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

Changes in haematocrit values were studied in hypoxaemic chronic bronchitis patients subjected to oxygen-therapy. A statistically significant decrease was observed in all cases after respiration of oxygen. This was partly attributable to resolution of vasoconstrictive reflexes imposed by prior oxygen starvation, due to shifting of part of the circulating mass from the systemic to the pulmonary circulation, and partly to improved ventilation yield; this, couplled with reduced cardiac frequency and output, facilitates a more efficient thoracic aspiration of the reflux blood.
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PMID:[Effects of oxygen therapy on the hematocrit value in hypoxemic, chronic bronchopneumopathies]. 444 23

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

Hydrogenomonas facilis and H. eutropha cultured in fructose medium retained high levels of ribulose-1,5-diphosphate carboxylase only when the following conditions were fulfilled: low aeration, FeCl(3) addition to fructose medium, and cell harvest at or prior to mid-exponential phase of growth. Repression of carboxylase synthesis was demonstrated under conditions of high oxygen tension during growth of H. eutropha on fructose. Upon depletion of fructose in the growth medium, carboxylase activity fell abruptly in both organisms. The decline could not be attributed to a repressive mechanism. Rapid inactivation of carboxylase was promoted by transfer of mid-exponential-phase H. eutropha to a basal salts medium lacking fructose. During severe fructose starvation, N(2), H(2), 80% H(2) to 20% air, 2,4-dinitrophenol, actinomycin D, streptomycin, bicarbonate, and magnesium ion deficiency spared carboxylase. Nitrogen starvation or chloramphenicol afforded no protection during severe starvation. In vitro inactivation was also demonstrated in crude cell-free extracts from nonstarved, fructose-grown H. eutropha. Substrate bicarbonate protected against this loss. Inactivation of the carboxylase could not be demonstrated either by starvation of autotrophically grown cells or in autotrophic extracts. Autotrophic extracts mixed with heterotrophic extracts lost their carboxylase activity, but mixing with heterotrophic extracts that had been heated to 50 C resulted in no loss of activity. Mechanisms are proposed to accommodate these observations.
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PMID:Factors affecting the synthesis and degradation of ribulose-1,5-diphosphate carboxylase in Hydrogenomonas facilis and Hydrogenomonas eutropha. 496 35

Cell-free extracts with high nitrogenase activity were prepared by sonic oscillation and French press treatment from the blue-gree alga Anabaena cylindrica. Extracts were prepared from cells grown on a 95% N(2)-5% CO(2) gas mixture followed by a period of nitrogen starvation under an atmosphere of 95% argon-5% CO(2). No increase in the specific activity of extracts was achieved by breaking heterocysts. Activity (assayed by acetylene reduction) was found to be dependent on adenosine triphosphate (ATP), an ATP-generating system, and a low-potential reductant. Na(2)S(2)O(2) employed as reductant supports higher rates of nitrogenase activity than reduced ferredoxin. The activity is associated with a small-particle fraction that can be sedimented by ultracentrifugation. In contrast to the particulate nitrogenase of Azotobacter, which is stable in air, the A. cylindrica nitrogenase is an oxygen sensitive as nitrogenase prepared from anaerobic bacteria.
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PMID:Nitrogenase activity in cell-free extracts of the blue-green alga, Anabaena cylindrica. 499 40

Forearm muscle metabolism was studied in eight obese subjects after an overnight, 3 and 24 day fast. Arterio-deep-venous differences of oxygen, carbon dioxide, glucose, lactate, pyruvate, free fatty acids, acetoacetate, and beta-hydroxybutyrate with simultaneous forearm blood flow were measured. Rates of metabolite utilization and production were thus estimated. Oxygen consumption and lactate and pyruvate production remained relatively constant at each fasting period. Glucose, initially the major substrate consumed, showed decreased consumption after 3 and 24 days of fasting. Acetoacetate and beta-hydroxybutyrate consumption after an overnight fast was low. At 3 days of fasting with increased arterial concentrations of acetoactate and beta-hydroxybutyrate, consumption of these substrates rose dramatically. At 24 days of fasting, despite further elevation of arterial levels of acetoacetate and beta-hydroxybutyrate, the utilization of acetoacetate did not increase further and if anything decreased, while five out of eight subjects released beta-hydroxybutyrate across the forearm. Acetoacetate was preferentially extracted over beta-hydroxybutyrate. At 24 days of starvation, free fatty acids were the principal fuels extracted by forearm muscle; at this time there was a decreased glucose and also ketone-body consumption by skeletal muscle.
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PMID:Human forearm metabolism during progressive starvation. 509 67

1. The rates of oxygen consumption were measured in 6-8-day-old rabbits at 34 and 15 degrees C after varying periods of starvation and cold exposure. At the start of the experiment the rabbits had been fasted for 24 hr. Eight rabbits were studied immediately, six after 24 and six after 48 hr in a cold environment (20 degrees C), and twelve after a further 48 hr in a warm environment (34 degrees C). All the animals had a similar increase in oxygen consumption during the final hour of cold exposure (15 degrees C).2. The rabbits kept at 20 degrees C lost 83% of the fat stored in their brown adipose tissue within 24 hr and a further 11% in the next 24 hr. The fat content of white adipose tissue had fallen by 75% at 48 hr. In contrast rabbits kept unfed at 34 degrees C had lost 47% of the fat in brown adipose tissue and 44% of the fat in white adipose tissue after 48 hr.3. In six rabbits subcutaneous thermocouples demonstrated that local heat production continued in brown adipose tissue after 48 hr cold exposure.4. In the rabbits kept at 34 degrees C the final cold exposure caused a large increase in the serum free fatty acid and glycerol concentrations. Much lower concentrations were found in rabbits kept at 20 degrees C.5. The results show that the fat stored in the brown adipose tissue of young rabbits exposed to cold is preferentially used for heat production. When this store of fat is exhausted, brown adipose tissue still produces heat presumably by oxidizing fat and glucose taken from the circulation.
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PMID:Fat metabolism and heat production in young rabbits. 534 20

1. 3-Hydroxybutyrate dehydrogenase (EC 1.1.1.30) activities in sheep kidney cortex, rumen epithelium, skeletal muscle, brain, heart and liver were 177, 41, 38, 33, 27 and 17mumol/h per g of tissue respectively, and in rat liver and kidney cortex the values were 1150 and 170 respectively. 2. In sheep liver and kidney cortex the 3-hydroxybutyrate dehydrogenase was located predominantly in the cytosol fractions. In contrast, the enzyme was found in the mitochondria in rat liver and kidney cortex. 3. Laurate, myristate, palmitate and stearate were not oxidized by sheep liver mitochondria, whereas the l-carnitine esters were oxidized at appreciable rates. The free acids were readily oxidized by rat liver mitochondria. 4. During oxidation of palmitoyl-l-carnitine by sheep liver mitochondria, acetoacetate production accounted for 63% of the oxygen uptake. No 3-hydroxybutyrate was formed, even after 10min anaerobic incubation, except when sheep liver cytosol was added. With rat liver mitochondria, half of the preformed acetoacetate was converted into 3-hydroxybutyrate after anaerobic incubation. 5. Measurement of ketone bodies by using specific enzymic methods (Williamson, Mellanby & Krebs, 1962) showed that blood of normal sheep and cattle has a high [3-hydroxybutyrate]/[acetoacetate] ratio, in contrast with that of non-ruminants (rats and pigeons). This ratio in the blood of lambs was similar to that of non-ruminants. The ratio in sheep blood decreased on starvation and rose again on re-feeding. 6. The physiological implications of the low activity of 3-hydroxybutyrate dehydrogenase in sheep liver and the fact that it is found in the cytoplasm in sheep liver and kidney cortex are discussed.
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PMID:Ketone body and fatty acid metabolism in sheep tissues. 3-Hydroxybutyrate dehydrogenase, a cytoplasmic enzyme in sheep liver and kidney. 548 53

1. In rabbits kept unfed for 4 or 24 or 48 hr after delivery by Caesarean section at term, noradrenaline infusion (I.V. for 30 min) caused a similar increase in oxygen consumption but the increase in serum free fatty acid concentration was greatest in rabbits kept unfed for 48 hr.2. The brown adipose tissue of anaesthetized rabbits under 3 hr old took glucose from the circulation but did not release fatty acids. In similar rabbits noradrenaline infusion stimulated the tissue to generate heat, but there was no release of fatty acids even though the rate of triglyceride hydrolysis was high (as judged by the rate of glycerol release).3. In rabbits kept unfed for 48 hr from birth in a warm environment, brown adipose tissue released small amounts of fatty acids but continued to take glucose from the circulation. Heat production in response to noradrenaline infusion was accompanied by an increased release of fatty acids. The fat content of the brown adipose tissue did not fall with starvation.4. The mean serum insulin concentration of rabbits at birth was 54 muu./ml. compared to 23 muu./ml. in the mother. In new-born rabbits kept unfed for 48 hr the insulin concentration had fallen to 14 muu./ml.5. It is concluded (i) that at birth brown adipose tissue has the capacity to generate heat but the tissue is slow to release its stores of fat in response to starvation, (ii) that brown adipose tissue has a high rate of glucose uptake even during starvation and (iii) that the high circulating concentration of insulin may be responsible for the tissue's slow adaptation to the demands of starvation.
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PMID:Brown adipose tissue metabolism in vivo and serum insulin concentrations in rabbits soon after birth. 557 36

Liver homogenates of avian species, but not of mammals, form glycogen from glucose, mannose, fructose and galactose. Incorporation of labelled glucose, fructose and mannose, but not of labelled galactose, into glycogen is diluted isotopically by unlabelled glucose. Except for fructose, glycogen formation from other substrates by pigeon liver homogenates compares favourably with that from the same substrates in pigeon liver slices. Optimum conditions for glycogen synthesis from glucose by pigeon liver homogenate are: medium of incubation, 0.175m-sucrose-45mm-potassium chloride-15mm-glycylglycine buffer, pH7.5; concentration of substrate, 15mm; concentration of tissue, less than 120mg./ml.; temperature of incubation, 37-43 degrees ; atmosphere, oxygen. Uncouplers of oxidative phosphorylation, Ca(2+), EDTA, PP(i), 2-deoxyglucose 6-phosphate and microsomal fraction of rat liver are inhibitory to glycogen synthesis from glucose. Starvation of pigeons for 24 and 48hr. leads to a slight stimulation of glycogen synthesis in their liver homogenates as compared with fed controls. Pigeon liver homogenates can be separated into subcellular fractions that on reconstitution can synthesize glycogen. All the enzymes of the glycogen pathway except soluble high-K(m) glucokinase are present in pigeon liver.
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PMID:Studies on glycogen synthesis in pigeon liver homogenates. Incorporation of hexose into glycogen. 558 93

1. The effect of semistarvation and complete starvation (sufficient to produce a loss of about 32 and 25% respectively of initial body weight) on the active transport of L-glucose has been studied by the use of sacs of everted mid-small intestine of rats. The animals were allowed free access to water.2. Sacs from animals on a restricted diet transported L-glucose against its concentration gradient, but sacs from fully fed rats did not. Even when sacs from fully fed rats were distended sufficiently to cause them to lose serosal volume, the L-glucose concentration in the final serosal fluid was never greater than that in the final mucosal fluid.3. The L-glucose active transport was independent of net water movement, needed oxygen, was not demonstrable at 27 degrees C, and required Na ions at a concentration of 83 mM or greater. It could be completely inhibited by 10(-6)M phlorrhizin, or 10 mM L-histidine, or 1.39 mM D-glucose. Phlorrhizin at a concentration of 10(-8)M reduced, but did not prevent, L-glucose active transport.4. It seems probable that L-glucose active transport is mediated by the mechanism that actively transports D-glucose.5. Un-incubated mid-small intestine of fully fed rats contained 37.8 mg D-glucose/100 g wet wt. of tissue, whereas semistarved intestine had only 10.8 mg D-glucose/100 g. The lack of demonstrable active transport of L-glucose by normal intestine may possibly have been caused, at least in part, by inhibition of the process by endogenous D-glucose.6. There appeared to be no metabolism of L-glucose by rat intestine, nor conversion to the D-form.7. The hypothesis that sugars require the D-pyranose ring structure for active absorption is no longer tenable.
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PMID:Active transport of L-glucose by isolated small intestine of the dietary-restricted rat. 568 90


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