine were compared in the two groups. An increase in blood glucose and decreases in plasma insulin, liver glycogen, and muscle glycogen occurred in both groups. The magnitude of these responses were similar in the two groups except for the decrease in muscle glycogen, which was smaller in the chronic epinephrine-treatment group. There were no changes in respiratory capacity, citrate synthase or succinate dehydrogenase activities, or in cytochrome c concentration in skeletal muscle in response to 6 wk of epinephrine treatment. These results are compatible with the suggestion that catecholamines may play a role in some of the metabolic and cardiac adaptations to exercise training. However, they argue strongly against the hypothesis that catecholamines are responsible for inducing the increase in muscle mitochondria that occurs in response to exercise training.
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PMID:Adaptive responses of rats to prolonged treatment with epinephrine. 645 52

This study examined how the duration of experimentally induced diabetes affects myocardial metabolism. Both acutely (2-day) and chronically (30-day and 90-day) streptozocin (STZ)-diabetic rats exhibited hyperglycemia and hyperketonemia, while hyperlipemia was evident only in the chronically diabetic rats. The activity of succinate dehydrogenase was lower, whereas that of 3-hydroxyacyl-CoA-dehydrogenase was higher in the hearts of chronically diabetic rats. Although myocardial concentrations of glucose-6-phosphate, glycogen, and triacylglycerols were elevated in diabetes, the patterns of alterations differed between acute and chronic diabetes. The fructose-1,6-diphosphate/fructose-6-phosphate ratio declined progressively after STZ administration, which was not accompanied by a reciprocal increase in citrate levels, although citrate concentrations were elevated. Impaired glucose oxidation was more severe in the freshly isolated heart cells from 30-day than from 2-day diabetic rats. For a given substrate concentration, the oxidation rates of palmitate and 3-hydroxybutyrate were markedly reduced in myocytes from 30-day diabetic rats. However, they were similar to or even higher than the rates found in their control counterparts under conditions that reflected the respective in vivo concentrations of the substrates. Incubating isolated myocytes from 2-day diabetic rats in the presence of insulin only partially restored the impaired glucose oxidation. Insulin administered to the animals 4 h before the experiments restored the impaired glucose oxidation by the cells. Insulin in vitro or single injection in vivo had little or no effect on glucose oxidation in isolated myocytes from 30-day diabetic rats.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:The effects of acute and chronic diabetes on myocardial metabolism in rats. 650 Jan 87

Nine male, insulin-dependent diabetic patients participated in a 16-wk training program consisting of 1 h of jogging, running, ball games, and gymnastics, performed 2-3 times/wk. The training resulted in an 8% increase of maximal oxygen uptake (P less than 0.01). Insulin sensitivity as determined by the insulin clamp technique increased 20% (P less than 0.05). Glycosylated hemoglobin showed no change (10.4 +/- 0.7% versus 11.3 +/- 0.5%), 24-h urinary glucose excretion was not reduced, and home-monitored urine tests were unchanged. The frequency of hypoglycemic attacks did not change during the training period and body weight remained constant. There was a 14% fall in plasma cholesterol (P less than 0.01) and a rise in the proportion of HDL-cholesterol from 24 +/- 2% to 30 +/- 3% (P less than 0.01). Thigh muscle oxidative capacity increased, as indicated by a 24% increase in succinate dehydrogenase activity (P less than 0.05). The number of capillaries/muscle fiber increased 15% (P less than 0.01). However, as the mean muscle fiber cross-sectional area increased to a similar extent (11%, P less than 0.05), capillary density (cap x mm-2) was unchanged. In conclusion, this study demonstrates that physical training in insulin-dependent diabetics results in increased peripheral insulin sensitivity, a rise in muscle mitochondrial enzyme activities, decreased total plasma cholesterol levels, and unchanged blood glucose control. The findings suggest that in the absence of efforts to alter dietary regulation and insulin administration, physical training consisting of 2-3 weekly bouts of moderate exercise may not of itself improve blood glucose control in type I diabetes.
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PMID:Increased peripheral insulin sensitivity and muscle mitochondrial enzymes but unchanged blood glucose control in type I diabetics after physical training. 675 18

In 120 patients with diabetes mellitus the indices of the blood and erythrocytic acid-alkali balance, glycemia level, blood lactate and pyruvate concentrations, the activity of serum malate dehydrogenase and lactate dehydrogenase, as well as of succinate dehydrogenase and alpha-glycerophosphate dehydrogenase in lymphocytic mitochondria were studied. A remarkable difference of the indices examined, depending on the disease severity, duration or compensation state of carbohydrate metabolism, was noted comparatively to those of normal. Insulin therapy and the diet No. 9, combined with hyperbaric oxygenation, was accompanied by a rapid (within 12 to 18 days) compensation of carbohydrate metabolism and good dynamics of all the tests. The results obtained are indicative of a significant improvement of the tissue metabolism both on the glycolysis level and in the cycle of tricarboxylic acids.
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PMID:[Effect of insulin therapy and hyperbaric oxygenation on the enzyme activity of tissue metabolism in diabetes mellitus]. 676 Jan 77

Administration of physiologically low doses of bicarbonate into rats caused an inhibition of oxidative phosphorylation and a transitory decrease in ATP content in liver mitochondria; at the same time, concentrations of malate and glutamate were unaltered and those of pyruvate and phosphoenolpyruvate were decreased. Insulin removed the bicarbonate effect on mitochondrial functions but affected only slightly the distribution of metabolites. Bicarbonate appears to activate pyruvate carboxylase and to inhibit succinate dehydrogenase as well as the operation of tricarboxylic acid cycle due to accumulation of oxaloacetate. The effect of insulin mimics acceleration of decarboxylation reactions in mitochondria.
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PMID:[Effect of bicarbonate and insulin on energy metabolism in the mitochondria of rat liver]. 676 May 41


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