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:1.3.5.1 (succinate dehydrogenase)
8,177 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Rat brown adipocytes were incubated for 24 h with or without norepinephrine (NE) in Dulbecco's modified Eagle's medium with albumin, calf serum, and antibiotics. Brown fat cells were viable as defined by unchanged cell morphology, ATP content, or basal and NE-stimulated respiration. However, a 24-h exposure to NE led to a decline in NE-stimulated respiration that was not due to loss of thermogenic capacity. Brown fat cells incubated with or without NE had similar protein, succinate dehydrogenase, and uncoupling protein (UCP) content. These results differ from those observed after food deprivation in rats where loss of mitochondrial proteins occurs within 24 h, suggesting that reduced exposure to NE is not the only factor responsible for brown fat atrophy. NE increased [35S]methionine incorporation into cellular proteins, mitochondrial proteins, and UCP. The effect of NE on cell protein synthesis was inhibited by propranolol but not by prazosin. It was also inhibited 95% by cycloheximide but only partially (50%) by actinomycin D in contrast to NE stimulation of UCP labeling, which required RNA transcription. Chloramphenicol-sensitive protein synthesis was stimulated by NE. These results indicate a trophic action of NE in brown adipocytes exerted both at the level of RNA transcription and translation.
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PMID:Characterization of norepinephrine-stimulated protein synthesis in rat brown adipocytes. 144 15

We report a functional and molecular analysis of nine oncocytic tumors of the human thyroid. In all the abundance of mitochondria observed ultrastructurally was accompanied by an increase in enzymatic activities of respiratory complexes 1 (NADH dehydrogenase), 11 (succinate dehydrogenase) IV (cytochrome c oxidase), and V (ATPase). Western blot analysis failed to detect uncoupling protein in the tumors. The elevated respiratory enzyme activities were paralleled by an increase in the mitochondrial DNA content. Restriction analysis of mitochondrial DNA gave no indication of heteroplasmy or other gross alterations. We conclude that the mitochondrial proliferation in oncocytic tumors is probably not the result of a compensatory mechanism for the deficiency in enzyme complexes of the mitochondrial respiratory chain.
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PMID:Functional and molecular analysis of mitochondria in thyroid oncocytoma. 167 11

Repeated injections of 6-hydroxydopamine in Syrian hamster neonates maintained under long-day (16L:8D) photoperiod for 30 days retarded body growth and cellular proliferation in brown adipose tissue but did not affect the cellular content of mitochondrial proteins. Sympathectomy reduced GDP binding to isolated mitochondria without affecting the organelle uncoupling protein (UCP) content. Unilateral surgical denervation of the brown fat pad of 30-day-old hamsters caused loss of tissue protein and succinate dehydrogenase as well as reductions in GDP binding and UCP content of isolated mitochondria but did not prevent an increase in GDP binding observed after 1 month exposure to a short-day photoperiod. The increased GDP binding was not due to increased UCP content. These results indicate that an adrenergic neural input may not be essential for UCP expression in Syrian hamsters and that changes in GDP binding observed in a short-day photoperiod environment can be observed in denervated tissue in the absence of changes in mitochondrial UCP content.
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PMID:Role of neural input in photoperiod-induced changes in hamster brown adipose tissue. 211 94

Mice selected for high body weight (QL522) had increased food intake, body weight gain, and fat deposition relative to mice without weight selection (QL521). Brown adipose tissue (BAT) thermogenic capacity, as determined by the tissue content of protein, DNA, and succinate dehydrogenase and by mitochondrial uncoupling protein content was similar or slightly higher in 2- and 10-mo-old QL522 mice relative to age-matched QL521 mice. When food intake of QL522 mice was restricted to the level of QL521 mice, body weight gain and fat deposition over 28 days were then comparable to those of QL521 mice. Food restriction had no effect on BAT composition of QL522 mice. Both QL521 and QL522 mice increased calorie intake by 40-50% when offered a palatable high-fat supplement (HF), but only QL522 mice increased weight gain and fat deposition significantly. QL521 mice fed a high-fat supplement showed a significant increase in brown fat succinate dehydrogenase content, whereas QL522 mice showed significant increases in brown fat weight, protein, and succinate dehydrogenase content relative to mice fed stock diet. Nonshivering thermogenic capacity, as assessed by norepinephrine-stimulated oxygen uptake in anesthetized animals at 30 degrees C was similar between QL521 and QL522 mice eating stock diet and was significantly increased by the high-fat supplement in both strains. Thus mice selected for high body weight are very susceptible to diet-induced obesity, and we have no evidence that a reduction in brown fat thermogenic capacity contributes to the increased fat deposition of QL522 mice as they grow old or when they are offered palatable energy-dense supplements.
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PMID:Weight gain and brown fat composition of mice selected for high body weight fed a high-fat diet. 231 10

In euthyroid mice, a 48-h fast caused brown fat (BAT) atrophy characterized by loss of tissue proteins, succinate dehydrogenase (SDH), and a significant reduction in mitochondrial uncoupling protein (UCP) content. Chemical sympathectomy and surgical denervation failed to mimic the changes in BAT protein and SDH contents observed after food deprivation. However, suppression of sympathetic activity could account for the loss of UCP from the mitochondria. In mice made hyperthyroid by repeated triiodothyronine injections, losses of tissue SDH and proteins caused by food deprivation or surgical denervation were markedly suppressed, while the loss of UCP from the mitochondria remained unchanged. These results suggest that reduced sympathetic activity to BAT in fasted mice is not the exclusive cause of the tissue atrophy and that thyroid hormones may play a role in the control of brown fat atrophy in mice.
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PMID:Importance of neural input and thyroid hormones in the control of brown fat atrophy in mice. 239 Jul 38

The rate of oxygen consumption measured at 32.5 degrees C of lightly anesthetized 129/ReJ dy/dy mice was greater than that of dy/+ or +/+ control mice. However, the norepinephrine-stimulated rates of oxygen consumption of dystrophic and normal mice were similar. Brown adipose tissue cellularity (DNA content) of dystrophic mice was unchanged, and the tissue protein and succinate dehydrogenase contents were slightly reduced. The mitochondrial concentration of the uncoupling protein, thermogenin, and purine nucleotide binding to mitochondria isolated from brown fat of normal or dystrophic mice, were similar. These results indicate that the nonshivering thermogenic capacity of dystrophic mice is not significantly altered.
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PMID:Unchanged nonshivering thermogenic capacity of dystrophic mice. 309 57

Mice fasted for 24 h showed reductions in carcass fat and gonadal fat depots and atrophy of brown adipose tissue (BAT) that was characterized by loss of protein and succinate dehydrogenase. These changes were reversed on 24 h of refeeding. Cycling mice experienced 14 cycles of 1 day of fast followed by 2 days of refeeding, whereas control mice were fed ad libitum. Weight loss during each fast remained constant, and the animals lost and regained in excess of twice their initial weights within 6 wk. However, final weight and carcass and gonadal fat weights were similar to those of animals fed ad libitum. Total food intake was similar between cycling mice and those fed ad libitum suggesting an increase in feeding efficiency. There was no development of resistance to food deprivation since the preceding fasting experience of the animal had no effect on weight and carcass fat loss during a 24- or 48-h fast. Norepinephrine-stimulated oxygen consumption that was reduced in cycling mice was probably the result of a reduction of BAT thermogenic capacity. BAT succinate dehydrogenase content and the concentration of uncoupling protein in isolated mitochondria were significantly reduced. These changes in BAT composition were not observed when the refeeding period of each cycle was increased to 6 days. These results suggest that reduced energy expenditure in BAT may play a role in the conservation of energy during intermittent and frequent bouts of food deprivation.
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PMID:Effects of repeated cycles of fasting-refeeding on brown adipose tissue composition in mice. 340 68

Hamster brown adipocytes were incubated for up to 24 h with or without norepinephrine (NE) in Dulbecco's modified Eagle's medium supplemented with bovine serum albumin, calf serum, and antibiotics. Brown fat cells were viable for 24 h as defined by their ability to respond to NE by a 10-fold increase in oxygen consumption. However, prolonged exposure of the cells to NE led to a decline in NE-stimulated rates of O2 consumption, which was not the result of loss of cell thermogenic capacity. Brown fat cells incubated for 24 h with or without NE showed no significant change in succinate dehydrogenase activity or uncoupling protein (UCP) content. However, cell recovery after 24 h was significantly reduced in the absence of NE. In brown adipocytes isolated from rat, NE increased [35S]methionine incorporation into cell proteins and UCP. In contrast, [35S]methionine incorporation in hamster brown adipocyte proteins and UCP was greater than in rat brown fat cells and was not increased by NE. These results indicate that although NE may be required for cell survival, it does not stimulate protein and UCP synthesis in hamster brown fat cells.
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PMID:Norepinephrine does not stimulate protein and UCP synthesis in brown adipocytes of golden Syrian hamsters. 834 73

The objective of this work was to evaluate the effects of ethanol consumption on brown adipose tissue (BAT) thermogenic capacity in mice. Mice offered only ethanol (10%; v/v) for 10 days as drinking fluid had significant reductions in total energy and fluid intakes relative to mice given water, but net weight gains were similar. BAT thermogenic capacity was reduced in mice drinking ethanol, as shown by decreases in tissue protein and succinate dehydrogenase (SDH) activity and in the uncoupling protein content of isolated mitochondria. Ethanol consumption differed greatly between mice offered a choice between ethanol and water for 25 days after a 10-day habituation period, with only ethanol as the drinking solution. Total energy intake of mice that continue to consume the most ethanol voluntarily (up to 25% of total fluid intake) was significantly reduced but carcass fat was increased, relative to mice consuming less or no ethanol. Brown fat thermogenic capacity was not significantly affected by the degree of ethanol consumption. Basal and norepinephrine-stimulated rates of oxygen uptake of isolated brown adipocytes were not affected by ethanol. Thus, changes in the animal capacity for energy expenditure in brown adipose tissue does not appear an important factor to explain the effects of ethanol consumption on fat deposition in mice.
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PMID:Effects of ethanol consumption on brown adipose tissue thermogenic capacity in mice. 884 Sep 29

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


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