Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0038187 (starvation)
 24,951 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The total activity of pyruvate dehydrogenase (PDH) complex in rat hind-limb muscle mitochondria was 76.4 units/g of mitochondrial protein. The proportion of complex in the active form was 34% (as isolated), 8-14% (incubation with respiratory substrates) and greater than 98% (incubation without respiratory substrates). Complex was also inactivated by ATP in the presence of oligomycin B and carbonyl cyanide m-chlorophenylhydrazone. Ca2+ (which activates PDH phosphatase) and pyruvate or dichloroacetate (which inhibit PDH kinase) each increased the concentration of active PDH complex in a concentration-dependent manner in mitochondria oxidizing 2-oxoglutarate/L-malate. Values giving half-maximal activation were 10 nM-Ca2+, 3 mM-pyruvate and 16 microM-dichloroacetate. Activation by Ca2+ was inhibited by Na+ and Mg2+. Mitochondria incubated with [32P]Pi/2-oxoglutarate/L-malate incorporated 32P into three phosphorylation sites in the alpha-chain of PDH; relative rates of phosphorylation were sites 1 greater than 2 greater than 3, and of dephosphorylation, sites 2 greater than 1 greater than 3. Starvation ( 48h ) or induction of alloxan-diabetes had no effect on the total activity of PDH complex in skeletal-muscle mitochondria, but each decreased the concentration of active complex in mitochondria oxidizing 2-oxoglutarate/L-malate and increased the concentrations of Ca2+, pyruvate or dichloracetate required for half-maximal reactivation. In extracts of mitochondria the activity of PDH kinase was increased 2-3-fold by 48 h starvation or alloxan-diabetes, but the activity of PDH phosphatase was unchanged.
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PMID:Reversible phosphorylation of pyruvate dehydrogenase in rat skeletal-muscle mitochondria. Effects of starvation and diabetes. 633 93

The effects of starving, refeeding, and restarving rats for different periods on content of sarcoplasmic and contractile proteins and on activity of the Ca2+-dependent proteinase (CAF) in skeletal muscle was determined. Groups of five to six male rats, 8 to 11 weeks old, were starved up to 8 days, refed up to 6 days, and in two experiments, restarved up to 10 days. CAF activity was assayed in P 0-45 crude CAF fractions prepared so as to remove a protein inhibitor of CAF; the assays were demonstrated to be specific for CAF. Sarcoplasmic protein content of rat skeletal muscle changed little until after 6 days of restarvation when it decreased to 68-89% of control level (P less than 0.05). Contractile protein content decreased to 65% of control level (P less than 0.01) after 8 days of starvation, remained at this level for 4 days of refeeding, then increased to approximately 80% of control level after 6 days of refeeding, remained at this level for 2 days of restarvation, and then decreased to approximately 65% of control level (P less than 0.01) after 6 and 8 days of restarvation. Muscle CAF activity did not change during the first 8 days of starvation but increased to 113% above control level (P less than 0.01) after 6 days refeeding and then decreased to only 29% of control level (P less than 0.01) after 8 days of restarvation. These changes in muscle CAF activity are consistent with the proposed role for CAF in initiating metabolic turnover of contractile proteins, but because actual measurements of myofibrillar protein were not made and because in vivo CAF activity is difficult to assess, they do not prove this role for CAF nor do they exclude participation of other proteinases.
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PMID:Effect of starvation and refeeding on activity of a Ca2+-dependent protease in rat skeletal muscle. 633 41

The capacity of Amoeba proteus to form pinocytotic channels after pretreatment with either puromycin, cycloheximide, emetine or a long period of starvation was studied. The effect on pinocytosis of the three inhibitors of protein synthesis was similar. They preferentially affected pinocytosis induced by Na+ with little effect on K+-induced pinocytosis. In Ca2+-deficient media, Na+-induced pinocytosis was inhibited, while the addition of Ca2+ restored channel formation. The degree of inhibition of Na+-induced pinocytosis was influenced by the concentration of Ca2+ in the inducing solution. Selective Ca2+-reversible inhibition of Na+-induced pinocytosis also occurred after starvation or treatment with a proteolytic enzyme, subtilisin. The membrane potential in starved or emetine-treated cells in culture medium was normal and their depolarising response to inducers was not diminished in solutions containing Na+. The resting input resistance of these cells was higher than in normal amoebae, but no significant difference in electrical parameters was observed after pinocytosis was induced. It is suggested that starvation, inhibition of protein synthesis, and enzyme digestion deplete the membrane of structures which are necessary for normal Ca2+ functions during induction of pinocytosis by Na+-like inducers.
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PMID:Selective inhibition of calcium-stimulated cation-induced pinocytosis by starvation and inhibitors of protein synthesis in Amoeba proteus. 638 52

The presence of high phosphoenolpyruvate carboxykinase (EC 4.1.1.32) activity in mouse islet cytosol has been demonstrated. The enzyme was activated by Mn2+ with a Ka of 100 X 10(-6) mol/l. The mean total activity of the Mn2+-stimulated phosphoenolpyruvate carboxykinase in islet cytosol estimated at 22 degrees C with saturating concentrations of the substrates oxaloacetate and ITP was 146 pmol/min per micrograms DNA. Km was calculated to be 6 X 10(-6) mol/l for oxaloacetate and 140 X 10(-6) mol/l for ITP. The islet phosphoenolpyruvate carboxykinase activity was not increased after starvation of the animals for 48 h. Preincubation of the cytosol at 4 degrees C with Fe2+, quinolinate, ATP, Pi, glucose 6-phosphate, fructose 1,6-bisphosphate, NAD+, NADH, oxaloacetate, ITP, cyclic AMP and Ca2+ had no effect on the enzyme activity. However, preincubation of the cytosol at 37 degrees C with ATP-Mg inhibited the Mn2+-stimulated phosphoenolpyruvate carboxykinase activity progressively with time and in a concentration-dependent manner. A similar but weaker inhibitory effect was observed with p[NH]ppA, whereas p[CH2]ppA, ADP, AMP, adenosine and Pi had no effect. It is tentatively suggested that ATP and p[NH]ppA either by adenylation or otherwise affect the interaction between islet phosphoenolpyruvate carboxykinase and the recently discovered Mr = 29000 protein modulator of the enzyme in such a way - perhaps by causing a dissociation between them - that phosphoenolpyruvate carboxykinase loses its sensitivity to Mn2+ activation.
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PMID:Phosphoenolpyruvate carboxykinase in mouse pancreatic islets. ATP-induced changes in sensitivity to Mn2+ activation. 638 41

A colorimetric method for the determination of lipid phosphorus in the nanomolar range was used to determine the total phospholipid content of isolated pancreatic islets. Freshly isolated islets of lean C57BL/6J mice contained significantly more phospholipids expressed per micrograms DNA as compared to C57BL/6J (ob/ob) mouse or Wistar rat islets. Starvation for 48 h (Wistar rats) or 60 h (NMRI mice) did not affect the islet phospholipid content. Phosphatidylcholine was the most abundant phospholipid class of NMRI mouse islets, followed by phosphatidylethanolamine, sphingomyelin, phosphatidylinositol, phosphatidylserine and lysophosphatidylcholine. When islets of NMRI mice were maintained for 5-7 days in tissue culture, the phospholipid content remained unchanged as compared to that of freshly isolated islets despite a considerable loss of the insulin stores. The islet phospholipid content was significantly increased when the glucose concentration of the culture medium was elevated from 3 to 28 mM. Leucine (10 mM) added to a low-glucose medium failed to increase the islet phospholipid content. Addition of glipizide (2 microM) to the culture medium decreased the islet insulin content significantly but failed to affect the total islet phospholipid content. Culture in a Ca2+-free medium containing 28 mM glucose increased the islet insulin content but, again, the phospholipid content remained unaffected. These data show that changes of the total phospholipid content of pancreatic islets are unrelated to the islet insulin content and presumably also to the content of secretory granules. Alterations of the islet content of phospholipids may rather reflect changes of the amount of endoplasmic reticulum of the islet cells.
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PMID:Effects of starvation and different culture conditions on the phospholipid content of isolated pancreatic islets. 639 54

The Leeds facility for in vivo neutron activation analysis has been modified and calibrated for the simultaneous measurement of nitrogen, potassium, sodium, chlorine, phosphorus and calcium in obese patients weighing up to 210 kg. The effects of body size and shape were incorporated into the calibration by measuring 14 anthropomorphic phantoms of known composition representing individual patients being treated for obesity. The phantoms were constructed from tissue substitutes representing lean, skeletal and adipose tissues, arranged to simulate the distributions of the corresponding tissues within the patients, as visualised by CT scanning. The precision of the method, determined by measuring a single phantom ten times over a period of ten weeks, is between two and three per cent for all elements except calcium, for which it is 11.3%. Accuracy is estimated to be similar to precision. The procedure has been used to study changes in body composition of patients undergoing therapeutic starvation.
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PMID:Multi-element analysis of the obese subject by in vivo neutron activation analysis. 646 4

Anion transport across the red cell membrane has been measured as sulfate self-exchange flux (Ja) in fresh and metabolically depleted human red cells. Depletion of metabolic stores by a starvation of the cells decreases Ja by 50%. A similar effect was observed when ATP was acutely and selectively depleted by iodoacetamide. This inhibition was independent of the presence of calcium and reversible after metabolic rejuvenation of the cells. Ghosts prepared from fresh red cells exhibited the same value of Ja as fresh red cells. By contrast, ghosts prepared from depleted red cells exhibited a decrease in Ja which was reverted by a physiological concentration of ATP. The effect of ATP was dependent on its concentration (Km approximately 40 microM) and on the duration of the metabolic depletion: complete restoration of Ja was obtained only in ghosts prepared from red cells acutely depleted of ATP by a 2 h incubation with iodoacetamide. After a 20 h starvation, Ja restoration was never more than 80%. We postulate that ATP acts primarily through the phosphorylation of band 3 protein, the anion exchanger; it acts also through the stabilization of the normal organization of the membrane. This latter effect may involve the phosphorylation of membrane components, but also a direct interaction, as shown by the influence of other organic phosphates (2,3-diphosphoglycerate and inositol hexaphosphate) on Ja in the absence of ATP.
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PMID:Organic phosphates modulate anion self-exchange across the human erythrocyte membrane. 648 27

The effects of Mg2+ and Ca2+ deprivation on survival and growth of normal and transformed cultured cells were studied. Normal fibroblast from several origins (mouse, hamster and human) did not grow in 2 microM Mg2+ medium, whereas transformed fibroblasts (mouse and rat) and tumor cells of other types (mouse adrenocortical and rat glial cells) grew optimal. All transformed or tumorogenic cells that showed low growth requirement for Mg2+ were able to develop colonies in agarose suspension cultures, i.e., were anchorage-independent fo growth. Mg2+ deprivation of normal cells did not lead to cell cycle arresting at G0/G1 and cell death accounts for the limited growth of these cells in medium containing low Mg2+ concentration. Contrary to Mg2+, starvation for serum or for Ca2+ caused normal cells to undergo cell cycle arrest at the G0/G1 phase. During the progressive spontaneous transformation of Swiss mouse 3T3 fibroblasts, the decrease in growth requirements for Mg2+ and Ca2+ do not occur at the same time. The requirement for external Ca2+ lowers before the onset of anchorage-independent growth while the Mg2+ requirement only decreases after cells become anchorage-independent. Therefore the reductions in growth requirement for Mg2+ and Ca2+ that take place in cell transformation are not linked events.
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PMID:Ca2+ and Mg2+ requirements for growth are not concomitantly reduced during cell transformation. 670 40

Plasma and urine electrolytes were measured in five healthy non-obese young adults before, during and after a four-day period of total starvation (distilled water only). Plasma sodium, chloride and bicarbonate concentrations decreased in all subjects by a mean value of 4 mmol/l, whereas the sum of acetoacetate and hydroxybutyrate concentrations increased by 4-6 mmol/l. These changes occurred without alterations in the state of hydration or vascular volume. Hydroxybutyrate and ammonium ions became the main urinary ions during starvation, whereas sodium and chloride, which were quantitatively the most important urinary electrolytes before starvation, decreased four-fold, and potassium two-fold. Plasma zinc concentrations rapidly increased in all subjects by a mean of 4 mumol/1 (25%) and returned to normal on refeeding. The excretion of zinc in urine trebled and continued to rise on refeeding. There were no major changes in the excretion of calcium, magnesium, phosphate or sulphate during the starvation period. From knowledge of the intracellular concentrations of various minerals and extent of breakdown of lean tissues (N excretion), it is suggested that most of the urinary calcium, magnesium and phosphate probably originates from bone, and that the amount of zinc in urine is only a small fraction of that which is likely to be released from the breakdown of lean tissues. It is also suggested that the continued excretion of zinc on refeeding is due to release of zinc from tissues which 'buffered' it during the starvation period. This study provides useful data in non-obese individuals with which to compare changes which occur in post-traumatic and post-infective starvation.
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PMID:Mineral metabolism during short-term starvation in man. 672 71

It is currently thought that lead is released from organic depots in response to internal or external stress to the organism. Using young Wistar rats, we were unable to confirm this view. Chronic lead levels, persisting over a period of 20 days, were achieved by the intraperitoneal injection of labelled (210Pb) lead acetate into rats (5 mg/kg body weight). The animals were divided into four groups. One group was maintained normally as a control, while two others were subjected to stress, i.e. starvation and injection of an autolysate of bacteria, respectively. All three of these groups showed identical behaviour with respect to total body radioactivity, femur radioactivity (representing the chief skeletal depot), and excretion of radioactivity. The fourth group received Na2Ca-EDTA (sodium salt of the calcium chelate of ethylenediaminetetraacetic acid). The decrease of total body radioactivity and femur radioactivity, and the relative excretion of 210Pb had almost levelled out by about 14 days, and was related mainly to the elimination of lead from the bones (in parenchymatous organs, the cell membrane forms a barrier to the therapeutic removal of intracellular lead). This illustrates the effectiveness of early treatment in lead poisoning, and the ineffectiveness of continuous therapy.
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PMID:[Elimination of lead from rats under biological stress, and application of Na2Ca-EDTA (author's transl)]. 677 29


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