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)

Brown adipose tissue (BAT) thermogenic activity has been measured in lactating rats on day 11 post-partum. In order to assess the response of this tissue to different rates of milk production, litter sizes were adjusted to give 2, 4, 8 or 12 pups/dam. In all lactating animals, BAT mass and protein content were markedly reduced, but thermogenic activity was only fully suppressed in dams nursing large litters. In those with 4 pups, guanosine diphosphate-binding activity (expressed as pmol GDP bound/mg mitochondrial protein) was lower than that of virgin control rats, but remained well above values obtained from control animals acclimated at thermoneutrality. Other estimates of BAT thermogenesis, cytochrome oxidase activity and noradrenaline-stimulated increase in oxygen consumption supported the inverse relationship between litter size and BAT function. Possible control mechanisms for the observed changes in BAT activity in lactating animals are discussed.
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PMID:Brown adipose tissue metabolism in lactating rats: the effect of litter size. 653 77

The effects of feeding high fat diets on thermogenesis in brown adipose tissue has been investigated in cold-acclimated mice. Two high fat diets of differing fatty acid composition were used, one of which was based on corn oil and the other on beef tallow. After 3 weeks of feeding the diets there was little difference in the weight, protein content and cytochrome oxidase activity of brown adipose tissue (interscapular plus subscapular) of mice fed the high fat diets from those given the low fat stock diet. However, the mice fed the high fat diets showed marked increases in mitochondrial GDP binding and in mitochondrial respiration, consistent with an augmentation in the activity of the proton conductance pathway. This increase in thermogenesis in brown adipose tissue mitochondria occurred without any elevation in digestible energy intake, and is therefore not a response to overfeeding. It is concluded that the activity of the proton conductance pathway in brown adipose tissue of cold-acclimated mice can be modulated by the level of dietary triglyceride independently of energy intake. We suggest that the effect of high fat diets on thermogenesis in brown adipose tissue may relate to the suppressive effects of dietary lipid on fatty acid synthesis in the tissue.
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PMID:Effect of high fat diets on the thermogenic activity of brown adipose tissue in cold-acclimated mice. 672 79

The properties and activity of brown adipose tissue have been investigated in suckling, pre-obese, ob/ob mice in order to determine whether decreased thermogenesis in the tissue precedes the development of obesity in this mutant. At 14 days of age there was no difference between the ob/ob and normal animals in the total amount of interscapular brown adipose tissue, and the DNA content, protein content, and cytochrome oxidase activity of the tissue were similar in the two groups of mice. Respiration rates of brown adipose tissue mitochondria in the presence of albumin were, however, greater in the normal than the ob/ob animals, although after the addition of GDP to recouple the mitochondria there was no difference between the two groups. The mitochondrial membrane potential, measured with [3H]methyltriphenylphosphonium, was less affected by exogenous GDP in ob/ob mice than in normal animals. GDP binding to brown adipose tissue mitochondria, an index of the proton conductance pathway, was much greater in normal than in ob/ob mice at both 10 and 14 days of age; the decreased GDP binding in the mutant animals was found to result from a reduction in the number of binding sites. It is concluded that brown adipose tissue mitochondria of pre-obese ob/ob mice are more tightly coupled than those of normal siblings, and that the activity of the 'thermogenic' proton conductance pathway is lower in the mutant animals. A decrease in thermogenesis in brown adipose tissue is therefore an early event in the development of the ob/ob mouse and precedes the appearance of obesity.
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PMID:Studies on the activity of brown adipose tissue in suckling, pre-obese, ob/ob mice. 709 44

In this study, oxygen consumption and H(2)O(2) release rate by succinate or pyruvate/malate supplemented mitochondria isolated from skeletal muscle of trained and untrained rats were investigated. The overall mitochondrial antioxidant capacity and the effect of preincubation of mitochondria with GDP, an inhibitor of uncoupling proteins UCP1 and UCP2, on both succinate-supported H(2)O(2) release and membrane potential were also determined. The results indicate that training does not affect mitochondrial oxygen consumption with both complex-I- and complex II-linked substrates. Succinate-supported H(2)O(2) release was lower in trained than in untrained rats both in State 4 and State 3. Even the antimycin A-stimulated release was lower in trained rats. When pyruvate/malate were used as substrates, H(2)O(2) release rate was lower in trained rats only in the presence of antimycin A. The increase of mitochondrial protein content (determined by the ratio between cytochrome oxidase activities in homogenates and mitochondria) in trained muscle was such that the succinate-supported H(2)O(2) release per g of tissue was not significantly different in trained and untrained rats, while that supported by pyruvate/malate was higher in trained than in untrained animals. The lack of training-induced changes in overall antioxidant capacity of mitochondria indicates that the decrease in mitochondrial H(2)O(2) release cannot be attributed to a greater capacity of mitochondria to scavenge the reactive oxygen intermediates derived from univalent O(2) reduction by respiratory chain components. In contrast, the above decrease seems to depend on the drop induced by training in mitochondrial membrane potential. These training effects are not due to an increased level of mitochondrial uncoupling protein, because in the presence of GDP the increase in both membrane potential and H(2)O(2) release was greater in untrained than in trained rats.
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PMID:Effect of training on H(2)O(2) release by mitochondria from rat skeletal muscle. 1060 Jan 70

In an effort to better characterize uncoupling protein-3 (UCP3) function in skeletal muscle, we assessed basal UCP3 protein content in rat intermyofibrillar (IMF) and subsarcolemmal (SS) mitochondrial subfractions in conjunction with measurements of state 4 respiration. UCP3 content was 1.3-fold (P < 0.05) greater in IMF compared with SS mitochondria. State 4 respiration was 2.6-fold greater (P < 0.05) in the IMF subfraction than in SS mitochondria. GDP attenuated state 4 respiration by approximately 40% (P < 0.05) in both subfractions. The UCP3 activator oleic acid (OA) significantly increased state 4 respiration in IMF mitochondria only. We used chronic electrical stimulation (3 h/day for 7 days) to investigate the relationship between changes in UCP3 protein expression and alterations in state 4 respiration during contractile activity-induced mitochondrial biogenesis. UCP3 content was increased by 1.9- and 2.3-fold in IMF and SS mitochondria, respectively, which exceeded the concurrent 40% (P < 0.05) increase in cytochrome-c oxidase activity. Chronic contractile activity increased state 4 respiration by 1.4-fold (P < 0.05) in IMF mitochondria, but no effect was observed in the SS subfraction. The uncoupling function of UCP3 accounted for 50-57% of the OA-induced increase in state 4 respiration in IMF mitochondria, which was independent of the induced twofold difference in UCP3 content due to chronic contractile activity. Thus modifications in UCP3 function are more important than changes in UCP3 expression in modifying state 4 respiration. This effect is evident in IMF but not SS mitochondria. We conclude that UCP3 at physiological concentrations accounts for a significant portion of state 4 respiration in both IMF and SS mitochondria, with the contribution being greater in the IMF subfraction. In addition, the contradiction between human and rat training studies with respect to UCP3 protein expression may partly be explained by the greater than twofold difference in mitochondrial UCP3 content between rat and human skeletal muscle.
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PMID:Role of UCP3 in state 4 respiration during contractile activity-induced mitochondrial biogenesis. 1514 19


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