Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: EC:1.9.3.1 (cytochrome oxidase)
 8,822 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In the paper the author is concerned with the histochemical estimation of the metabolic adaptation of the heart muscle of albino rats during an early experimental alloxan diabetes. It has been found that the state of experimentally produced insulin deficiency directly influences metabolism of the heart muscle and the changes observed in the histochemical reactions prove this. An increase in the intensity of histochemical reactions concerns the PAS-positive reaction and the reactions to the NADH and NADPH tetrazole reductase activities. Alkaline phosphatase shows a decrease in the enzymatic activity, whose nature is transitional and reversible with regard to cytochrome oxidase and ATP-ase. The histochemical picture of metabolic changes depends on the duration time of experimental diabetes.
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PMID:Some histochemical observations on the myocardial metabolism in experimental conditions. Part I. 21 83

The effects of norepinephrine and insulin on thermogenesis were investigated in adipocytes isolated from brown adipose tissue (BAT) of obese non-diabetic LA/N-cp rats (obese LA), obese diabetic SHR/N-cp rats (obese SHR), and their corresponding lean controls. The maximal calorigenic response (Vmax) and the sensitivity [50% effective concentration (EC50)] to norepinephrine (1 microM) were markedly reduced in brown adipocytes from obese SHR rats compared with their lean controls (3- to 4-fold decrease in the Vmax and 50% increase in the EC50 value). In the same cells, there was a similar decrease in the respiratory response to dibutyryl adenosine 3',5'-cyclic monophosphate, indicating the presence of a major postreceptor defect. Remarkably, total BAT cytochrome oxidase activity (an index of cellular mitochondrial content) was also diminished three to four times in obese SHR rats, suggesting that a reduced BAT mitochondrial content is responsible for the decreased thermogenesis. Ultrastructural studies revealed that the cytoplasm of brown adipocytes from obese SHR rats contained a large lipid droplet, numerous tiny droplets, and few atypical mitochondria with loosely packed cristae. Adipocytes from obese SHR rats were also characterized by a significant resistance to the antithermogenic effect of insulin but not to that of the nonmetabolizable adenosine analogue N6-phenylisopropyl adenosine. In contrast, all the above biochemical parameters were normal in obese LA rats. These results demonstrate that the marked insulin resistance in BAT of obese SHR rats is associated with a decreased responsiveness and sensitivity to norepinephrine, indicating the presence of receptor and postreceptor defects. It is suggested that insulin resistance and/or diabetes in SHR/N-cp rats lead to a decreased mitochondriogenesis in BAT, which results in a reduced thermogenic capacity, thereby contributing to the development of obesity.
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PMID:Major thermogenic defect associated with insulin resistance in brown adipose tissue of obese diabetic SHR/N-cp rats. 165 55

We previously reported that the decreased sensitivity of brown adipose tissue (BAT) from obese Zucker rats to the calorigenic effects of norepinephrine is associated with a marked resistance to insulin, and we suggested that this defect may explain, at least in part, the increased energy gain efficiency of fa/fa rats. To test whether insulin resistance and/or diabetes leads to a reduced BAT thermogenesis in other genetic models of obesity, we compared BAT metabolic properties of obese Zucker rats with that of obese-nondiabetic LA/N-cp and obese-diabetic SHR/N-cp rats. It was found that the responsiveness and sensitivity of isolated brown adipocytes to the calorigenic effects of norepinephrine (10-100 mM) were markedly reduced in SHR/N-cp rats as compared to their lean controls (the Vmax was decreased by 3-4 times and the EC50 value was doubled). In the same cells, there was a similar decrease in the respiratory effects of dibutyryl cAMP (DBcAMP), revealing the presence of a major post-receptor defect. Remarkably, total cytochrome oxidase activity (an index of cell mitochondrial content) was also decreased by 3-4 times in SHR/N-cp rats, suggesting that a reduced BAT mitochondrial content is responsible for the defective thermogenesis. Similarly to Zucker rats, adipocytes isolated from SHR/N-cp rats were resistant to the metabolic effects of insulin (glucose transport and antithermogenesis). Cells from obese Zucker rats were also desensitized to the metabolic effects of norepinephrine and insulin but their thermogenic capacity was not reduced. In contrast, all the above parameters were normal in obese-nondiabetic LA/N-cp rats.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Mechanism linking insulin resistance to defective thermogenesis in brown adipose tissue of obese diabetic SHR/N-cp rats. 166 83

1. Forty-eight pigs weaned at 3 weeks old and acclimated to the experimental temperatures for 2 weeks before the start of the experiment, were fed ad lib and used between 9 and 33 kg live weight to determine the effects of warm exposure (31.5 vs 18.5 degrees C) on adipose tissue and muscle metabolism. 2. Warm exposure induced a decline in the lipid content (P less than 0.01) of backfat whereas degree of saturation (P less than 0.05) and adipocytes size were increased (P less than 0.05). 3. At 31.5 degrees C, as compared to 18.5 degrees C, activities of malic enzyme and glucose-6-phosphate dehydrogenase were depressed by an average 33% in backfat (P less than 0.01) and 23% in leaf fat (P less than 0.05) while lipoprotein-lipase activity was stimulated by 60% (P less than 0.01) in leaf fat. 4. In warm conditions, the activities of the enzymes indicative of oxidative and glycolytic metabolism in muscle, i.e. lactate dehydrogenase, beta-hydroxyacyl coenzyme-A dehydrogenase, citrate synthase and cytochrome oxidase, were reduced in the longissimus dorsi muscle (P less than 0.05) and to a lesser extent in the trapezius muscle. 5. At 31.5 degrees C, pigs exhibit lower average plasma levels of insulin, T3 and T4 than those maintained at 18.5 degrees C.
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PMID:Effects of warm exposure on adipose tissue and muscle metabolism in growing pigs. 168 95

Ginseng polysaccharides (GH1) 50-200 mg/kg ip or sc reduced blood glucose and liver glycogen of mice. Adrenalectomy did not affect this action. GH1 increased the content of pyruvic acid, but decreased the content of lactic acid by weakening the activity of lactate dehydrogenase. GH1 accelerated oxidative-phosphorylation of carbohydrate since the activities of succinate dehydrogenase (SDH) and cytochrome oxidase (CCO) were obviously stimulated. Besides the promotion of the activity of SDH in human embryonic lung fibroblasts (HELF), GH1 decreased the content of polysaccharides in HELF of the 24th age generation, but increased that of the 40th age generation. On the other hand, GH1 stimulated the release of insulin. It is suggested that the reduction of blood glucose and liver glycogen induced by GH1 be primarily due to the increase of carbohydrate utilization and the decrease of glycogenesis.
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PMID:[Effects of ginseng polysaccharides on reducing blood glucose and liver glycogen]. 196 54

The role of insulin in the regulation of the thermogenic activity and capacity (uncoupling protein content) of brown adipose tissue (BAT) has been investigated using mice made diabetic with streptozotocin and then subsequently infused with different doses of insulin. After 12 days of diabetes, the animals received either 0, 8, 16, or 32 units of insulin.kg body wt-1.day-1 delivered by osmotic minipumps implanted subcutaneously for 12 days. After 12 days of diabetes, body weight, interscapular BAT, and epididymal white adipose tissue weights were each reduced. In BAT, significant decreases (P less than 0.05) in the mitochondrial protein content (63%), cytochrome oxidase activity (79%), mitochondrial GDP binding (51%), and the specific mitochondrial concentration and total tissue content of uncoupling protein (71 and 89%, respectively) were obtained, indicating that the thermogenic activity and capacity of the tissue were reduced in diabetes. The infusion of insulin at a dose of 8 units.kg-1.day-1 normalized mitochondrial GDP binding and doubled the concentration of uncoupling protein. Body weight, epididymal white adipose tissue weight, and the mitochondrial protein content of BAT were restored with 16 units of insulin.kg-1.day-1. Higher doses of insulin did not further increase the specific mitochondrial concentration of uncoupling protein, but the mitochondrial content (and thereby the total uncoupling protein content) of BAT was increased and blood glucose normalized. There was a significant correlation between the dose of insulin replacement and several of the parameters measured in BAT: mitochondrial protein content (r = 0.68, P less than 0.001), cytochrome oxidase activity (r = 0.54, P less than 0.001), and total uncoupling protein content (r = 0.68, P less than 0.001).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Regulation of the level of uncoupling protein in brown adipose tissue by insulin. 213 90

The effects of insulin and norepinephrine on oxygen consumption, lipolysis, and glucose transport were investigated in adipocytes isolated from brown adipose tissue (BAT) of adult (4-5 mo) lean (Fa/?) and obese (fa/fa) Zucker rats. Total BAT protein content and cytochrome oxidase activity were similar in both phenotypes, suggesting that obese rats have a normal mitochondrial content. Light and electron micrographs revealed that brown adipocytes from obese rats contained very large multilocular triglyceride droplets, but their mitochondrial ultrastructure was normal. Norepinephrine, when added in excess (1 microM), stimulated brown adipocyte respiration 8-10 times above basal levels both in lean and obese animals. However, dose-response experiments disclosed that the 50% effective concentration (EC50) was significantly higher in cells isolated from obese rats compared with lean ones (EC50 115 vs. 43 nM, P less than 0.05). The lipolytic sensitivity to norepinephrine was also reduced in adipocytes isolated from obese animals (EC50 83 vs. 12 nM, P less than 0.05). Addition of dibutyryl adenosine 3',5'-cyclic monophosphate to respiring obese rat brown adipocytes restored to normal the defective response to norepinephrine, suggesting that the reduction in catecholamine sensitivity resulted from a deactivation of the receptor-adenylate cyclase complex. On the other hand, the antilipolytic and antithermogenic actions of physiological concentrations of insulin were significantly reduced in obese BAT cells. The sensitivity and responsiveness of obese rat brown adipocytes for insulin-stimulated glucose transport were also markedly decreased (EC50 1 vs. 0.3 nM, P less than 0.05; maximal velocity 3-fold vs. 7-fold).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Defective metabolic effects of norepinephrine and insulin in obese Zucker rat brown adipose tissue. 215 35

1. Sprague-Dawley rats were injected for 16 d with long-acting insulin, and energy balance was calculated using the comparative carcass technique. Two experiments were carried out with females (starting weights 150 and 90 g respectively), and one with males (starting weight 150 g). In a fourth experiment, cytochrome c oxidase (EC 1.9.3.1) activity was measured as an indicator of the capacity for substrate oxidation. 2. Insulin increased weight gain by up to 57% (P less than 0.01 for all studies). Metabolizable energy intake (kJ/d) was also consistently higher in the treated groups, by up to 34% (P less than 0.01 for all studies). The excess weight gained by the insulin-treated rats was predominantly due to fat deposition. 3. Energy expenditure, calculated as the difference between metabolizable intake and carcass energy gain, was expressed on a whole-body basis, or relative to either metabolic body size (kg body-weight0.75) or fat-free mass. Insulin consistently raised energy expenditure, regardless of the method of expression, but this change reached statistical significance in only two of the nine comparisons. 4. Cytochrome c oxidase activity was not affected by insulin treatment in either interscapular brown adipose tissue or gastrocnemius muscle. In liver, total enzyme activity (U/tissue) was increased from 2928 (SE 162) in the controls to 3940 (SE 294) in the treated group (P less than 0.02), but specific activity (U/mg protein) was unchanged. 5. It is concluded that, despite causing substantial hyperphagia, insulin treatment only slightly increases energy expenditure in rats. The costs of increased tissue deposition may account for this change.
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PMID:Energy balance in rats given chronic hormone treatment. 1. Effects of long-acting insulin. 254 25

Oxygen consumption and 3H-guanosine diphosphate (GDP) binding were determined in brown adipocytes and mitochondria from 28-day gestation fetuses of alloxan-diabetic rabbit does and saline-injected controls. Maternal diabetes was classified as severe or mild determined by whether maternal blood glucose values were greater or less than 200 mg/dL, respectively, at death. Basal oxygen consumption and adipocyte diameters did not vary among groups. A significant reduction in maximal norepinephrine (NE) stimulated O2 consumption by fetal brown adipose tissue (BAT) cells was seen in offspring of severely diabetic pregnancies when compared with control values (248 +/- 53 +/- v482 +/- 32 microL O2/10(6) cells/h; P less than .005). In contrast, a significant increase in maximal NE-stimulated O2 consumption by fetal BAT cells occurred in offspring of mild diabetic pregnancies (807 +/- 60, P less than .001 v controls). A highly significant inverse correlation between serum glucose levels and maximal O2 consumption by fetal BAT was observed in fetuses from mild and severe diabetic pregnancies (r = -.98, P less than .005), and there was no correlation between these two parameters in offspring of normal pregnancies. A significant inverse correlation was observed between maximal O2 consumption by fetal BAT cells and serum insulin levels in offspring of both control and diabetic pregnancy (r = -.74; P less than .02). Tissue cytochrome oxidase activity was lower in offspring of severely affected diabetic does, indicating a reduction in BAT mitochondrial content compared with controls. BAT mitochondria from fetuses of severely diabetic does exhibited reduced 3H-GDP capacity, which was 2.5-fold lower than controls.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Oxygen consumption and guanosine diphosphate binding by fetal brown adipose tissue in diabetic pregnancy. 254 31

The role of insulin in norepinephrine turnover (NE) and thermogenesis in brown adipose tissue (BAT) after acute cold-exposure was studied using streptozocin (STZ)-induced diabetic rats. NE turnover was estimated by the NE synthesis inhibition technique with alpha-methyl-p-tyrosine. BAT thermogenesis was estimated by measuring mitochondrial guanosine-5'-diphosphate (GDP), cytochrome oxidase activity and mitochondrial oxygen consumption in BAT at an ambient temperature of 22 degrees C and during a six-hour cold-exposure at 4 degrees C. In insulin-deficient diabetic rats, the NE turnover, mitochondrial GDP binding, cytochrome oxidase activity and mitochondrial oxygen consumption in BAT at 22 degrees C were significantly reduced, compared with those of control rats. Treatment of STZ-induced diabetic rats with insulin prevented a decrease in NE turnover and BAT thermogenesis. Acute cold-exposure increased the NE turnover of BAT in insulin-deficient diabetic rats. The BAT thermogenic response to acute cold-exposure, however, did not occur in insulin-deficient diabetic rats. These results suggest that insulin is not essential in potentiating NE turnover in BAT after acute cold-exposure, but is required for cold-induced thermogenesis.
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PMID:The role of insulin in norepinephrine turnover and thermogenesis in brown adipose tissue after acute cold-exposure. 255 47


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