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

The low calcium response of wild type Yersinia pestis, the causative agent of bubonic plague, and of enteropathogenic Yersinia pseudotuberculosis and Yersinia enterocolitica is known to be mediated by a shared Lcr plasmid of about 70 kb. At 37 degrees C in Ca2+-deficient medium, this element promotes restriction of growth with concomitant production of virulence functions including the common V antigen and a set of yersiniae outer membrane peptides termed YOPs (Lcr+). The latter are expressed by the enteropathogenic species but not by wild type Y. pestis which possesses a unique 10 kb Pst plasmid associated with pesticinogeny (Pst+). We show in this report that, after pulse with 35S-methionine, peptides with molecular weights corresponding to YOPs of 78, 47, 45, 44, 36, and 26 kDa are synthesized during the low calcium response by both Lcr+, Pst+ and Lcr+, Pst- cells of Y. pestis. Although stable in the latter, radioactivity in YOPs of wild type was rapidly chased into lower molecular weight degradation products. At least four soluble peptides, including V, were also labeled during starvation for Ca2+; these structures were stable in both Lcr+, Pst+ and Lcr+, Pst- yersiniae. These findings suggest that a product encoded by the Pst plasmid of Y. pestis is required for post-translational regulation of outer membrane but not soluble peptides mediated by a second unrelated Lcr plasmid.
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PMID:Post-translational regulation of Lcr plasmid-mediated peptides in pesticinogenic Yersinia pestis. 350 47

The influence of a physiologic range of palmitate concentrations (0, 0.25, 0.5, and 1.0 mmol/L) on glucose ability to modify insulin secretion, (U-14C) palmitate oxidation, and (U-14C) glucose incorporation into lipids has been studied in islets isolated from either fed or 48-hour starved rats. Palmitate potentiated the insulin response of fed islets to glucose in a particular dose-related manner. Glucose stimulated secretion was accompanied by a decreased palmitate oxidation and an increased (U-14C) glucose incorporation into di-, tri-acylglycerols, and predominantly into phospholipids. These metabolic parameters showed also a positive dependence on palmitate concentration. Starvation increased islet capacity to oxidize palmitate, rendered it insensitive to glucose inhibition, and inhibited both (U-14C) glucose incorporation into all lipid fractions and sugar induced insulin release. The stimulation of islet lipid synthesis by glucose seems to be limited by the exogenous supply of fatty acids and their rate of oxidation. As judged from (U-14C) glucose incorporation data, the rate of phospholipid biosynthesis showed a significant and positive correlation with insulin secretion. This metabolic pathway might provide islet cells with some lipid intermediates (diacylglycerol and/or specific phospholipids) that have been considered as possible mediators of the calcium messenger system.
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PMID:Glucose stimulation of insulin secretion in islets of fed and starved rats and its dependence on lipid metabolism. 351 58

The influence of Ca2+ on myofibrillar proteolysis was evaluated in the isolated extensor digitorum longus muscle incubated in vitro with agents previously shown to increase the intracellular concentration of Ca2+. Myofibrillar proteolysis was evaluated by measuring the release of N tau-methylhistidine, and total proteolysis was evaluated by measuring tyrosine release by incubated muscles after the inhibition of protein synthesis with cycloheximide. Incubated muscles released measurable quantities of N tau-methylhistidine, and muscle contents of the amino acids remained stable over 2 h of incubation. The release of N tau-methylhistidine by incubated muscles was similar to its release by perfused rat muscle in response to brief starvation, indicating the integrity of the incubated muscles. Ca2+ ionophore A23187, dibucaine, procaine, caffeine and elevated K+ concentration increased lactate release by incubated muscles and decreased tissue contents of ATP and phosphocreatine to varying degrees, indicating the metabolic effectiveness of the agents tested. Only A23187 and dibucaine increased total cell Ca2+, and they increased tyrosine release. Caffeine and elevated [K+] increased neither cell Ca2+ nor tyrosine release; however, only A23187 and dibucaine increased tyrosine release significantly. On the other hand, these agents were without effect on myofibrillar proteolysis as assessed by N tau-methylhistidine release by incubated muscles and changes in tissue contents of the amino acid. In fact, some of the agents tested tended to decrease myofibrillar proteolysis slightly. These results indicate that acute elevation of intracellular Ca2+ is associated with increased breakdown of non-myofibrillar but not myofibrillar proteins. Because of this, the role of elevated Ca2+ in muscle atrophy in certain pathological states is questioned. The data also indicate that the breakdown of myofibrillar and non-myofibrillar proteins in muscle is regulated independently and by different pathways, a conclusion reached in previous studies with perfused rat muscle.
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PMID:Differential effects of acute changes in cell Ca2+ concentration on myofibrillar and non-myofibrillar protein breakdown in the rat extensor digitorum longus muscle in vitro. Assessment by production of tyrosine and N tau-methylhistidine. 356 5

Dietary control of sodium intake was utilized in weanling rats to study the relationships among body growth, tissue composition and extracellular fluid volume (ECFV). Forty 3-wk-old rats were divided into groups receiving 30, 150, 300, 600 or 900 mu eq sodium/d for 5 wk. The minimal daily requirement for normal growth was 300 mu eq Na, or about 60 mu eq/g of new growth. Lower doses caused dose-related growth failure associated with a reduced ECFV. Analyses of carcass, muscle and bone composition were carried out. In sodium-deprived animals there was retarded growth of protoplasm, fat and bone; the mineral composition of muscle was not altered, whereas in bone calcium concentration was reduced. Plasma concentrations of sodium, potassium and chloride remained normal. Pair-feeding indicated that sodium-deficiency growth retardation could not be attributed to starvation. Sodium-deficient animals ingested a greater amount of food per gram of weight gain, possibly reflecting an increased energy expenditure. Sodium deprivation initially permitted protoplasmic growth to proceed at a rate disproportionate to that of the ECFV. Subsequently, both continued to grow at a reduced but similar rate, suggesting that ECFV may be a controller of protoplasmic growth.
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PMID:Sodium deprivation growth failure in the rat: alterations in tissue composition and fluid spaces. 365 41

1. The respiration rate of rat liver mitochondria was stimulated by up to 70% when the extramitochondrial Ca2+ concentration was raised from 103 to 820 nM. This occurred when pyruvate, 2-oxoglutarate, or threo-(Ds)-isocitrate was employed as substrate, but not when succinate was used. 2. Ruthenium Red prevented the stimulation of mitochondrial respiration by extramitochondrial Ca2+, showing that the effect required Ca2+ uptake into the mitochondrial matrix. 3. Starvation of rats for 48 h abolished the stimulation of mitochondrial respiration by extramitochondrial Ca2+ when pyruvate was used as substrate, but did not affect the stimulation of 2-oxoglutarate oxidation by extramitochondrial Ca2+. 4. Our findings are in accord with proposals that oxidative metabolism in liver mitochondria may be stimulated by Ca2+ activation of intramitochondrial dehydrogenases.
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PMID:Stimulation of the respiration rate of rat liver mitochondria by sub-micromolar concentrations of extramitochondrial Ca2+. 366 47

Microplasmodia of Physarum polycephalum differentiate into spherules when the CaCl2 concentration of their nutrient medium is increased to 54mM (high-calcium). The salts starvation medium routinely used to induce differentiation contains 8mM CaCl2. This medium will not induce spherulation in the absence of a calcium salt; no other metal is essential. High-calcium also induces the spherulation of a strain of Physarum that had not been previously observed to spherulate. The striking increase in superoxide dismutase activity (SOD) and the decrease in glutathione concentration (GSH) that are characteristic of salts-induced spherulation do not occur in salts media containing high-calcium. In the absence of calcium, no significant change in SOD is observed and very little change in GSH occurs. The immediate effect of the oxidative stress associated with spherulation may be the release of calcium stores into the cytosol. The parameters modulating this stress are, in turn, sensitive to exogenous calcium concentrations.
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PMID:Superoxide dismutase activity and glutathione concentration during the calcium-induced differentiation of Physarum polycephalum microplasmodia. 366 5

The sulfhydryl-reducing agent beta-mercaptoethanol preferentially stimulates the synthesis of glucose-regulated proteins (GRPs) in mammalian cells. The rapid and large increase in GRPs is due to transcriptional activation of GRP94 and GRP78 genes, resulting in a rapid increase in the steady-state levels of GRP transcripts. From analysis of 5'-deletion mutants, the region of beta-mercaptoethanol responsiveness in the GRP78 promoter was mapped within 450 nucleotides upstream of the TATA sequence. This same general region was demonstrated to be important for induction of the GRP78 gene by the calcium ionophore A23187, glucose starvation, and a temperature-sensitive mutation in a K12 cell line defective in protein glycosylation.
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PMID:Transcriptional activation of the glucose-regulated protein genes and their heterologous fusion genes by beta-mercaptoethanol. 367 Mar 3

Larval Schistosoma mansoni have been shown to induce morphological changes to the internal calcium reserves (in particular the calcareous inclusions in Type A calcium cells and to the inner, nacreous layer of the shell) of Biomphalaria glabrata within 48 h of miracidial penetration. Control experiments have shown that these changes were not due to either the experimental procedures used, mechanical damage or to starvation effects. The effects were, however, analogous to experimentally induced acidosis, suggesting that the rapidly transforming miracidium-sporocyst quickly induces changes in the host's metabolism, presumably by the production and release of CO2 and waste metabolites into the haemolymph.
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PMID:Biomphalaria glabrata: changes in calcium reserves following parasitism by larval Schistosoma mansoni. 369 64

In vivo kinetics of mucosal uptake of luminal 59Fe2+ by tied segments of normal mouse duodenum are characterised by a Km of approx. 100 microM and a Vmax of approx. 9 pmol/min per mg wet weight of intestine. These values were determined at pH 7.25 in the presence of excess sodium ascorbate. Studies with luminal Fe2+ concentrations of 100 microM reveal: uptake is relatively independent of ascorbate: Fe ratio and luminal pH and uptake is potently inhibited by 1 mM Co2+ or Mn2+ and large luminal NaCl concentrations but not by Ca2+. 3 days of hypoxia (0.5 atmospheres) yields no significant increase in subsequent total mucosal uptake by in vivo tied segments while uptake is significantly reduced by semi-starvation. Quantitative comparison of in vivo mucosal uptake with subsequent determination of isolated brush-border membrane 59Fe2+ transport in individual mice reveals a positive correlation (P less than 0.01) between the two parameters. These results, in conjunction with studies of isolated mouse duodenal brush-border membrane (Simpson, R.J. and Peters, T.J. (1985) Biochim. Biophys. Acta, 814, 381-388 and (1986) Biochim. Biophys. Acta 856, 109-114) suggest that the Fe2+ transport properties of isolated brush-border membrane are quantitatively adequate to explain in vivo mucosal uptake in normal and hypoxic mice at Fe2+ concentrations up to 100 microM.
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PMID:Fe2+ uptake by mouse intestinal mucosa in vivo and by isolated intestinal brush-border membrane vesicles. 374 52

The effects of 48-hour starvation on some characteristics of the Ca2+ transport system as well as on lipid content and free fatty acids composition in rat liver mitochondria were determined. The ion fluxes in mitochondria in steady state and oscillations were measured using Ca2+, Sr2+ and H+ sensitive electrodes. The Ca2+ uptake in liver mitochondria was changed after starvation. In the case of equal amounts of endogenous mitochondrial Ca2+ the capability of liver mitochondria to accumulate and store exogenous Ca2+ was decreased after starvation. After inhibition of the energy dependent (active) Ca2+ transport by ruthenium-red (RR) the rate of the passive Ca2+ efflux was activated and this could be explained by the induction of the electroneutral 2H+/Me2+ exchange after starvation. The disproportion in the amounts of linoleic and docosahexaenoic acids in mitochondrial phospholipids after starvation is considered to be the possible cause of the changes in the structure and permeability of the mitochondrial membrane.
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PMID:The influence of starvation on some characteristics of the Ca2+ transport system and lipid content in rat liver mitochondria. 376 64


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