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

The ATP and ADP content of planarians subjected to starvation for two weeks followed by feeding for the same period was investigated. The ATP and ADP content during fasting increased and then, after feeding, returned to normal. The ATP/ADP ratio varied in the same way, which is consistent with the view that the adenylic nucleotide pool is implicated in the regulation of the energy metabolism of the organism.
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PMID:Change in ATP and ADP content of fasting and feeding planarians (Polycelis nigra). 55 28

Amino acid starvation of Ehrlich ascites cells leads to a significant decrease of the intracellular ATP concentration concomitant with a marked decrease in nucleolar RNA polymerase activity. Addition of 8-bromoguanosine 3':5'-monophosphate (br8cGMP) to the amino-acid-deficient culture medium increased the cellular ATP levels and restored the rRNA synthesis capacity of nucleoli to control levels. Exogenous br8cAMP overcame the effects of br8cGMP. Administration of br8cAMP to exponentially growing ascites cells resulted in a shrinkage of ATP levels and in an inhibition of nucleolar RNA synthesis similar to that observed under shift-down conditions. These effects of br8cAMP could be antagonized by exogenous br8cGMP or hypoxanthine. Since the br8cGMP-induced increase in the total adenine nucleotides was abolished in the presence of azaserine (an inhibitor of the amidation of formylglycineamide ribonucleotide) it is concluded that cyclic nucleotides exert at least a part of their regulatory effects on cell proliferation by regulating nucleotide biosynthesis de novo.
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PMID:The effect of cyclic nucleotides on cellular ATP levels and ribosomal RNA synthesis in Ehrlich ascites cells. 56 46

Methods are described for preparing and analyzing single preimplantation mouse embryos for a variety of metabolites and cofactors (glucose-6-P, fructose-6-P, fructose-1,6-bisphosphate, ATP, AMP, Pi, citrate, isocitrate, alpha-ketoglutarate, and malate). Oil-well and enzymatic cycling techniques are combined to provide the sensitivity needed to measure the amounts present (10(-12) to 1o(-15) moles). After experimental treatment, embryos are collected on glass slides and freeze-dried. They can then be stored indefinitely under vacuum at -25 degrees C without deterioration. With these procedures, the embryos were collected at successive stages of development and subjected to starvation and refeeding with glucose, pyruvate or both. The results confirm the existence of a block at early stages at the P-fructokinase step. This may be due to inhibition by the very high citrate levels present. The data suggest that glycolysis is turned on late in preimplantation development by the rise in fructose-6-P, a deinhibitor of P-fructokinase. In the citrate cycle, no step between citrate and alpha-ketoglutarate is rate-limiting, but a step between alpha-ketaglutarate and malate appears to impede the flux at early embryonic stages.
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PMID:Measurement of metabolites in single preimplantation embryos; a new means to study metabolic control in early embryos. 58 Feb 93

A system for in situ perfusion of rat hindquarters using a fluorocarbon for oxygen and CO2 exchange, and a polyol to provide oncotic pressure is described. Perfusion with glucose plus insulin resulted in no significant change in the tissue level of citrate cycle intermediates, phosphocreatine, ATP, ADP, AMP, and glycogen. Glucose was consumed at a linear rate, and lactate, pyruvate, alanine, glutamine, glutamate, and citrate were released into the perfusing medium. Inclusion of pyruvate resulted in elevation of citrate cycle intermediates and alanine, whereas acetate elevated the level of cycle intermediates without significant effect on tissue alanine or its release. Radioactivity from NaH[14C]O3 was incorporated into citrate cycle intermediates, glutamate, aspartate, and lactate by glucose-perfused hindquarters, the extent of which was markedly elevated as the tissue pyruvate was increased. When pyruvate was in the physiological range, acetate caused elevation in incorporation of CO2 into these metabolites, increased the concentration of citrate, and doubled the concentration of acetyl-CoA. Thirty-five to forty-four per cent of 14C incorporated into citrate was retained after enzymic degradation to 2-oxoglutarate. Perfusion with [2-14C-]propionate led to elevation in the level of citrate cycle intermediates, and radioactivity was incorporated into the latter, as well as glutamate, aspartate, lactate, pyruvate, alanine, and CO2. Two independent calculations estimated the rate of flux of 4-carbon cycle intermediates to 3-carbon metabolites of about 68 mumol/h (approximately 38 nmol/min/g of tissue), a rate in excess of those reported for alanine release from human or rat muscle during starvation. Arsenite blocked carbohydrate flux through the citrate cycle and effected accumulation of lactate, pyruvate, alanine, and 2-oxoglutarate. Flux from 4- to 3-carbon acids was diminished by arsenite, apparently as a result of lowered substrate concentration for decarboxylation. 3-Mercaptopicolinic acid, an inhibitor of phosphoenolpyruvate carboxykinase, was without effect on the parameters studied, suggesting that this enzyme is not involved in the decarboxylation reaction. It is concluded that (a) a constant level of citrate cycle intermediates is maintained in part by continuous flux of carbon into and out of the cycle by carboxylation and decarboxylation reactions; (b) the carbon skeleton of alanine released from skeletal muscle is derived in part from other amino acids which are catabolized to cycle intermediates; and (c) the subsequent removal of these intermediates is probably mediated by malic enzyme(s) (EC 1.1.1.40, or 1.1.1.36, or both.
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PMID:Carboxylation and decarboxylation reactions. Anaplerotic flux and removal of citrate cycle intermediates in skeletal muscle. 76 69

Bacillus subtilis cells accumulate unusual phosphorylated substances at the end of logarithmic growth in a semi-synthetic medium. Two of these substances are guanosine 3'(2')-diphosphate 5'-diphosphate (ppGpp) and guanosine 3'(2')-diphosphate 5'-triohosphate (pppGpp) which, in contrast to amino-acid-starved Escherichia coli cells, are not degraded in sporulating cells of B. subtilis after the addition of chloramphenicol. Moreover, inhibition of protein synthesis in growing cells of B. subtilis causes accumulation of ppGpp and pppGpp, which is also in contrast to E. coli. This was shown by isolation and characterization of substances produced in these cells after the addition of chloramphenicol. Other inhibitors of protein synthesis acting at the ribosomal level also cause the accumulation of ppGpp and pppGpp. There is no difference between the action of antibiotics affecting 50-S and/or 30-S ribosomal subunits, since chloramphenicol, tetracycline erythromycin and neomycin cause the accumulation of almost equal amounts of these nucleotides. This apparently resolves the close connection between ppGpp accumulation and the rate of stable RNA synthesis, which was believed to exist also in B. subtilis because of the stringent response observed after amino acid starvation coupled with ppGpp accumulation. Antibiotics which inhibit protein synthesis differently than by affecting the ribosomes (puromycin) or which inhibit RNA (rifampicin) or DNA (nalidixic acid) synthesis do not cause ppGpp accumulation. The accumulation of ppGpp and pppGpp in the presence of charged tRNA provided by chloramphenicol treatment suggests that the signal for the synthesis of unusual nucleotides is an inhibition of the binding of tRNA (charged or uncharged) to the acceptor site of the ribosome. This activates the rel gene product which forms ppGpp and pppGpp from GTP and ATP. Sporulating cells of B. subtilis without chloramphenicol treatment produce besides ppGpp and pppGpp other unusual substances, which are likely to be highly phosphorylated nucleotides contained adenine as base moiety.
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PMID:Studies on the control of development. Accumulation of guanosine tetraphosphate and pentaphosphate in response to inhibition of protein synthesis in Bacillus subtilis. 80 77

These studies were undertaken to determine the mechanism by which intravenously administered lead salts inhibit hepatic gluconeogenesis. Within 1 h after the intravenous administration of lead acetate (10 mg), there is 97% inhibition of CO2 fixation in isolated rat liver mitochondria. This effect is concentration-dependent. The induction of phosphoenolpyruvate carboxykinase activity observed with starvation was also inhibited by intravenously administered lead acetate, but the activities of pyruvate kinase, glucose 6-phosphate dehydrogenase and pyruvate carboxylase were unaffected, as was the oxidation of palmitate and palmitoyl-CoA by mitochondria from Pb2+-treated animals. The addition of reduced glutathione to mitochondria from Pb2+-treated animals had no effect on the inhibited CO2 fixation. ATP concentrations in mitochondria from Pb2+-treated animals are decreased and the dose-response relationships for the effect of Pb2+ on CO2 fixation and ATP concentrations correspond. We conclude that the decrease in mitochondrial ATP in Pb2+-treated animals is probably responsible for the marked inhibition ov CO2 fixation, and hence the impairment of gluconeogenesis from alanine, lactate and pyruvate observed by others.
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PMID:Inhibition of carbon dioxide fixation by lead acetate in rat liver mitochondria. 90 20

Higher omega-oxidation activities in the diabetic mammal and the starved one suggest that omega-oxidation mechanism plays an important role under these conditions. Dicarboxylic acid that is the final product of omega-oxidation can be metabolized further by beta-oxidation, subsequently, formation of succinyl-CoA and short-chain dicarboxylic acid might be increased in the liver. The physiological significance of omega-oxidation might consist in supplying the substrate of TCA cycle for utilization of acetyl-CoA and excreting the short-chain dicarboxylate in urine resulting in the decrease of ketone bodies in the blood, especially in diabetes and starvation. On the bases of these information, it is important to investigate the metabolism of dicarboxylic acids. Generally, fatty acids must be activated before they enter the metabolic pathway. By in vitro studies with rat liver homogenate, we have recently demonstrated that octadecaned-ioic acid must be activated by ATP-Mg2+ and CoA as monocarboxylic acid is. However, it has not been studied to compare the activity of acyl-CoA synthetase on mono and dicarboxylic acid. So, in this report, we assayed the activity of acyl-CoA synthetase in beef liver preparations using palmitic or hexadecanedioic acid (C1;16) as substrate. The results are as follows 1) Activation capacity of the supernatant of sonicated mitochondria was less than that of sonicated microsome for either palmitate or hexadecanedioate. 2) Activation capacity for hexadecanedioate was less than that for palmitate in both supernatant of sonicated mitochondria and that of sonicated microsome. 3) In our experiment, it might be suggested that the subcellular distribution of hexadecanedioate activation is almost identical with that of palmitate activation.
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PMID:[Acyl-CoA synthetase activity of long-chain mono and dicarboxylic acid in beef liver preparations (author's transl)]. 94 21

The influence of amino acid starvation on both the pool sizes of nucleoside triphosphates and the rRNA synthetic capacity of Ehrlich ascites cells was studied. The results indicate that under shiftdown conditions, an immediate shrinkage of the cellular ATP and GTP levels occurs. Concomitant with this, protein and rRNA syntheisis are markedly inhibited. If the pool sizes of purine nucleaside triphosphates are expanded by adding adenosine or guanosine to cells cultured in histidine-free medium, the nucleolar RNA synthesis is fully restored, while protein synthesis remains inhibited. The results suggest that the rate of pre-rRNA transcription may be controlled by the actual nucleoside triphosphate levels of the cells rather than by short-lived protein(s), as has been previously postulated.
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PMID:Control of nucleolar RNA synthesis by the intracellular pool sizes of ATP and GTP. 94 52

The stimulatory effect of starvation on omega oxidation of stearate by the 20,000 X g supernatant fluid of rat liver homogenates was studied. The effect was obtained after starvation for 24 hours. Starvation for longer times did not further increase omega oxidation. The stimulatory effect of starvation on omega oxidation of stearic acid was accompanied by a reduced incorporation of stearic acid into phosphatidic acid, diglycerides, and triglycerides. Substitution of the 100,000 X g supernatant fluid from liver homogenate of starved rats with 100,000 X g supernatant fluid from liver homogenates of control rats reduced the microsomal omega oxidation of stearic acid with a simultaneous increase in incorporation of stearic acid into the different glycerides. Under the latter conditions almost no free stearic acid could be isolated from the incubation mixture after the incubation. Of three different soluble factors necessary for glyceride formation, ATP appeared to be the most important from a regulatory point of view. Thus the soluble fraction of liver homogenate from a starved rat was shown to contain suboptimal concentrations of ATP. Addition of physiological amounts of ATP to the 20,000 X g supernatant fluid of homogenate of liver of starved rats had the same effect as addition of 100, 000 X g supernatant fluid from liver homogenate of control rats, i.e. decrease in omega oxidation and increase in formation of glycerides. Addition of sn-glycerol 3-phosphate and CoA-SH in amounts optimal for glyceride formation to the 20,000 X g supernatant fluid of liver homogenate of starved rats had only small effects on omega oxidation and glyceride formation. The results are consistent with a competition for free fatty acids between the acyl-CoA synthetases involved in biosynthesis of glycerides and the microsomal hydroxylase(s) involved in omega oxidation of fatty acids. The concentration of ATP in the soluble fraction is of importance in this competition. The possibility is discussed that this competition is of importance also under in vivo conditions and that a decreased rate of esterification in the starved state is responsible for the higher excretion of omega-oxidized fatty acids in urine in the ketotic state.
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PMID:On the mechanism of regulation of omega oxidation of fatty acids. 95 85

Under starvation conditions, rhodopsin-containing halobacteria show a light-accelerated death under aerobic conditions. This is attributed to photooxidative processes. Under anaerobic conditions, halobacteria die rapidly in the dark, and light prevents death. Since it has been shown by others that lightdriven ATP synthesis can occur under anaerobic conditions, it is postulated that rhodopsin-mediated photophosphorylation is of survival value for this organism in the brines in which it lives, especially because the solubility of oxygen is low in highly saline waters and anaerobic conditions can often develop.
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PMID:Some effects of light on the viability of rhodopsin-containing halobacteria. 96 70


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