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 kinetics of D-xylose transport were studied in Rhodotorula glutinis. Analysis of the saturation isotherm revealed the presence of at least two carriers for D-xylose in the Rhodotorula plasma membrane. These two carriers exhibited Km values differing by more than an order of magnitude. The low-Km carrier was repressed in rapidly growing cells and derepressed by starvation of the cells. Several hexoses were observed to inhibit D-xylose transport. In the studies reported here, the inhibitions produced by D-galactose and 2-deoxy-D-glucose were examined in some detail in order to define the interactions of these sugars with the D-xylose carriers. 2-Deoxy-D-glucose competitively inhibited both of the D-xylose carriers. In contrast, only the low-Km carrier was competitively inhibited by D-galactose.
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PMID:A kinetic analysis of D-xylose transport in Rhodotorula glutinis. 56 57

The basic characteristics of hexose uptake and regulation of the glucose transporter (GLUT1) by D-glucose and insulin were studied in primary cultures of bovine brain microvessel endothelial cells (BMECs). A non-metabolizable glucose analog, 3-O-[3H]methyl-D-glucose [( 3H]3MG), was used as a model substrate, and the uptake was studied using BMECs grown in tissue culture plates. Uptake of [3H]3MG was equilibrative, temperature-dependent, and independent of sodium. The uptake also decreased gradually with culture age from 7 to 13 days. Saturation kinetics were observed for [3H]3MG uptake and the apparent Km and Vmax values were determined to be 13.2 mM and 169 nmol/mg per min, respectively. Pre-incubation with high concentrations of D-glucose and 3MG accelerated [3H]3MG uptake by BMECs by a counter-transport mechanism. D-Glucose, 2-deoxy-D-glucose, D-mannose, D-xylose, D-galactose and D-ribose showed significant competitive inhibition with [3H]3MG, whereas L-glucose, D-fructose, and sucrose did not affect [3H]3MG uptake by BMECs. [3H]3MG uptake was inhibited significantly by cytochalasin B and phloretin but not by phlorizin, 2,4-dinitrophenol, or ouabain. D-Glucose starvation of BMECs by incubation with D-glucose-free media for 24 h resulted in a significant increase (40-70%) in uptake of [3H]3MG compared with control conditions (7.3 mM D-glucose). Low D-glucose treatments (2.43 and 1.83 mM) for 7 days induced a slight but significant increase (20%) in [3H]3MG uptake, while long-term high glucose treatments (25 mM) showed no significant effect on [3H]3MG uptake irrespective of exposure time. The increase in [3H]3MG accumulation following D-glucose starvation was dependent upon starvation time (12 to 48 hr) and protein synthesis. Refeeding of D-glucose (7.3 mM) to D-glucose-starved BMECs resulted in a return of [3H]3MG uptake to control levels in 48 h. The D-glucose-starvation-induced increase in [3H]3MG uptake was shown to result from an increase in Vmax; the Km remained constant. In addition, D-glucose-starved BMECs were shown to have an increased level of GLUT1 using an antibody against human GLUT1 and an enzyme-linked immunosorbent assay (ELISA). The increased uptake following D-glucose starvation was not significantly affected by the presence of L-glucose, was partially impaired by the presence of D-galactose, D-fructose, and D-xylose, and was completely inhibited by the presence of D-mannose and 3MG. Furthermore, preincubation of BMECs with insulin (10 micrograms/ml) for 20 min did not affect the uptake of [3H]3MG or 2-deoxy-D-[3H]glucose ([3H]2DG).(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Hexose uptake in primary cultures of bovine brain microvessel endothelial cells. I. Basic characteristics and effects of D-glucose and insulin. 175 15

According to the directed mutation hypothesis, certain mutations in bacteria occur more frequently in environments in which the resulting phenotype is selectively favoured than in non-selective environments. This hypothesis therefore challenges the fundamental tenet that mutations occur spontaneously, irrespective of effects on the organism's fitness. One purported case of directed mutation is the excision of a Mu sequence from Escherichia coli strain MCS2 in minimal lactose-arabinose medium. Here, we show that this case can be more simply explained by an accelerated rate of excision mutation in response to non-specific physiological stresses of starvation and by slight growth of MCS2 on minimal lactose-arabinose medium.
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PMID:New data on excisions of Mu from E. coli MCS2 cast doubt on directed mutation hypothesis. 213 15

1. Small-intestinal absorption and permeability were measured in nine patients with malnutrition who were receiving liquid enteral nutrition after different periods of starvation, in five patients receiving enteral nutrition without starvation, in six healthy subjects after starvation for 36 h and in two obese subjects starved for 11 days. 2. Absorption, expressed by the plasma 60 min D-xylose level and the plasma 60 min D-xylose/3-O-methyl-D-glucose ratio, was greatly decreased (P less than 0.001) in the nine patients receiving enteral feeding after starvation, whereas permeability, denoted by the 5 h urinary lactulose/rhamnose ratio, was increased (P less than 0.05). 3. The five patients receiving enteral feeds without prior starvation had normal intestinal absorption and permeability. 4. Starvation of the healthy subjects reduced absorption (P less than 0.05) and this was detectable at 36 h. Permeability, however, was not increased by 36 h starvation. Starvation of the obese subjects also progressively reduced absorption, and this was reversed with refeeding. 5. Changes in intestinal function during enteral feeding are similar to those seen in intestinal diseases. They develop rapidly and are not caused or reversed by liquid enteral feeds. Starvation, before beginning feeding, may explain some of the changes found.
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PMID:Small-intestinal function during enteral feeding and starvation in man. 250 27

1. In the first experiment D-xylose, L-arabinose, D-galacturonic and D-glucuronic acids were fed ad libitum to young chicks for 2 weeks at 200 g/kg of diet and weight gains and food consumption were recorded. 2. L-arabinose and D-xylose did not depress food consumption in the first week but prolonged feeding caused food consumption to decrease and weight gain to be adversely affected. 3. D-galacturonic acid and D-glucuronic acid caused severe growth retardation as early as the first week of feeding, primarily because of voluntary starvation. 4. Apparent metabolisable energy values for the diets were obtained when chicks were 19 to 21 d of age and were 14.04 +/- 0.52, 12.03 +/- 0.61, 11.77 +/- 1.21, 11.68 +/- 0.34 and 11.66 +/- 0.45 KJ/g for the basal diet with glucose, xylose, arabinose, galacturonic and glucuronic acids respectively. 5. True metabolisable energy values for the diets were obtained from adult cockerels and were 15.07 +/- 0.16, 13.45 +/- 0.16, 13.12 +/- 0.37, 12.29 +/- 0.26 and 12.69 +/- 0.23 KJ/g for basal diet with glucose, xylose, arabinose, galacturonic and glucuronic acids respectively. 6. In the second experiment D-galactose, D-xylose, L-arabinose, D-galacturonic and D-glucuronic acid were fed ad libitum to young chicks for 3 weeks at 50 g/kg of diet and weight gains and food consumption were recorded. 7. Chicks grew and ate well on all diets. 8. The digestibilities of sugars and uronic acids were obtained by measurement of these constituents in diets and digesta using titanium dioxide as a marker. The digestibilities were 1.000 +/- 0.0, 0.997 +/- 0.002, 0.936 +/- 0.041, 0.628 +/- 0.103, 0.588 +/- 0.059, and 0.645 +/- 0.089 for D-glucose, D-galactose, D-xylose, L-arabinose, D-galacturonic and D-glucuronic acids respectively. 9. Both at 200 and 50 g/kg dietary inclusion there was noticeable caecal fermentation from L-arabinose, D-galacturonic and D-glucuronic acid. Only at 200 g/kg dietary inclusion did D-xylose produce significant evidence of caecal fermentation.
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PMID:Digestibility of pentose sugars and uronic acids and their effect on chick weight gain and caecal size. 340 82

Transport regulation by different metabolizable and nonmetabolizable sugars was studied in human fibroblasts. Sugars were classed as glucose-like (D-mannose, 3-0-methyl-D-glucose, thio-D-glucose, and D-allose) and starvation-like (D-galactose, D-fructose, L-glucose, D-xylose, 6-deoxy-D-glucose and 2-deoxy-D-glucose) based on their competence in curbing glucose starvation enhanced transport. No significant correlation existed between the ability of a sugar to curb hexose transport and the KI of that sugar in inhibiting hexose transport. Independence of the transport curb from glucose metabolism was observed since nonmetabolizable analogs of D-glucose when substituted for D-glucose in the culture medium effected glucose [i.e. 3-0-methyl-D-glucose (3-OMG)] and starvation-like (i.e. 6- and 2-deoxy-D-glucose) effects. The KI of inhibition pf 2-deoxy-D-glucose transport for 3-OMG was 8.5 mM, similar to those obtained for 6-deoxyglucose and 2-deoxyglucose on 2-deoxyglycose transport (7.5 and 3.5 mM, respectively) and on 3-0-methylglucose transport (3.5 and 2.5 mM, respectively). An equimolar mixture of D-glucose and 3-OMG (5.55 mM each) was more effective than 11.1 mM D-glucose or 3-OMG alone in curbing hexose transport or reversing hexose starvation induced increases in transport. The effect of 3-OMG may be independent of glucose metabolism but it is possible that 3-OMG structurally mimics a metabolite of glucose that may interact with intracellular regulators of carrier degradation and or expression.
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PMID:Control of sugar transport in human fibroblasts independent of glucose metabolism or carrier-substrate interaction. 403 32

Paigen, Kenneth (Roswell Park Memorial Institute, Buffalo, N.Y.). Phenomenon of transient repression in Escherichia coli. J. Bacteriol. 91:1201-1209. 1966.-A family of mutants has been obtained in Escherichia coli K-12 in which beta-galactosidase is not inducible for approximately one cell generation after the cells are transferred to glucose from other carbon sources. After that period; the enzyme can be induced at the level appropriate to glucose-grown cultures of the parent cells. Among a wide variety of carbon sources, the only one capable of eliciting a state of transient repression is glucose. Conversely, transient repression occurs when cells are transferred to glucose from any of a variety of other carbon sources. The only exceptions to this so far discovered are lactose, gluconate, and xylose. Susceptibility to transient repression in mutants can also be induced in glucose-grown cells by a period of starvation. Mutant cells which have become susceptible to transient repression lose susceptibility in the presence of glucose only when they are under conditions which permit active protein synthesis. The presence of an inducer of beta-galactosidase is not required during this time, nor does pre-induction for beta-galactosidase diminish the susceptibility of mutants. At least two other catabolite repression-sensitive enzymes (galactokinase and tryptophanase) are also sensitive to transient repression, and the two phenomena are probably related. The absolute specificity of glucose and the pattern of response seen after growth in different carbon sources suggest that the endogenous metabolite which produces these repressions is far more readily derived from glucose in metabolism than it is from any other exogenous carbon source.
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PMID:Phenomenon of transient repression in Escherichia coli. 532 97

Two galactose uptake systems were found in the mycelia of Neurospora crassa. In glucose-grown mycelia, galactose was transported by a low-affinity (Km = 400 mM) constitutive system which was distinct from the previously described glucose transport system I (R. P. Schneider and W. R. Wiley, J. Bacteriol. 106:479--486, 1971). In carbon-starved mycelia or mycelia incubated with galactose, a second galactose transport activity appeared which required energy, had a high affinity for galactose (Km = 0.7 mM), and was shown to be the same as glucose transport system II. System II also transported mannose, 2-deoxyglucose, xylose, and talose and is therefore a general monosaccharide transport system. System II was derepressed by carbon starvation, completely repressed by glucose, mannose, and 2-deoxyglucose, and partially repressed by fructose and xylose. Incubation with galactose yielded twice as much activity as starvation. This extra induction by galactose required protein synthesis, and represented an increase in activity of system II rather than the induction of another transport system. Glucose, mannose, and 2-deoxyglucose caused rapid degradation of preexisting system II; fructose and xylose caused a slower degradation of activity.
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PMID:Characterization and regulation of galactose transport in Neurospora crassa. 644 43

Hyperosmolar infusions of the inert pentose sugar, xylose (MW 150), were used to induce hyperosmolar states in non-starved and starved rats. Using 51Cr EDTA and RIHSA the extracellular fluid (ECF) and plasma fluid volumes (PV) were determined before and after infusions. The cause of weight loss after 24-30 h starvation was also examined. Equal osmolar provocation in starved and non-starved animals caused the same degree of hyperosmolality. The greater the osmolality increase the larger the volume of intracellular fluid mobilised. Despite the total ECF volume increments being large relative to PV, this fluid compartment remained hardly effected by the fluid released from the cells. No evidence could be found to support 24-30 h starvation as causing a measurable fluid balance defect, a finding of considerable importance when considering short term problems arising out of starvation. The strict control of PV in normovolemic rats has again been confirmed.
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PMID:Mobilised fluid volumes after induced hyperosmolality in the rat. 688 May 43

The culturability of Vibrio cholerae O1 serotype Inaba strain 569B was decreased by the addition of glucose to cell suspensions in starvation media. A similar effect was observed with sucrose, maltose, and fructose. We term this inhibitory effect glucose shock. It was not observed with arabinose or xylose or with carboxylates, such as acetate and pyruvate. No acidification of the medium occurred in the presence of these carbohydrates. Glucose shock was prevented by the addition of nitrogen or phosphorus sources. In the presence of phosphate, the bacterium produced formic acid from glucose. The phenomenon of glucose shock was also observed in V. cholerae O1 serotype Inaba strain RIMD 2203082 but not in strain RIMD 2203088 (O1 Inaba), IID 936 (O1 Ogawa), or RIMD 2214034 (non-O1). The culturability of Escherichia coli, Enterobacter aerogenes, and Listonella anguillarum did not decrease in starvation media with added glucose. Hence, the phenomenon should have ecological significance in determining the distribution of bacteria in marine ecosystems in situations where carbohydrates are abundant, but nitrogen and phosphorus are limiting.
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PMID:Decrease in culturability of Vibrio cholerae caused by glucose. 761 70


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