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

---

Query: EC:2.3.1.21 (CPT)
4,580 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A total of 35 pigs were obtained by cesarean section, placed in individual sterile isolators, and randomly allotted to treatment groups. Thirty pigs received purified, isoenergetic liquid diets containing 2 or 32% butterfat (dry matter basis) and were killed at 1, 7, or 21 days of age. Five pigs were killed at 2 hours post delivery and received no diet. Twenty-one-day old pigs showed a tendency for higher weight gain and feed consumption when consuming the 32% fat diet although the differences were not significant. The rate of oxidation of [U-14C]palmitate to CO2 and acid soluble products was measured in homogenates of liver, kidney, heart, and leg muscle (biceps femoris) from pigs 0, 1, 7, and 21 days of age. The relative rates of oxidation of [U-14C]myristate, [U-14C]palmitate, and [U-14C]stearate were measured in homogenates of liver from 7-day old pigs. Palmitate oxidation was stimulated by carnitine in all four tissues and the rate of carnitine-stimulated palmitate oxidation to acid soluble products in heart and to CO2 in liver was higher in tissues from pigs consuming the 32% fat diet. The rate of palmitate oxidation increased with age in liver, kidney and leg muscle tissues and was maximum at 21 days in kidney and leg muscle and at 7 days in liver. The rate of palmitate oxidation in heart tended to decrease with animal age. In homogenates of liver from 7-day old pigs, palmitate was oxidized at a faster rate than stearate or myristate. The activities of carnitine palmitoyltransferase (CPT) (EC 2.3.1a) and succinate dehydrogenase (EC 1.3.99.1) in mitochondria isolated from liver, kidney, heart, and leg muscle did not vary considerably with age although CPT activity tended to be higher in those tissues from pigs consuming the high fat diet. Changes in the rate of palmitate oxidation with age tended to parallel changes in the level of mitochondrial protein per g of wet tissue and suggested an increased ability to utilize fat as an energy substrate during early development of the neonatal pig.
...
PMID:Effect of age and dietary fat level on fatty acid oxidation in the neonatal pig. 70 4

To study possible factors in the pathogenesis of the ethanol-induced fatty liver, we investigated the effect of chronic ethanol consumption on the metabolism of fatty acids by isolated hepatic mitochondria. Chronic ethanol consumption resulted in decreased fatty acid oxidation, as evidenced by a reduction in oxygen uptake and CO2 production associated with the oxidation of fatty acids. The State 3 rate of oxygen uptake was depressed to a greater extent than the State 4 or the uncoupler-stimulated rate; the respiratory control ratio was also decreased. Therefore, one site of action of chronic ethanol feeding is on oxidative phosphorylation. The reduction in fatty acid oxidation, in general, is not due to an effect on the activation or translocation of fatty acids into the mitochondria. There was no effect by ethanol feeding on the activity of palmitoyl coenzyme A synthetase, whereas carnitine palmitoyltransferase activity was increased. The use of an artificial system (formazan production) to study beta oxidation in the absence of the electron transport chain is described. In the presence of fluorocitrate, which inhibits citric acid cycle activity, ketogenesis and formazan production were increased by chronic ethanol consumption. Thus beta oxidation to the level of acetyl-CoA is not impaired by chronic ethanol consumption. Total oxidation of fatty acids to CO2 is depressed by chronic ethanol intoxication because of effects on oxidative phosphorylation or the citric acid cycle (or both). Neither nutritional deficiency, cofactor depletion, nor the presence of ethanol in vitro explains these effects. Several of the effects of chronic ethanol consumption on fatty acid oxidation are mimicked by acetaldehyde and acetate, products of ethanol oxidation. Chronic ethanol consumption leads to persistent impairment of mitochondrial oxidation of fatty acids to CO2. However, oxidation of fatty acids to acetyl-CoA is not decreased by chronic ethanol consumption.
...
PMID:Effect of chronic ethanol ingestion on fatty acid oxidation by hepatic mitochondria. 117 Oct 98

Depressed fatty acid (FA) oxidation found previously in various types of cardiomyopathies has been attributed to the lack of carnitine in heart muscle. This is not the case in the cardiac lesion of hamsters, strain BIO 14.6, between the ages of 3 and 6 months. We observed depressed CO2 production by heart homogenates of diseased animals from labeled acetate (1/20), butyrate (1/15), octanoate (1/3, and palmitate (1/4) in the presence of carnitine. The activity of carnitine palmitoyltransferase (forward reaction) and FA activating enzymes was unchanged. The oxidation of 1,4-labeled succinate as well as acetyl CoA was depressed to approximately 40% of the control, whereas [2-14C]pyruvate and [U-14C]oxoglutarate were oxidized at 60 to 70% of the control level. The CO2 production from [1-14C]pyruvate and [1-14C]oxoglutarate showed no reduction. No significant difference was found in myocardial triglyceride content and palmitate esterification into neutral lipids. The possible cause of different magnitudes of depressed oxidation of these substrates is unknown. It may be that the acetyl-CoA derived from FAs and that derived from pyruvate are metabolized by the TCA cycle to different extents, or that the endogenous metabolism participates to different degrees in the presence of different substrates.
...
PMID:Metabolic changes in the myocardium of hamsters with hereditary muscular dystrophy. 119 85

1. Extracellular field potentials were recorded to study the role of endogenous adenosine during hypoxia in area CA1 of rat hippocampal slices. 2. Hypoxic conditions, induced by 15 min exposure to 95% N2-5% CO2 at 32 degrees C and in high-glucose incubation medium, produced a rapid and reversible depression of evoked synaptic potentials. 3. In slices from young Sprague-Dawley rats, the hypoxia-induced synaptic depression was reduced in a concentration-dependent manner by the adenosine antagonist 8-cyclopentyltheophylline (8-CPT; 100 nM-2.0 microM). 4. Recovery of synaptic potentials after hypoxia was complete under each experimental condition. 5. Extended periods of hypoxia lasting 30 min likewise produced a rapid and near total suppression of the evoked synaptic potentials. In the presence of 8-CPT, both the population excitatory postsynaptic potential (EPSP) slope and population spike amplitude were significantly preserved throughout the hypoxic episode. 6. Neither the onset rate nor the degree of the hypoxia-induced synaptic depression were significantly different in slices from young, adult, or aged Fischer 344 rats. Reduction of the hypoxia-induced response depression by 8-CPT was also similar in all age groups. 7. These findings have further characterized the important involvement of endogenous adenosine in the potentially neuroprotective synaptic depression observed in hippocampal slices from young and aged rats during hypoxia.
...
PMID:Endogenous adenosine contributes to hypoxic synaptic depression in hippocampus from young and aged rats. 152 79

Objectives of this study were to quantitate metabolite fluxes in ruminant liver and to delineate effects of recombinant bST on patterns of nutrient metabolism by liver. Nineteen multiparous cows ranging in previous lactational performance from 6400 to 13,500 kg per 305-d lactation were treated with either placebo or bST (40 mg/d) from wk 11 to 18 of lactation. Liver tissue was collected at slaughter. Tissue slices were incubated with various 14C-labeled substrates, and rates of conversion of label to CO2 and metabolites were measured. In vivo recombinant bST treatment increased in vitro conversion of [1-14C]propionate and [2-14C]acetate to glucose more than twofold. At 2.5 mM propionate, bST-treated cows converted propionate to glucose at 90% efficiency. Recombinant bST increased [14C]bicarbonate incorporation into glucose five-fold. Overall, bST treatment resulted in greater C flow from propionate and acetate through the TCA cycle. Acetate had only small effects on propionate metabolism and no effects on lactate plus pyruvate metabolism. Unexpectedly, propionate decreased acetate conversion to ketone bodies. Suggested mechanisms for this observation include depletion of coenzyme A and allosteric regulation of carnitine palmitoyltransferase I by methylmalonyl-coenzyme A formed from propionate. In summary, bST treatment resulted in increased rates of gluconeogenesis and oxidation in liver in support of lactation.
...
PMID:Effects of somatotropin and substrates on patterns of liver metabolism in lactating dairy cattle. 157 17

The support of Xenopus laevis spermatogenesis in vitro by different energy-yielding substrates has been investigated. Isolated spermatogenic cells maintained their levels of adenosine-triphosphate for 24 h in serum-free medium containing only amino acids as energy substrates. DL-Aminocarnitine, an inhibitor of carnitine palmitoyltransferase, reduced cell viability 87% during a 15-h culture in the same medium, indicating that beta oxidation of endogenous fatty acids is a significant source of energy when exogenous substrates are unavailable. Isolated spermatocytes developed into spermatids for 7 days in medium supplemented with either pyruvate, oxaloacetate, or lactate, with maximal survival and development at 0.5 mM pyruvate, 2.0 mM oxaloacetate, and 4.0 mM lactate. Few spermatocytes survived more than 3 days in serum-free medium supplemented with only glucose and amino acids as energy substrates. In contrast, glucose-supplemented medium supported spermatocyte differentiation for 14 days in testis fragment culture and 7 days in spermatocyte-Sertoli cell cocultures due to the excretion of lactate and pyruvate by Xenopus Sertoli cells during culture in glucose-supplemented medium. Glucose also enhanced spermatocyte development in medium containing dialyzed, heat-inactivated fetal calf serum. Spermatogenic cells oxidized glucose to CO2 with C1 oxidized 6- to 7-fold more than C6, suggesting that glucose may be metabolized in the hexose monophosphate shunt. The results are discussed in comparison to energy metabolism in mammalian testes and spermatogenic cells.
...
PMID:Support of Xenopus laevis spermatogenesis in vitro by different energy substrates. 234 Mar 34

Dependence of gluconeogenesis on beta-oxidation and ketogenesis from long-chain fatty acids was examined in isolated sheep hepatocytes. Hepatocytes were incubated with a combination of gluconeogenic precursors (2 mM pyruvate, 20 mM lactate, and 5 mM propionate) plus other fatty acids, in the presence and absence of tetradecylglycidic acid, an inhibitor of the carnitine palmitoyltransferase reaction. Palmitate oxidation to total acid-soluble metabolites or beta-hydroxybutyrate was markedly inhibited by the addition of tetradecylglycidic acid. In general, oxidation of palmitate to carbon dioxide was not altered by tetradecylglycidic acid. Glucose production was inhibited 28 to 50% in the presence of tetradecylglycidic acid. Addition of acetate and butyrate inhibited gluconeogenesis, but octanoate addition had a slight stimulatory effect. In the presence of tetradecylglycidic acid, butyrate, but not acetate, addition further reduced gluconeogenesis. In contrast, addition of octanoate in the presence of tetradecylglycidic acid restored gluconeogenic rates to control values. The results are consistent with observations in several nonruminant species and suggest that, as in those species, ruminant gluconeogenesis requires at least a basal rate of beta-oxidation and ketogenesis from long-chain fatty acids to support maximum gluconeogenic rates.
...
PMID:Gluconeogenic dependence on ketogenesis in isolated sheep hepatocytes. 234 43

The effects of ethanol administration on activity and regulation of carnitine palmitoyltransferase I (CPT-I) were studied in hepatocytes isolated from rats fed a liquid, high-fat diet containing 36% of total calories as ethanol or an isocaloric amount of sucrose. Cells were isolated at several time points in the course of a 5-week experimental period. Ethanol consumption markedly decreased CPT-I activity and increased enzyme sensitivity to inhibition by exogenously added malonyl-CoA. Changes in enzyme activity occurred sooner than those in enzyme sensitivity. Fatty acid oxidation to CO2 and ketone bodies was depressed in hepatocytes from ethanol-fed animals during the first part of the treatment. At the end of the 35-day period, there were no longer differences in the rate of ketogenesis between the two groups. At that time, however, the rate of CO2 formation was still impaired in the ethanol-fed animals. Furthermore, addition of ethanol or acetaldehyde to the incubation medium strongly depressed CPT-I activity and rates of fatty acid oxidation in hepatocytes from ethanol-treated rats, whereas these effects were much less pronounced in cells from control animals. The response of CPT-I activity to insulin, glucagon, vasopressin, and phorbol ester was blunted in cells derived from ethanol-fed rats. These changes in the regulation of CPT-I activity corresponded with those observed in the rate of fatty acid oxidation. It is concluded that CPT-I may play a role in the generation of the ethanol-induced fatty liver.
...
PMID:Effects of ethanol feeding on the activity and regulation of hepatic carnitine palmitoyltransferase I. 306 12

The monosynaptic reflex (MSR), recorded extracellularly from the ventral root isolated, superfused spinal cords of neonatal rats (6-10 days post-partum), was rapidly depressed to 35-45% of control values by either cessation of superfusion (4 min stop-flow period) or by superfusion with anoxic medium (95% N2-5% CO2; 4 min). The depression was reversible, 85-115% recovery occurring after 15 min of restoration of flow or normoxic (95% O2-5% CO2) superfusion. 2-Chloroadenosine, a metabolically stable adenosine analogue, also reversibly inhibited the MSR, an effect which was antagonised by 10(-6) M 8-cyclopentyltheophylline (8-CPT). The depression of the MSR, caused by 4 min of hypoxia (either stop-flow or anoxic superfusion), was prevented by 10(-6) M 8-CPT. These results provide strong evidence for a critical involvement of adenosine in mediating early synaptic depression evoked by a brief period of hypoxia.
...
PMID:Involvement of adenosine in synaptic depression induced by a brief period of hypoxia in isolated spinal cord of neonatal rat. 319 1

The oxidation of palmityl-coenzyme A and acetate to CO2 by mitochondria isolated from rat small intestine increases 10-fold at the time of weaning (18-21 days of age). Carnitine palmitoyltransferase (EC 2.3.1.21) activity is 2-fold greater in mitochondria of suckling rat intestine compared to postweaned intestine. These data indicate that carnitine palmitoyltransferase does not control the increase in intestinal fatty acid oxidation during weaning. We have previously reported that the estimated intramitochondrial [NADH]/[NAD+] as determined by the ratio of tissue levels of 3-hydroxybutyrate and acetoacetate is fivefold greater in suckling rat intestine compared to postwean animals. High intramitochondrial [NADH]/[NAD+] which is present in suckling rat small intestine is associated with a decrease in citric acid cycle activity and beta oxidation. The addition of acetoacetate causes a decrease in intramitochondrial [NADH]/[NAD+]. The oxidation of acetate and glucose to CO2 by suckling rat intestine mitochondria was stimulated by the addition of 1 mM acetoacetate. These data suggest that the lower rate of fatty acid oxidation by suckling rat small intestine is controlled by elevated intramitochondrial [NADH]/[NAD+].
...
PMID:Control of fatty acid oxidation by intramitochondrial [NADH]/[NAD+] in developing rat small intestine. 335 71


1 2 3 4 Next >>

---