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At least 667 records · Page 37Linked to original sources
PubMed2000

Unlike leptin, ciliary neurotrophic factor does not reverse the starvation-induced changes of serum corticosterone and hypothalamic neuropeptide levels but induces expression of hypothalamic inhibitors of leptin signaling.

Leptin mediates neuroendocrine responses to fasting and restores the starvation-induced changes of several hypothalamic neuropeptides. Ciliary neurotrophic factor (CNTF), a cytokine closely related to leptin, reduces food intake and reverses obesity, but its role in restoring the starvation-induced changes of hormones or hypothalamic neuropeptides remains largely unknown. To comparatively assess the roles of CNTF and leptin in reversing the starvation-induced changes of hypothalamic neuropeptides and endocrine function and in inducing expression of hypothalamic inhibitors of leptin and CNTF signaling (suppressor of cytokine signaling 3 [SOCS-3]) and mediators of energy expenditure (cyclo-oxygenase 2 [COX-2]), we studied the effect of CNTF and leptin administered by intraperitoneal injections (1 microg/g twice daily) in C57Bl/6J mice fasted for 48 h. Serum corticosterone levels increased with fasting, and leptin administration partially normalized them, whereas CNTF administration had no effect. Hypothalamic neuropeptide Y (NPY) and agouti-related protein (AgRP) mRNA expression increased and pro-opiomelanocortin (POMC) decreased in response to fasting. Leptin administration decreased NPY and AgRP and increased POMC mRNA levels toward baseline, but CNTF administration in fasted mice had no effect of comparable significance. Both leptin and CNTF administration in fasted mice resulted in an induction of SOCS-3 mRNA expression. CNTF also induced hypothalamic SOCS-2 mRNA expression. Finally, neither leptin nor CNTF administration in mice fasted for 48 h alters hypothalamic COX-2 expression. Our data suggest that only falling leptin levels mediate the starvation-induced alterations in corticosterone levels and expression of hypothalamic neuropeptides, but inhibitors of leptin signaling are induced by both leptin and CNTF. This may be of clinical importance because both agents are now being evaluated for the treatment of obesity in humans.

Actins↗
PubMed1997

The endogenous polysaccharide utilization rate of mixed ruminal bacteria and the effect of energy starvation on ruminal fermentation rates.

When mixed ruminal bacteria were starved in vitro for 24 h, cellular ATP decreased, but there was little change in cell protein. Starved ruminal bacteria derived most of their ATP from cellular polysaccharide. Because polysaccharide declined at a first-order rate of 23%/h, it was possible to estimate the endogenous polysaccharide utilization rate at various stages of starvation by multiplying the amount of utilizable polysaccharide remaining at each time point by 0.23. The bacteria initially had a rate of soluble carbohydrate fermentation that was > 717 micrograms of hexose equivalent/mg of protein per h. Starvation had little impact on the rate of soluble carbohydrate fermentation until 8 to 12 h, and the endogenous polysaccharide utilization rate was < 10 micrograms of hexose/mg of protein per h. The bacteria digested ball-milled cellulose at a rate of 24 micrograms of hexose/mg of protein per h for 8 to 12 h. Even bacteria that had been starved for 24 h fermented cellulose at a rate of 16 micrograms of hexose/mg of protein per h. The rate of methane production was initially 70 nmol of methane/mg of protein per min. Short periods of starvation (< 12 h) had little impact on methane production, but longer times caused an almost complete inhibition of methanogenesis. The rate of amino acid deamination was initially 31 nmol of ammonia/mg of protein per min, and the critical phase of starvation was again 8 to 12 h. Ruminal bacteria that were harvested at 24 h after feeding had 10-fold less polysaccharide than did bacteria that were harvested at 2 h after feeding, but this polysaccharide supported high rates of soluble carbohydrate and cellulose fermentation, deamination, and methane production.

Adenosine Triphosphate↗
PubMed2004

Radiation resistance and virulence of Listeria monocytogenes Scott A following starvation in physiological saline.

The influence of starvation on the resistance of Listeria monocytogenes Scott A to electron beam irradiation in 0.85% (wt/vol) NaCl (saline) and in ground pork was investigated. Exponential- or stationary-phase cells (control) were grown at 35 degrees C in tryptic soy broth supplemented with 0.6% yeast extract. Washed cells were starved for 12 days in saline, and virulence of the pathogen was evaluated at 0, 8, and 12 days during starvation. Samples of saline and irradiation-sterilized ground pork, inoculated with control or starved cells, were irradiated at doses ranging from 0.0 to 2.5 kGy. L. monocytogenes survivors were determined by plating diluted samples of saline or pork on tryptic soy agar supplemented with 0.6% yeast extract and counting bacterial colonies following incubation (35 degrees C, 48 h). Virulence of starved cells and control was not significantly different (P > 0.05). Cells exhibited the highest radiation resistance at 8 days of starvation. Irradiation (0.5 kGy) in saline resulted in approximately 7.14, 5.55, and 2.38 log reduction in exponential, stationary, and starved cells, respectively. Irradiation of ground pork at 2.5 kGy reduced controls by approximately 6.0 log, whereas starved cells were reduced by only 3.8 log. Starved cells consistently exhibited higher irradiation D10-values than controls (P < 0.05). D10-values for exponential, stationary, and starved cells were 0.07, 0.09, and 0.21 kGy and 0.35, 0.42, and 0.66 kGy in saline and ground pork, respectively. These results indicate that starvation cross-protects L. monocytogenes Scott A against radiation inactivation and should be considered when determining this pathogen's irradiation D-value.

Adaptation, Physiological↗
PubMed2005

Analysis of differential-expressed proteins of Acidithiobacillus ferrooxidans grown under phosphate starvation.

Acidithiobacillus ferrooxidans is one of the most important bacterium used in bioleaching, and can utilize Fe(2+) or sulphide as energy source. Growth curves for Acidithiobacillus ferrooxidans under phosphate starvation and normal condition have been tested, showing lag, logarithmic, stationary and aging phases as seen in other bacteria. The logarithmic phases were from 10 to 32 hours for Acidithiobacillus ferrooxidans cultivated with normal cultivating condition and from 20 to 60 hrs for Acidithiobacillus ferrooxidans cultivated phosphate starvation. Differences of protein patterns of Acidithiobacillus ferrooxidans growing in case of normal or phosphate starvation were separately investigated after cultivation at 30(o)C by the analysis of two-dimensional gel electrophoresis (2-DE), matrix-assisted laser desorption/ionization (MALDI)-Mass spectrometry. There were total 6 protein spots identified, which were Recombination protein recA, RNA helicase, AP2 domain-containing transcription factor, NADH dehydrogenase I chain D, Hyothetical protein PF1669, and Transaldolase STY3758. From the 6 identified protein spots, 3 proteins were found to be decreased in expression at the cultivating condition of phosphate starvation, while another three upregulated.

Acidithiobacillus thiooxidans↗
PubMed2000

[Function of an inhibitor of cyclin-dependent kinase p27/Kip in cells transformed by E1A + E1B19 kDa + E1A + cHa-Ras, differing in their ability to realize a G1-block during serum starvation].

We studied the capability of E1A + cHa-ras and E1A + E1B19kDa transformants to undergo the G1/S arrest of the cell cycle following depletion of serum growth factors. It has been shown that serum starvation induced the G1/S arrest both in normal rat embryo fibroblasts (REF) and in E1A + E1B19kDa transformants, whereas E1A + cHa-ras transformed cells lost this feature. To analyse the mechanisms underlying these differences, we studied the expression of p27/KIP, its intracellular distribution and association with E1A oncoproducts. The content of the p27/KIP inhibitor of cyclin-dependent kinases was found to change a little upon transformation by two complementary oncogene pairs. However, serum starvation for 24 h led to a significant increase in the content of p27/KIP in E1A + E1B19kDa transformants, while E1A + cHa-ras cells accumulated p27/KIP less markedly. According to the immunofluorescence study, the p27/KIP inhibitor is located in the nucleus of both normal and transformed cells. Moreover, serum starvation did not lead to its inhibition due to redistribution to the cytoplasm in both cell lines. Also, we were unable to detect association of p27/KIP with E1A oncoproducts in immunoprecipitated complexes. The obtained data indicate that, in contrast to E1A + cHa-ras transformants, in E1A + E1B19kDa cells the p27/KIP inhibitor is functional and it is capable of inducing the G1/S block after serum starvation.

Adenovirus E1 Proteins↗
PubMed2001

Negative regulation of phosphate starvation-induced genes.

Phosphate (Pi) deficiency is a major nutritional problem faced by plants in many agro-ecosystems. This deficiency results in altered gene expression leading to physiological and morphological changes in plants. Altered gene expression is presumed to be due to interaction of regulatory sequences (cis-elements) present in the promoters with DNA binding factors (trans-factors). In this study, we analyzed the expression and DNA-protein interaction of promoter regions of Pi starvation-induced genes AtPT2 and TPSI1. AtPT2 encodes the high-affinity Pi transporter in Arabidopsis, whereas TPSI1 codes for a novel gene induced in the Pi-starved tomato (Lycopersicon esculentum). Expression of AtPT2 was induced rapidly under Pi deficiency and increased with decreasing concentrations of Pi. Abiotic stresses except Pi starvation had no affect on the expression of TPSI1. DNA mobility-shift assays indicated that specific sequences of AtPT2 and TPSI1 promoter interact with nuclear protein factors. Two regions of AtPT2 and TPSI1 promoters specifically bound nuclear protein factors from Pi-sufficient plants. Interestingly, the DNA binding activity disappeared during Pi starvation, leading to the hypothesis that Pi starvation-induced genes may be under negative regulation.

Arabidopsis↗
PubMed2005

[Concentration of hydrochloric acid and pepsin in gastric juice in dogs after starvation and refeeding].

Feeding fogs with meat after a 3-day period of starvation increased hydrochloric acid concentration with subsequent return of the parameter to normal values. Under the same conditions, pepsin concentration decreased and raised up after re-feeding. Histamine administration following the starvation decreased hydrochloric acid concentration with subsequent normalising. In three days after re-feeding and histamine administration, pepsin concentration drooped owing, probably, to a decrease of parietal cell H2-receptor affinity to histamine. Pentagastrin administration after the starvation increased hydrochloric acid concentration. The findings suggest G-cell function inhibition occurring after a 3-day starvation which is important for the stomach mucous membrane protection.

Animals↗
PubMed2005

Effects of starvation conditions on biomass behaviour for minimization of sludge production in membrane bioreactors.

The behaviour of an activated sludge system in starvation conditions was examined in batch according to substrate impulses defined by different S0/X0 ratio. The answer was characterised by an exogenous phase followed by a starvation one. If at high S0/X0 ratio, bacterial cell multiplication was the main synthesis process during exogenous phase, at low S0/X0 ratio the observed phenomenon was compound storage. In starvation conditions, for the lowest S0/X0 ratio, a rapid decrease in the MLVSS without soluble proteins production was observed. No bacterial lysis occurred and this phenomenon was due to consumption of the storage compounds with a decrease rate equal to 0.74d(-1). For high S0/X0 ratio, as soon as the exogenous phase was completed, a decrease of the MLVSS simultaneously to a soluble protein production was observed. An immediate bacterial lysis occurred with a decay rate equal to 0.53 d(-1). Because MBR systems work generally in low F/M conditions, the activity of the present microbial population is close to the one observed in starvation phase. This work points out that these conditions do not allow net bacterial growth and cells just use lysis products to satisfy their maintenance requirements. These assumptions confirm the feasibility of a decrease of the net biomass production in a MBR when high sludge retention time is operated.

Bacteria↗
PubMed1995

Modulation of apoptosis by starvation: morphological and biochemical study of rat intestinal mucosa.

Morphology at light and electron microscopic levels, expression and activation of transglutaminase and DNA fragmentation at internucleosomal sites were used as markers to study the effect of starvation on the apoptosis of small intestinal epithelial cells. The cells entering apoptotic programme in well-fed animals undergo many morphological changes in apical cytoplasm involving alterations in actin cytoskeleton organisation which may cause a discharge of microvilli. Some free floating cells in the intestinal lumen show characteristics of apoptotic cell death, e.g. shrinkage of cell and peripheral condensation of chromatin, while mitochondria and lysosomes remain unchanged. Apoptotic bodies are also seen in scanning electron micrographs. During progressive starvation, epithelial cells do not enter the apoptotic cell death programme. Biochemical markers for apoptosis such as increased transglutaminase activity and DNA fragmentation are clearly discernible in normally fed animals. The percentage of cells labelled immunohistochemically by antibody against transglutaminase decreased during starvation while DNA fragmentation was absent. The exact mechanism for suppressing apoptosis in intestinal cells under starvation is not known. However, the data presented here support the existence of such a regulatory process.

Journal Article↗
PubMed1985

Phosphoribosylpyrophosphate synthesis from glucose decreases during amino acid starvation of human lymphoblasts.

When cultured human lymphoblasts are starved 3 h for an essential amino acid, rates of purine nucleotide synthesis decrease markedly because of a decrease in the intracellular phosphoribosylpyrophosphate concentration (Boss, G.R., and Erbe, R.W. (1982) J. Biol. Chem. 257, 4242-4247; Boss, G. R. (1984) J. Biol. Chem. 259, 2936-2941). In amino acid-starved cells, glucose transport was not changed, whereas total glucose consumption and lactate production decreased by approximately 25 and 10%, respectively. Carbon flow through the oxidative pentose phosphate pathway, measured by 14CO2 release from [1-14C]glucose, decreased by 18% during amino acid starvation. However, kinetic studies of ribulose-5-phosphate 3-epimerase and phosphoriboisomerase suggested that the ribulose 5-phosphate produced by this pathway is converted mostly to xylulose 5-phosphate instead of to ribose 5-phosphate so that this pathway produces little phosphoribosylpyrophosphate. The activity of the nonoxidative pentose phosphate pathway, measured by high performance liquid chromatography following the incorporation of [1-14C]glucose into phosphoribosylpyrophosphate, ATP, and GTP, decreased by approximately 55% during amino acid starvation. None of the enzymes of either pathway changed in specific activity during amino acid starvation. We conclude that the nonoxidative pentose phosphate pathway is the major source of phosphoribosylpyrophosphate for purine nucleotide synthesis and that this pathway is regulated by a metabolite which changes in concentration during amino acid starvation.

Aldose-Ketose Isomerases↗
PubMed1985

Alteration in the characters of CDP-choline synthetase and phospholipid-choline exchange enzyme upon choline starvation in Chinese hamster ovary cells.

When CHO-K1 cells are cultivated under choline-deficient conditions, the specific activity of CDP-choline synthetase increases and conversely phospholipid-choline exchange enzyme activity decreases, whereas the other three known enzyme activities related to synthesis of phosphatidylcholine remain unchanged. The changes of the former two enzyme activities take place immediately after removal of choline from the medium. The altered activities readily revert to the control levels upon resupplementation of choline to the starved cell culture. The changes upon choline starvation are sensitive to cycloheximide, while the restoration processes are insensitive to the drug. The activity of CDP-choline synthetase in unstarved control cells is found in both the soluble and membrane fractions. The Km value of the enzyme in the soluble fraction for choline phosphate differs from that in the membrane fraction. Asolectin alters the Km value of the former to a value close to that of the latter and raises its Vmax value, whereas it hardly affects the Km and Vmax values of the latter. In choline-starved cells, the activity is exclusively found in the membrane fraction. The change in the subcellular distribution of the activity upon choline starvation is sensitive to cycloheximide. The altered subcellular distribution reverts to the initial status upon resupplementation of choline even in the presence of cycloheximide. The activity of the phospholipid-choline exchange enzyme is exclusively found in the membrane fraction for both starved and control cells. The properties of the enzyme are altered upon choline starvation with respect to the Vmax value for choline and the Km and Vmax values for Ca2+. These altered kinetic parameters are changed by egg yolk phosphatidylcholine so as to be indistinguishable from those in unstarved control cells. We discuss the mechanism of the alterations in the characters of both enzymes in response to choline starvation.

Animals↗
PubMed1980

The effect of amino acid starvation on nucleoside uptake and RNA synthesis in Tetrahymena.

The uptake of nucleosides and the synthesis of RNA in Tetrahymena thermophila were examined following amino acid starvation. Omission of leucine, phenylalanine, or arginine from the medium resulted in a rapid decrease in the incorporation of [3H]uridine into the acid-soluble pool and acid-insoluble material (RNA). Amino acid starvation inhibited the uptake of all ribo- and deoxyribonucleosides tested but did not affect the uptake of amino acids or glucose. In addition, under the conditions used, the omission of an amino acid did not result in a large decrease in amino acid incorporation into total protein. Treatment of cells with cycloheximide or emetine gave results similar to the effects of amino acid starvation, but in these experiments the inhibition of protein synthesis was essentially complete. Nucleotide pool sizes were also measured following amino acid starvation. ATP and UTP levels were essentially unchanged, but the dTTP pool size was decreased by 40%. The decrease in RNA synthesis in vivo in the absence of an essential amino acid was reflected in the endogenous RNA synthetic activity of isolated nuclei. However, when solubilized RNA polymerase activity was measured with calf thymus DNA as template, no significant difference was observed between control and amino acid-starved cells.

Amino Acids↗
PubMed1983

The role of glucose and aminoacid starvation in the sensitivity of protein and RNA synthesis to cycloheximide and erythromycin in the yeast Saccharomyces cerevisiae.

In Saccharomyces cerevisiae dependence of ribonucleic acid synthesis on protein synthesis occurring during nutritional shift down conditions was evidenced. The results obtained indicated that yeast had "stringent control" of ribonucleic acid synthesis and that this control was reversed by cycloheximide only under glucose starvation or ammonia starvation in the presence of acetate as carbon source (phenotypic relaxation). Therefore, it appeared that the "phenotypic relaxation" of RNA synthesis depended on the carbon source present in the medium suggesting that the process could be negatively controlled by glucose or by some glucose catabolite(s). Such a phenotypic relaxation was sensitive to erythromycin treatment. On the other hand, total protein synthesis carried out during amino-acid starvation in the presence of glucose or ammonia starvation in the presence of acetate was 30%-40% inhibited by erythromycin, showing that in these conditions sensitivity to a non legitimate inhibitor could be triggered off in an haploid strain, and that such sensitivity did not depend on the presence of glucose in the medium.

Amino Acids↗
PubMed1980

Accumulation of ppGpp in a relA mutant of Escherichia coli during amino acid starvation.

In Escherichia coli, amino acid starvation triggers the rapid synthesis of two guanosine polyphosphates, pppGpp and ppGpp (the 3'-pyrophosphates of GTP and GDP, respectively). Determination of the turnover rate of the ppGpp pool indicated that during serine deprivation, as opposed to other amino acid starvations, the rate of ppGpp degradation is dramatically decreased. This results in a slow but significant accumulation of this regulatory nucleotide in a relA mutant during serine starvation. Similar ppGpp accumulation can be seen during serine starvation in different serine auxotrophic mutants carrying different relA alleles. On the other hand, no ppGpp accumulation is induced in various relaxed strains by serine hydroxamate treatment.

Escherichia coli↗
PubMed1983

Simultaneous regulation of amino acid influx and efflux by system A in the hepatoma cell HTC. Ouabain simulates the starvation-induced derepression of system A amino acid transport.

In the cultured hepatoma cell HTC, amino acid starvation stimulated both influx and efflux of 2-(methylamino)isobutyric acid (MeAIB) across the plasma membrane with little effect on the ultimate cellular accumulation of this amino acid. In agreement, prior amino acid starvation had little effect on the cellular steady state levels reached for various natural amino acids during subsequent incubation in an amino acid-rich medium containing cycloheximide. Furthermore, efflux of [14C]MeAIB was markedly increased by amino acid starvation. These findings do not mean that adaptive regulation of neutral amino acid transport is pointless. If membrane transport rather than metabolism is the rate-limiting step for net amino acid production or consumption, or becomes so during times of elevated formation or catabolism of an amino acid, then proportionate changes of both the opposed fluxes should enhance its net generation or consumption. Amino acid starvation enhances MeAIB-dependent Na+ influx. Alteration of the external [Na+] changes the Km, not the Vmax, for MeAIB influx when the degree of System A derepression is stabilized with cycloheximide. In both starved and unstarved cells, Km/Vmax for MeAIB entry yields a linear function with the reciprocal of the external [Na+], supporting at least for influx a rapid equilibrium-ordered kinetic model in which Na+ binds to the carrier site before the amino acid. Elevated cellular [Na+] obtained by ouabain treatment increased MeAIB efflux in parallel. Trans-inhibition of MeAIB influx by accumulated MeAIB, and as a related phenomenon by cellular Na+, was as effective in unstarved as in starved cells, showing independence of this kinetic phenomenon from adaptive regulation. The decreased MeAIB accumulation resulting from decreased influx and increased efflux occurring at high internal [Na+] applies both to unstarved and starved cells. We conclude that cellular Na+ accumulations, produced by increasing levels of ouabain, reversibly reduce the ability of MeAIB to repress System A because its interior concentration is prevented from rising, although transport in both directions continues; accordingly, the repressive signal appears to come from the internal amino acid levels rather than from occupation of the carrier site for System A flux.

3-O-Methylglucose↗
PubMed1983

Regulation of hexose carriers in chicken embryo fibroblasts. Effect of glucose starvation and role of protein synthesis.

Regulation of hexose transport was investigated in chicken embryo fibroblasts (CEF) which develop 4- to 8-fold enhanced hexose transport activity during glucose starvation. The presence of cycloheximide in low (0.5 micrograms/ml) concentrations during starvation largely blocked the enhancement of transport activity. Glucose refeeding of CEF in the starvation state led to a decline in transport to the basal level. This decline was either potentiated or blocked by the presence of cycloheximide in low or high (50 micrograms/ml) concentrations, respectively. Exposure of CEF in the fed state to low concentrations of cycloheximide resulted in a 70% decrease of transport within 6 h, whereas exposure to high concentrations of cycloheximide led to only a modest loss (35% decrease). In the glucose-starved state, CEF had no significant decline of transport when exposed to cycloheximide at either high or low concentrations. The uptake of 3-O-methylglucose by fed, starved, or cycloheximide-treated CEF correlated closely with D-glucose transport activity and [3H]cytochalasin B binding by plasma membranes prepared from CEF exposed to the same conditions. Hexose transport activity of CEF seems to largely depend on the number of functioning carriers in the plasma membrane, which apparently reflect the balance between carrier synthesis and inactivation. These two processes require protein synthesis, but are differentially sensitive to the effects of cycloheximide, such that low concentrations of cycloheximide appear to block primarily synthesis while high concentrations block both processes. Furthermore, during starvation the enhancement of transport appears largely due to decreased carrier inactivation in the face of continued carrier synthesis.

Animals↗
PubMed1982

[Polyphosphate and ATP content of Propionibacterium shermanii cells in nitrogen starvation].

When Propionibacterium shermanii was cultivated in a medium with glucose under the conditions of nitrogen deficiency, the content of high molecular weight polyphosphates (salt-soluble fraction, alkali-soluble fraction, and fraction extracted with hot perchloric acid) decreased. In contrast, it rose in a medium with lactate within two and three days of starvation. The culture growth stopped after a day under these conditions, the energy substrate was assimilated during the entire process of starvation, and the content of ATP continuously decreased. When ammonium sulfate was added after two and three days of starvation, the intracellular content of polyphosphates (in all of the three fractions) increased in the medium with glucose. If ammonium sulfate was added after three days of starvation in the medium with lactate, the content of polyphosphates rose in the fraction extracted with hot perchloric acid while the content of salt-soluble and alkali-soluble polyphosphates decreased. The culture started to grow again and the content of ATP in its cells rose abruptly when ammonium sulfate was added under these conditions. If the culture was grown in the medium with glucose and ammonium sulfate, the content of acid-insoluble polyphosphates increased twofold during the first day and dropped to the initial level by the third day of growth.

Adenosine Triphosphate↗
PubMed1980

[Renal function in therapeutic starvation (author's transl)].

There are many publications on various complications of therapeutic starvation, but only few cases and of renal complications have been described. During starvation two characteristic changes in kidney function occur: a reduction in glomerular filtration rate by about 50% and a decrease in renal uric acid clearance by impairment of tubular uric acid secretion with consequent hyperuricaemia. During fasting ketone bodies compete with uric acid for a common tubular secretion site. The development of some of the renal complications described in the literature so far can be explained bal failure with uric acid nephropathy, renal ischaemia and pre-existing kidney disease have been published. Furthermore reversible salt-losing nephropathies were observed. It is essential in the prophylaxis of renal complications during fasting to ensure that a sufficient fluid intake is maintained and the urinary output is controlled. Before therapeutic starvation is commenced parameters of renal function (urinalysis, blood urea, serum creatine, serum uric acid) must be determined and then monitored at regular intervals. After starvation has commenced the administration of uricosuric agents must be avoided and intravenous pyelography is contraindicated.

Acidosis↗