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

High-field pulsed Fourier-transform nuclear magnetic resonance spectroscopy (NMR) was used to quantify the adenylate levels of sea anemones (Aiptasia pulchella) with and without symbiotic dinoflagellates (Symbiodinium sp.). Animals were fed to repletion, then starved in darkness for up to six days before collection of in vivo NMR spectra. The host adenylate ratio of ATP: (ATP + ADP) declined significantly with increasing periods of starvation in both symbiotic and aposymbiotic hosts (P less than 0.05). However, the decline in the animal adenylate ratio was significantly more rapid in animals bearing symbiotic algae (P less than 0.05). This suggests that symbiotic algae in darkness cause more rapid depletion of host energy reserves, possibly by drawing on host pools of organic substrates. In vivo NMR spectroscopy was also used to evaluate the effect on A. pulchella of photosynthesis by zooxanthellae. Symbiotic anemones were fed to repletion, then starved under high irradiance (300 to 320 mu Ein m-2 s-1) or low irradiance (70 to 80 mu Ein m-2 s-1) conditions for up to five days. The host adenylate ratio declined significantly (P less than 0.01) with starvation under both treatments, but no significant difference was detected between treatments (P greater than 0.35). Blotted wet weight of anemones under high and low irradiance declined by 50% over eight days of starvation, but there was no significant difference in the rate of weight loss by anemones in the two treatments. There results suggest that translocation of photosynthate from symbiotic zooxanthellae does not significantly affect host adenylate ratio or have a sparing effect on host biomass during starvation in this symbiotic sea anemone.
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PMID:Impact of symbiotic algae on sea anemone metabolism: analysis by in vivo 31P nuclear magnetic resonance spectroscopy. 287 64

ADP-ribosyl transferase (ADPRT) is a DNA-dependent chromatin-associated enzyme which covalently attaches ADP-ribose moieties derived from NAD+ to protein acceptors to form poly(ADP-ribose). ADPRT activity is strongly stimulated by breaks in DNA, and it is suggested that its activity is required for efficient DNA excision repair. In this paper, a cell-cycle-dependent fluctuation of basal ADPRT activity was demonstrated by measuring it in permeabilized FL cells. The cell used was subjected to arginine starvation for 48 h before being released from the block by replacement of deficient medium with complete medium and cells in different proliferating stages were traced by [3H]TdR pulse labelling and obtained at different intervals after block release. The peak basal ADPRT activity appeared 4-6 h after the appearance of the peak of DNA synthesis. After treating the cells with MNNG (10(-4) M), MMS (10(-3)-10(-4) M) and 4NQO (10(-5) M) for 90 min just after release of the block, the ADPRT activity was markedly stimulated. It was further demonstrated that the effects of MNNG/4NQO and cell cycle influence on the level of poly(ADP-ribose) synthesis appear to be additive. While concerning MMS, quite a different pattern of ADPRT stimulation in the cell cycle was demonstrated, i.e., the activity of ADPRT stimulation of 10(-3) M MMS was found to be completely dependent on the basal ADPRT activity. In the cells with the highest basal ADPRT activity 12 h after block release, the MMS-induced ADPRT stimulation could not be observed. It was suggested that more than one pathway might be present in ADPRT stimulation induced by DNA-damaging chemicals, and the cells synchronized in late G1 stage might be the most suitable for demonstrating poly(ADP-ribose) synthesis after DNA damage.
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PMID:Cell cycle effects on the basal and DNA-damaging-agent-stimulated ADPRT activity in cultured mammalian cells. 308 45

The quantitative determination of adenyl nucleotides based on the separation of their dansyl derivatives by thin layer chromatography has made it possible to study the dynamics of changes in the pool of ATP, ADP and AMP in Escherichia coli K-12 during its synchronous growth after glucose starvation. The energy parameters (the adenylate pool, energy charge, teh ATP/ADP ratio, the rates of oxygen uptake and ATP generation, the economic coefficients of oxygen and ATP utilization) were compared with changes in the growth characteristics (the rate of growth and biomass concentration). This comparison allowed the authors to draw the conclusion about the uncoupled constructive and energy metabolism and about the possible regulatory role of energy parameters in the synchronised culture growth.
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PMID:[Energy aspects of the growth of Escherichia coli synchronized by starvation]. 329 94

The effects of riboflavin deficiency on mitochondrial and peroxisomal substrate oxidation were examined in young (treatment begun at weaning) and adult Sprague-Dawley rats that were fed diets low and high in fat. State 3 respiration rates (ADP-stimulated) were used as an estimate of mitochondrial oxidation rates. The oxidation of palmitoyl-CoA and palmitoylcarnitine, and to a lesser extent, glutamate, pyruvate and succinate, by hepatic mitochondria isolated from the young rats was depressed with riboflavin deficiency. There was no effect of dietary fat level on mitochondrial substrate oxidation. Carnitine palmitoyltransferase-A (CPT-A) Vmax was increased with riboflavin deficiency and with increasing dietary fat. Cyanide-insensitive palmitoyl-CoA oxidation was used to estimate peroxisomal palmitate oxidation. Expressed as total hepatic capacity, peroxisomal palmitate oxidation was depressed with riboflavin deficiency. This effect was the result of the reduced feed intake rather than riboflavin deficiency per se. Increasing dietary fat resulted in increased peroxisomal palmitate oxidation. Starvation of young rats did not change mitochondrial oxidation rates, although riboflavin-deficient starved rats exhibited increased rates of palmitoyl-CoA oxidation as well as increased CPT-A Vmax. In adult rats, after 5 wk of deficiency, only palmitoyl-CoA and palmitoylcarnitine oxidation rates were depressed. Dietary fat level did not interact with riboflavin deficiency. However, CPT-A Vmax was increased with riboflavin deficiency and with increased dietary fat level. Further, depressed hepatic fatty acid oxidation can occur in adult rats as a sequel to the feeding of riboflavin-deficient diets.
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PMID:Hepatic mitochondrial and peroxisomal oxidative capacity in riboflavin deficiency: effect of age, dietary fat and starvation in rats. 377 26

Starvation of the mouse hepatoma cell line Hepa for an essential amino acid (Trp, His, Leu, Ile or Phe) stimulated the incorporation of [3H]adenosine as ADP-ribose monomer into an 80,000-Mr protein, P80. Two-dimensional electrophoresis of Hepa proteins showed that P80 was the only protein labeled under starvation conditions. Time course experiments showed that the ADP-ribosylation of P80 was a consequence rather than the cause of reduced translational activity. Cycloheximide treatment and incubation at reduced temperatures also reduced the rate of protein synthesis and stimulated the ADP-ribosylation of P80. Starvation-dependent ADP-ribosylation of P80 was shown to occur in three other cell lines (Chang, Neuro-2a, and chick comb fibroblasts).
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PMID:Translational control of ADP-ribosylation in eucaryotic cells. 379 12

In incubated colonocytes isolated from rat colons, the rates of utilization O2, glucose or glutamine were linear with respect to time for over 30 min, and the concentrations of adenine nucleotides plus the ATP/ADP or ATP/AMP concentration ratios remained approximately constant for 30 min. Glutamine, n-butyrate or ketone bodies were the only substrates that caused increases in O2 consumption by isolated incubated colonocytes. The maximum activity of hexokinase in colonic mucosa is similar to that of 6-phosphofructokinase. Starvation of the donor animal decreased the activities of hexokinase and 6-phosphofructokinase, whereas it increased those of glucose-6-phosphatase and fructose-bisphosphatase. Isolated incubated colonocytes utilized glucose at about 6.8 mumol/min per g dry wt., with lactate accounting for 83% of glucose removed. These rates were not affected by the addition of glutamine, acetoacetate or n-butyrate, and starvation of the donor animal. Isolated incubated colonocytes utilized glutamine at about 5.5 mumol/min per g dry wt., which is about 21% of the maximum activity of glutaminase. The major end-products of glutamine metabolism were glutamate, aspartate, alanine and ammonia. Starvation of the donor animal decreased the rate of glutamine utilization by colonocytes, which is accompanied by a decrease in glutamate formation and in the maximum activity of glutaminase. Isolated incubated colonocytes utilized acetoacetate at about 3.5 mumol/min per g dry wt. This rate was not markedly affected by addition of glucose or by starvation of the donor animal. When colonocytes were incubated with n-butyrate, both acetoacetate and 3-hydroxybutyrate were formed, with the latter accounting for only about 19% of total ketones produced.
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PMID:Fuel utilization in colonocytes of the rat. 407 34

1. Glucose uptake or glucose formation has been studied in kidney cortex slices to investigate metabolic control of phosphofructokinase and fructose-diphosphatase activities. 2. Glucose uptake is increased and glucose formation is decreased by anoxia, cyanide or an uncoupling agent. Under these conditions the intracellular concentrations of glucose 6-phosphate and ATP decreased whereas that of fructose diphosphate either increased or remained constant, and the concentrations of AMP and ADP increased. 3. Glucose uptake was decreased, and glucose formation from glycerol or dihydroxyacetone was increased, by the presence of ketone bodies or fatty acids, or after starvation of the donor animal. Under these conditions, the concentrations of glucose 6-phosphate and citrate were increased, whereas those of fructose diphosphate and the adenine nucleotides were unchanged (see also Newsholme & Underwood, 1966). 4. It is concluded that anoxia and cell poisons increase glucose uptake and decrease gluconeogenesis by stimulating phosphofructokinase and inhibiting fructose diphosphatase, whereas ketone bodies, fatty acids or starvation increase gluconeogenesis and decrease glucose uptake through the citrate inhibition of phosphofructokinase.
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PMID:Control of glycolysis and gluconeogenesis in rat kidney cortex slices. 429

1. The ratio [ATP]/[ADP][P(i)], as measured by direct determination of the three components in rat liver, was found in various nutritional states to have approximately the same value as the ratio [ATP]/[ADP][P(i)] calculated from the concentrations of lactate, pyruvate, glyceraldehyde phosphate and 3-phosphoglycerate on the assumption that lactate dehydrogenase, glyceraldehyde phosphate dehydrogenase and 3-phosphoglycerate kinase are at near-equilibrium in the liver. This implies that the redox state of the NAD couple in the cytoplasm is linked to, and partially controlled by, the phosphorylation state of the adenine nucleotides. 2. The combined equilibrium constant of the glyceraldehyde 3-phosphate dehydrogenase and 3-phosphoglycerate kinase reactions at 38 degrees C and I0.25, was found to be 5.9x10(-6). 3. The fall of the [NAD(+)]/[NADH] ratio in starvation and other situations is taken to be the consequence of a primary fall of the [ATP]/[ADP][HPO(4) (2-)] ratio.
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PMID:Equilibrium relations between the cytoplasmic adenine nucleotide system and nicotinamide-adenine nucleotide system in rat liver. 431 32

1. The intracellular location and maximal activities of enzymes involved in phosphoenolpyruvate synthesis have been investigated in pigeon liver. Enolase and pyruvate kinase were cytoplasmic, and the activities were 50-60 and 180-210mumoles/min./g. dry wt. at 25 degrees respectively. Phosphoenolpyruvate carboxykinase was present exclusively, and nucleoside diphosphokinase predominantly, in the mitochondria; the particles had to be disrupted to elicit maximal activities, which were 27-33 and 400-600mumoles/min./g. dry wt. at 25 degrees respectively. The activities of all four enzymes did not change significantly during 48hr. of starvation. 2. Conditions for incubation of washed isolated mitochondria were established, to give high rates of synthesis of phosphoenolpyruvate, linear with time and proportional to mitochondrial concentration. Inorganic phosphate and added adenine nucleotides were stimulatory, whereas added Mg(2+) inhibited, partly owing to activation of contaminant pyruvate kinase. Phosphoenolpyruvate formation occurred from oxaloacetate, malate, fumarate, succinate, alpha-oxoglutarate and citrate, in decreasing order of effectiveness. 3. The steady-state ATP/ADP ratio of mitochondrial suspensions was decreased in the presence of added 2.5mm-Mg(2+) (owing to stimulation of adenylate kinase and possibly of an adenosine triphosphatase), 0.5mm-Ca(2+) or 0.4mm-dinitrophenol. In each case the rate of substrate removal and oxygen uptake was increased, whereas phosphoenolpyruvate synthesis was inhibited. Citrate formation was enhanced, owing to de-inhibition of citrate synthase. These effects were not primarily related to changes in the oxaloacetate concentration. 4. Both phosphoenolpyruvate carboxykinase and nucleoside diphosphokinase were active within the atractylosidesensitive barrier to the mitochondrial metabolism of added adenine nucleotides. There was no correlation between the rate of substrate-level phosphorylation associated with the oxidation of alpha-oxoglutarate, and the synthesis of phosphoenolpyruvate. 5. The results suggest that phosphoenolpyruvate formation in pigeon-liver mitochondria is regulated partly by the phosphorylation state of the adenine and guanine nucleotides, and partly by variations in the oxaloacetate concentration, all in the mitochondrial matrix. 6. Phosphoenolpyruvate is assumed to be the metabolite transported from the mitochondria to the cytoplasm during gluconeogenesis from oxaloacetate in pigeon liver.
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PMID:The regulation of phosphoenolpyruvate synthesis in pigeon liver. 496 63

1. A comparison was made of the effects of starvation on available cellular energy in two crayfish species which possess different inherent metabolic rates associated with habitat adaptations. 2. Starvation for 45 days did not significantly lower phosphoadenylate concentrations or adenylate energy charge [AEC = (ATP + 1/2 ADP)/(ATP + ADP)] in dorsal tail muscle of either the epigean (surface) crayfish. Procambarus clarkii or the cave species, Orconectes inermis inermis. 3. After 5, 15 and 30 days of starvation, P. clarkii contained greater ATP and total adenylate concentrations in dorsal tail muscle than control crayfish which were fed. 4. The greater phosphoadenylate concentrations in unfed crayfish may be associated with increased motor activity previously documented in another surface crayfish species under conditions of starvation. 5. However, starvation did not induce changes in adenylate concentrations in O. i. inermis. 6. This could be due to the lack of sufficient nutritional stress to elicit a response in this more slowly metabolizing species.
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PMID:The effects of starvation on muscle phosphoadenylate concentrations and adenylate energy charge of surface and cave crayfish. 612 Jul 79


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