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Query: UMLS:C0038187 (starvation)
 24,951 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Alterations in content of long-chain acyl-CoA and value of phosphate potential (PP) were studied in liver tissue after administration of phenobarbital and corn oil into rats, starved within 4 hrs and 12 hrs before the experiment. As compared with the 4 hrs period, starvation within 12 hrs caused an accumulation of acyl-CoA and a decrease in PP (ATP/ADP X Pi) in liver tissue. The same alterations in the patterns studied were found after administration of corn oil. However, the 12 hrs starvation amplified distinctly the effect of oil administration on the content of acyl-CoA and on the PP value. Phenobarbital, administered simultaneously with the oil, removed completely the effect of corn oil on the patterns studied during the both periods of starvation, but it caused only slight influence on the starvation induced alterations in acyl-CoA and PP. The data obtained suggest that within the two periods of starvation studied it has been possible to differentiate the unspecific effects of starvation and the alterations induced by specific agents.
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PMID:[Effect of various periods of starvation on the character of exhibited changes of energy metabolism in the rat liver during the administration of phenobarbitol and corn oil]. 674 Sep 91

The effect of long-chain acyl-CoA on subcellular adenine nucleotide systems was studied in the intact liver cell. Long-chain acyl-CoA content was varied by varying the nutritional state (fed and starved states) or by addition of oleate. Starvation led to an increase in the mitochondrial and a decrease in the cytosolic ATP/ADP ratio in liver both in vivo and in the isolated perfused organ as compared with the fed state. The changes were reversed on re-feeding glucose in liver in vivo or on infusion of substrates (glucose, glycerol) in the perfused liver, respectively. Similar changes in mitochondrial and cytosolic ATP/ADP ratios occurred on addition of oleate, but, importantly, not with a short-chain fatty acid such as octanoate. It is concluded that long-chain acyl-CoA exerts an inhibitory effect on mitochondrial adenine nucleotide translocation in the intact cell, as was previously postulated in the literature from data obtained with isolated mitochondria. The physiological relevance with respect to pyruvate metabolism, i.e. regulation of pyruvate carboxylase and pyruvate dehydrogenase by the mitochondrial ATP/ADP ratio, is discussed.
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PMID:Effect of long-chain fatty acyl-CoA on mitochondrial and cytosolic ATP/ADP ratios in the intact liver cell. 674 76

1. Carnitine palmitoyltransferase and carnitine octanoyltransferase activities were measured in mitochondria at various acyl-CoA concentrations before and after sonication, thus permitting assessment of both overt and latent activities. 2. Overt carnitine palmitoyltransferase in liver and adipocyte mitochondria and overt carnitine octanoyltransferase in liver mitochondria were inhibited by malonyl-CoA. None of the latent activities were affected by this metabolite. 3. 5,5'-Dithiobis-(2-nitrobenzoic acid) stimulated latent hepatic carnitine palmitoyltransferase at low [palmitoyl-CoA]. 4. Starvation (24 h) decreased overt carnitine palmitoyltransferase activity in adipocyte mitochondria, but did not alter the sensitivity of this activity to malonyl-CoA.
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PMID:The effect of malonyl-CoA on overt and latent carnitine acyltransferase activities in rat liver and adipocyte mitochondria. 686 Mar 13

Urine samples were collected before and after a starvation period of 14-16 h from patients with glycogen storage disease, one with type III (amylo-1,6-glucosidase deficiency), four with type VIII (phosphorylase-b-kinase deficiency), and one with an unclassified type. The excretion of adipic, suberic, and 3-hydroxybutyric acid was measured by combined gas chromatography-mass spectrometry. The tendency towards ketosis seemed to decline with age in the patients with type VIII. In the non-ketotic patients no excess amounts of dicarboxylic acids were excreted. Therefore, glycogen storage disease per se seems to have no direct relationship to the excretion of adipic or suberic acid. A positive correlation was, however, found between the urinary excretion of on one side 3-hydroxybutyric and on the other adipic (correlation coefficient (Kendall's tau) +0.64, P less than 0.002 (one-sided test)) or suberic (+0.61, P less than 0.003) acid. The two dicarboxylic acids are most probably formed from long-chain monocarboxylic acids by omega- and beta-oxidation. It is speculated that succinyl-CoA formed by this pathway may counteract the tendency to ketosis in patients with glycogen storage disease.
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PMID:Dicarboxylic aciduria during ketotic phases in various types of glycogen storage disease. 694 27

1. Activities of 3-oxo acid CoA-transferase, D-3-hydroxybutyrate dehydrogenase, hexokinase and carnitine palmitoyltransferase have been measured in the gastrointestinal tract. 2. Activity of 3-oxo acid CoA-transferase in the glandular mucosa of the stomach was as high as that in heart and kidney, and was 2--4 times greater than that in other regions of the gastrointestinal tract. It is suggested that metabolism of acetoacetate might support acid secretion on re-feeding after a period without food. 3. All regions of the gastrointestinal tract have the capacity to use ketone bodies, and it is likely that both muscle and mucosa will contribute to their utilization. 4. Activity of hexokinase was twice the rate of glucose utilization by the jejunum under anaerobic conditions. The maximal rate of glucose metabolism in the jejunum may not be substantially different from that in other regions of the gastrointestinal tract. 5. Starvation decreased the capacity for metabolism of glucose in several regions of the intestine. 6. Activities of carnitine palmitolytransferase in the stomach, jejunum and colon were similar, and about one-third of that in the liver. Activity in the jejunum was much higher than the apparent rate of oxidation of exogenous fatty acid. 7. The results do not suggest any large variation between tissues of the gastrointestinal tract in metabolism of glucose or fatty acids, whereas metabolism of ketone bodies may be more prominent in the stomach.
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PMID:Activity of 3-oxo acid CoA-transferase, D-3-hydroxybutyrate dehydrogenase, hexokinase and carnitine palmitoyltransferase in the stomach and small and large intestine of the rat. 695 79

Effects of starvation and re-feeding on adipocyte glycerolipid formation were investigated in young (age 48-55 days) and old rats (age 83-94 days). Adipocyte homogenates were used to assay glycerophosphate acyltransferase and Mg2+-dependent phosphatidase phosphohydrolase. Glycerophosphate acyltransferase was measured in the presence of [14C]glycerol 3-phosphate, palmitate, ATP, CoA and Mg2+. The release of inorganic phosphate from aqueous dispersed phosphatidase was taken as a measure of phosphatidate phosphohydrolase activity. Young rats starved for 48-72 h showed a 2-fold decline in the glycerophosphate acyltransferse activity. Older rats did not show any change in the glycerophosphate acyltransferase activity during 96 h starvation. Re-feeding of starved rats with chow for 48 h caused significant increases in the glycerophosphate acyltransferase activity. These changes were mainly limited to N-ethylmaleimide-sensitive glycerophosphate acyltransferase activity. These changes were mainly limited to N-ethylmaleimide-sensitive glycerophosphate acyltransferase. Phosphatidate phosphohydrolase activity decreased significantly (2-fold) during starvation in both young and old rats. Phosphatidate phosphohydrolase activity was regained completely after re-feeding of starved rats. Initial changes in the glycerophosphate acyltransferase and phosphatidate phosphohydrolase activities were very slow. Most notable increases in the glycerophosphate acyltransferase and phosphatidate phosphohydrolase activities were observed between 24 and 48 h after initiation of a re-feeding schedule. Mean adipocyte size decreased during starvation of rats for 72 h. Although considerable increases in the activities of both glycerophosphate acyltransferase and phosphatidate phosphohydrolase were apparent by re-feeding of starved rats for 48 h, mean adipocyte size did not change during this period. Thus, enzyme changes which occurred after re-feeding were independent of the adipocyte size. To separate the effects of age from the cell size on adipocyte glycerolipid formation during starvation and re-feeding periods, adipocytes from older rats were subjected to filtration through a nylon screen to obtain adipocytes of similar sizes. These studies suggest that the age of the animal significantly influences the effects of starvation and re-feeding on adipocyte glycerolipid formation.
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PMID:Glycerolipid biosynthesis in rat adipose tissue. 10. Changes during a starvation and re-feeding cycle. 715 Jun 32

1. The concentrations of malonyl-CoA, glycerol 3-phosphate, non-esterified carnitine, acid-soluble and acid-insoluble acylcarnitines, acetoacetate, 3-hydroxybutyrate and acid-insoluble acyl-CoA were measured in rapidly-frozen liver samples from fed or starved (24h) virgin, pregnant (19-20 days), lactating (2, 10-12 and 18-20 days) and weaned (for 24h, on 10th day of lactation) rats. The activities of total and N-ethylmaleimide-sensitive and -insensitive glycerophosphate acyltransferase (acyl-CoA:sn-glycerol 3-phosphate O-acyltransferase; EC 2.3.1.15) were also measured. 2. The concentration of malonyl-CoA was significantly higher in liver of fed pregnant, mid- and late-lactating rats than in liver of fed virgin rats. After starvation for 24h hepatic malonyl-CoA concentrations were higher in mid-lactating rats and lower in pregnant and weaned rats than in virgin animals. 3. After starvation for 24h the hepatic concentrations of glycerol 3-phosphate, ketone bodies, acid-soluble acylcarnitines and the value for the [3-hydroxybutyrate]/[acetoacetate] ratio were all highest in pregnant rats, intermediate in virgin, 2-day lactating and weaned animals and lowest in mid- and late-lactating rats. The concentrations of acid-insoluble acylcarnitines also increased most in pregnant rats, after starvation. The concentration of acid-insoluble acyl-CoA increased equally after starvation in virgin and pregnant animals but did not increase significantly in all other animals studied. 4. The total concentration of carnitine was similar in livers of fed virgin, pregnant and 2-day lactating animals but fell markedly by the 10th day of lactation and remained low in late-lactating animals. The concentration of non-esterified carnitine followed the same pattern. After starvation for 24h the hepatic concentration of non-esterified carnitine decreased significantly in virgin, pregnant and 2-day lactating animals, but remained unchanged in mid- and late-lactating or weaned animals. 5. The activities of N-ethylmaleimide-sensitive and -insensitive glycerophosphate acyltransferase both increased significantly in livers of mid-lactating animals. After starvation for 24h the activity of the N-ethylmaleimide-insensitive O-acyltransferase decreased in livers of virgin, pregnant and mid-lactating animals, whereas the activity of the N-ethylmaleimide-sensitive O-acyltransferase was unchanged in virgin animals but decreased markedly in livers of pregnant and lactating rats. 6. The results are discussed in relation to the importance of different metabolic parameters in the regulation of long-chain acyl-CoA metabolism in the liver.
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PMID:Regulation of hepatic fatty acid metabolism. The activities of mitochondrial and microsomal acyl-CoA:sn-glycerol 3-phosphate O-acyltransferase and the concentrations of malonyl-CoA, non-esterified and esterified carnitine, glycerol 3-phosphate, ketone bodies and long-chain acyl-CoA esters in livers of fed or starved pregnant, lactating and weaned rats. 732 3

The experiments reconfirm the powerful inhibitory effect of malonyl-CoA on carnitine acyltransferase I and fatty acid oxidation in rat liver mitochondria (Ki 1.5 microM). Sensitivity decreased with starvation (Ki after 18 h starvation 3.0 microM, and after 42 h 5.0 microM). Observations by Cook, Otto & Cornell [Biochem. J. (1980) 192, 955--958] and Ontko & Johns [Biochem. J. (1980) 192, 959--962] have cast doubt on the physiological role of malonyl-CoA in the regulation of hepatic fatty acid oxidation and ketogenesis. The high Ki values obtained in the cited studies are shown to be due to incubation conditions that cause substrate depletion, destruction of malonyl-CoA or generation of excessively high concentrations of unbound acyl-CoA (which offsets the competitive inhibition of malonyl-CoA towards carnitine acyltransferase I). The present results are entirely consistent with the postulated role of malonyl-CoA as the primary regulatory of fatty acid synthesis and oxidation in rat liver.
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PMID:Importance of experimental conditions in evaluating the malonyl-CoA sensitivity of liver carnitine acyltransferase. Studies with fed and starved rats. 734 Aug 31

The arteriovenous differences in the caecum of the rat have been compared for volatile fatty acids (VFA) and for electrolytes. Our results suggest the possibility of an exchange between VFA and chloride at the level of the caecal wall, rather than a net exchange between VFA and bicarbonate; however, the role of bicarbonate or Cl- at the cellular level is still unknown. Acetate uptake by the liver was enhanced when acetate in the afferent plasma was increased in fed as in starved rats, showing that acetyl CoA synthetase was still active during starvation. A release of endogenous acetate was only observed in situations of very active ketogenesis (starvation at the end of pregnancy). In physiological conditions, propionate and butyrate reaching the liver were almost quantitatively removed. However, butyrate was taken up by the liver at a higher rate than propionate after intracecal loads. Propionate was very efficiently utilized as a glucogenic substrate and without noticeable disturbance of lactate metabolism. After administration of acetate loads in starved rats, hepatic ketogenesis increased slightly. There was a marked difference between ketogenesis from butyrate in fed and starved rats. The low ketogenesis from butyrate in the fed rats stressed the important role of metabolic pathways of acetyl-CoA utilization in the control of ketogenesis. In contrast to alanine or lactate, propionate was poorly antiketogenic in the rat.
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PMID:Origin and utilization of volatile fatty acids in the rat. 734 86

The fuel selection of muscle fibres at rest is dependent on substrate availability. Increased lipid availability results in an increase citrate concentration with inhibition of glycolysis. Fat utilization also increases the concentration ratio acetyl-CoA:CoASH, with inhibition of PDH transformation to the active form. The result is an inhibition of carbohydrate utilization in conformity with the classical glucose-fatty acid style. During exercise fuel selection is dependent on the intensity of exercise, the recruitment pattern of fibre type and the availability of fuels. During exercise at maximum intensity the main fuels are PCr and muscle glycogen, the highest energy release occurring with type II fibres. At exercise intensities between 70 and 100% VO2max carbohydrate is the main fuel after the intake of normal mixed or carbohydrate-rich diets. No inhibition of PDHa formation was observed by increased concentration ratio acetyl-CoA:CoASH during the exercise, but the activation and transport of fatty-acyl groups from NEFA may be inhibited by a decrease in the concentration of CoASH. This mechanism may limit the contribution of fat to metabolism during exercise at intensities above 60% VO2max, after an intake of carbohydrate-rich diets. After carbohydrate starvation or an infusion of a fat emulsion, there was a substantial increase in the utilization of fat which, after the infusion, was concomitant with a high PDHa and a high lactate production. This is thought to be due to a decrease in glycolysis and in the catalytic activity of PDHa, especially in type I fibres, while lactate production continues in type II fibres. When exercise intensities fall below 60% VO2max, fat becomes the dominant fuel during prolonged exercise. At the same time the recruitment pattern is shifted toward type I fibres which have the lowest activation threshold and the highest oxidative capacity.
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PMID:Fuel selection, muscle fibre. 756 45


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