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)

Inositol-requiring mutants of Saacharomyces cerevisiae were tested in cell extracts for the ability to convert glucose-6-phosphate to inositol-phosphate (IP synthetase) and inositol (IP phosphatase). Mutants representing any one of 10 unlinked loci conferring the inositol requirement were unable to synthesize either compound in an assay with glucose-6-phosphate as the substrate. These results indicate that the mutants lack IP synthetase activity and that at least 10 genes control the conversion of glucose-6-phosphate to inositol-phosphate. In addition, a mutation known to be unlinked with the ino1 locus interacts with a leaky ino1 allele and may play a role in the regulation of IP synthetase. This mutation causes a 47% reduction in wild-type IP synthetase activity and, when combined in a haploid strain with the leaky ino1 allele, it reduced IP synthetase activity to a level below that which is growth supporting. Wild-type and IP synthetase-deficient strains were tested for reduced nicotinamide adenine dinucleotide (NADH) accumulation, since NAD+ is required in the conversion of glucose-6-phosphate to inositol. No detectable accumulation of NADH was observed in the wild-type strain, presumably because the NADH generated is rapidly oxidized during subsequent partial reactions of IP synthetase. Mutants representing three different loci accumulate NADH and may, therefore, lack the NADH-mediated reductase activity of IP synthetase. Other mutants tested fail to accumulate NADH and may, therefore, lack the NAD+-mediated oxidase activity of IP synthetase. Phospholipid synthesis was studied by 32P pulse labeling in one mutant under conditions of inositol supplementation and starvation. Starved cells incorporate 32P into phospholipids normally for 2 h, followed by a period in which the rate of phosphatidylinositol synthesis decreases and the rate of phosphatidylcholine synthesis increases. After 5 to 6 h starvation, all cellular phospholipid synthesis ceases.
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PMID:Control of inositol biosynthesis in Saccharomyces cerevisiae; inositol-phosphate synthetase mutants. 17 96

1. Glucokinase was absent from chicken liver and only the low Km hexokinases, inhibited by AMP, ADP but not ATP, were present. 2. The Km of chicken liver glucose-6-phosphatase for glucose-6-phosphate was reduced from 5.65 to 3.75 mM following starvation, and the enzyme was inhibited by glucose. 3. Starvation of chickens for 24 hr slightly lowered the hexokinase activity and doubled glucose-6-phosphatase activity; it did not change subcellular distribution of the enzymes. Oral glucose rapidly restored the activities to fed values. 4. It was concluded that glucose uptake into, and efflux from, chicken hepatocytes, was regulated by the activity and kinetic characteristics of glucose-6-phosphatase and by the glucose-6-phosphate concentration, and that the hexokinases had little regulatory function.
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PMID:Glucose phosphorylation and dephosphorylation in chicken liver. 23 87

The responses of liver glycogen and glucose-6-phosphate dehydrogenase (G6PD) (EC 1.1.1.49) to a high glucose, adequate protein diet were compared between rats previously starved 2 days, then refed a high protein, carbohydrate-free diet for 2 days, and rats previously fed the high protein diet for 4 days. Glycogen levels increased dramatically during the first day the high carbohydrate diet was fed, then decreased gradually on the second day. The response was the same regardless of whether the rats had been starved more before the high protein diet was fed. Liver G6PD activity also increased when the high carbohydrate diet was fed, and continued to increase on the second day. The increase in G6PD, however, was significantly greater in the rats which had been starved before the high protein diet was fed. It is suggested that some process occurs during starvation that predisposes the induction of G6PD upon refeeding a high carbohydrate diet, over and above any effect of glycogen accumulation and breakdown. Glucose or glucose-6-phosphate derived from glycogen does not appear to be the primary inducer of G6PD in rat liver.
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PMID:Independence of glycogen accumulation and glucose-6-phosphate dehydrogenase induction in rat liver. 92 58

The effects of one vs. two episodes of starvation-refeeding were studied in young male rats as a function of elapsed time between the two episodes of starvation-refeeding. Starved-refed rats ate more and gained weight faster than ad libitum-fed rats. The difference in weight gains could be attributed to the greater amount of body fat in the starved-refed rats. The responses of four NADP-linked liver dehydrogenases:isocitrate dehydrogenase (ICD)/LS-isocitrate:NADP oxidoreductase (decarboxylating) (EC 1.1.1.42), glucose-6-phosphate dehydrogenase (G6PD)/D-glucose-6-phosphate:NADP oxidoreductase (EC 1.1.1.49); 6-phosphogluconate dehydrogenase (6PGD/6-phospho-D-gluconate:NADP oxidoreductase (decarboxylating) (EC 1.1.1.44); and malic enzyme (ME)/L-malate:NADP oxidoreductase (decarboxylating) (EC 1.1.1.40) were studied. Starvation-refeeding caused an overshoot of G6PD, 6PGD, and ME, but not of ICD. A second episode of starvation caused an even greater enzyme overshoot; this difference persisted for 3 weeks with G6PD and for 2 weeks with 6PGD and ME. No significant differences in blood cholesterol were detected.
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PMID:Long-term effects of starvation-refeeding in the rat. 122 70

The periplasmic acid glucose-1-phosphatase (G-1-Pase) encoded by gene agp is necessary for the growth of Escherichia coli in a minimal medium containing glucose-1-phosphate (G-1-P) as the sole source of carbon. From a mutant in which the agp gene was inactivated, suppressors were isolated which recovered the ability to utilize G-1-P as carbon source. The mutants constitutively expressed hexose phosphate permease activity (encoded by uhpT). The mutation involved mapped in the uhp region and, unlike those of wild-type strains, bacteria of the suppressed strains required phosphoglucomutase (pgm), to grow on G-1-P. Surprisingly, in a minimal medium deprived of inorganic phosphate, uhpT+ bacteria lacking the two enzymes, alkaline-phosphatase (phoA) and glucose-1-phosphatase (agp), could utilize G-1-P as the sole source of phosphate, and also as both the sole phosphate and carbon source provided the integrity of pgm and of uhpT was conserved. Although glucose-6-phosphate, the inducer of UhpT permease, was not present in the medium, the activity of uhpT was greatly stimulated by inorganic phosphate depletion. This phosphate-starvation-induced bypass of G-1-Pase by UhpT + Pgm systems shows that agp is essential for G-1-P assimilation as a carbon source only in a high-phosphate medium, a result in agreement with the lack of agp regulation by inorganic phosphate.
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PMID:Utilization of exogenous glucose-1-phosphate as a source of carbon or phosphate by Escherichia coli K12: respective roles of acid glucose-1-phosphatase, hexose-phosphate permease, phosphoglucomutase and alkaline phosphatase. 164 77

1. Activities of trout liver glucose dehydrogenase (GDH, EC 1.1.1.47) and glucose-6-phosphate dehydrogenase (G6PD, EC 1.1.1.49) were increased after a sudden drop in water temperature, but not in long-time cold acclimated as compared with warm acclimated trout. 2. Possibly, the activities of GDH and G6PD were temporarily increased in connection with metabolic adaptation to the lower temperature. 3. The activities of GDH and G6PD were not changed by the stress of handling. 4. Partially purified trout liver GDH has a lower activation energy with glucose than with glucose-6-phosphate as substrate, and the Km (glucose) decreases with decreasing assay temperature. 5. At low temperatures, the activity of trout liver GDH with glucose as substrate may be comparable to that of glucose-6-phosphate. 6. Partially purified beef liver GDH has a high activation energy with glucose as substrate, and the Km (glucose) does not change with the assay temperature. 7. Hexokinase (HK, EC 2.7.1.1) and GDH activities were unchanged when trout were deprived of food for 4 weeks. Apparently, the trout liver glucose utilization did not adapt to the starvation.
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PMID:Glucose dehydrogenase, glucose-6-phosphate dehydrogenase and hexokinase in liver of rainbow trout (Salmo gairdneri). Effects of starvation and temperature variations. 176 17

The effect of intrauterine growth retardation and neonatal hypoglycemia on cerebral metabolic intermediates were determined in newborn dogs subjected to 5 days of maternal canine starvation (MCS) before birth. Birth weight was reduced 23% (232 +/- 6 versus 300 +/- 10 g). Circulating blood glucose was reduced after 3 h of neonatal fasting in MCS pups (2.7 +/- 0.4 +/- versus 5.7 +/- 1.1 mM). Cerebral cortical levels of glucose were also reduced at this time. Cerebral glucose-6-phosphate was not altered; nonetheless fructose-6-phosphate was lower in MCS pups at 6 and 9 h, while fructose 1,6-diphosphate appeared elevated at 3 h. These data suggest that cerebral glycolytic activity may be increased by increased activity of phosphofructokinase. Cerebral glutamine appeared reduced in fasting MCS pups at 3, 6, and 8 h of age. A considerable disturbance of the adenine nucleotide pool was noted between 3-9 h in MCS pups; while the cerebral energy reserve was diminished in MCS pups between 3-24 h. The data of reduced cerebral energy status and reserve suggest that cerebral energy production was diminished. Although glucose levels were low at 3 h, subsequent recovery was not immediate as adenine-nucleotides remained low beyond the period of hypoglycemia. The combined effects of intrauterine growth retardation and transient neonatal hypoglycemia appear to result in reduced cerebral oxidative metabolism; this occurs despite an apparent enhanced utilization of alternate fuels.
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PMID:Cerebral metabolic intermediate response following severe canine intrauterine growth retardation. 372 65

The reason for the failure of early-stage mouse embryos to grow on glucose alone was investigated by measurement of glucose-6-phosphate, fructose-1,6-bisphosphate plus triose phosphates, citrate, and malate in individual embryos during starvation and refeeding with glucose or glucose plus pyruvate. The results indicate a block at the 6-phosphofructokinase (EC 2.7.1.11) step at early stages, which is later removed. Although there seems to be no early difficulty in phosphorylation of glucose, maximum glucose-6-phosphate levels (and probably fructose-6-phosphate levels) are much lower at early stages than at later stages. The increase in fructose-6-phosphate with age may be the major cause of the increase in 6-phosphofructokinase activity. Unusually high citrate levels at all ages may help to keep this enzyme strongly inhibited until the increase in fructose-6-phosphate occurs. The changes in metabolite levels also indicate an early defect in mobilization of glycogen and a probably less important defect in the citrate cycle.
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PMID:The explanation for the blockade of glycolysis in early mouse embryos. 427 92

The uptake of nutrients (glucose, glutamine, and N-acetylglucosamine), the intracellular concentrations of metabolites (glucose-6-phosphate, cyclic AMP, amino acids, trehalose, and glycogen) and cell wall composition were studied in Candida albicans. These analyses were carried out with exponential-phase, stationary-phase, and starved yeast cells, and during germ-tube formation. Germ tubes formed during a 3-h incubation of starved yeast cells (0.8 X 10(8) cells/mL) at 37 degrees C during which time the nutrients glucose plus glutamine or N-acetylglucosamine (2.5 mM of each) were completely utilized. Control incubations with these nutrients at 28 degrees C did not form germ tubes. Uptake of N-acetylglucosamine and glutamine was inhibited by cycloheximide which suggests that de novo protein synthesis was required for the induction of these uptake systems. The glucose-6-phosphate content varied from 0.4 nmol/mg dry weight for starved cells to 2-3 nmol/mg dry weight for growing yeast cells and germ tube forming cells. Trehalose content varied from 85 nmol/mg dry weight (growing yeast cells and germ tube forming cells) to 165 nmol/mg weight (stationary-phase cells). The glycogen content decreased during germ-tube formation (from 800 to 600 nmol glucose equivalent/mg dry weight) but increased (to 1000 nmol glucose equivalent/mg dry weight) in the control incubation of yeast cells. Cyclic AMP remained constant throughout germ-tube formation at 4-6 pmol/mg dry weight. The total amino acid pool was similar in exponential, starved, and germ tube forming cells but there were changes in the amounts of individual amino acids. The overall cell wall composition of yeast cells and germ tube forming cells were similar: lipid (2%, w/w); protein (3-6%), and carbohydrate (77-85%). The total carbohydrates were accounted for as the following fractions: alkali-soluble glucan (3-8%), mannan (20-23%), acid-soluble glucan (24-27%), and acid-insoluble glucan (18-26%). The relative amounts of the alkali-soluble and insoluble glucan changed during starvation of yeast cells, reinitiation of yeast-phase growth, and germ-tube formation. Analysis of the insoluble glucan fraction from cells labelled with [14C]glucose during germ-tube formation showed that the chitin content of the cell wall increased from 0.6% to 2.7% (w/w).
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PMID:An analysis of the metabolism and cell wall composition of Candida albicans during germ-tube formation. 632 47

A close study of the metabolic regulation of hexose transport in a hamster fibroblast mutant, highly defective in the enzyme phosphoglucose isomerase (PGI mutant), reveals the requirement for at least three vectors for transport regulation. The downward regulation of the hexose transport system, called the "transport curb," requires (i) a ligand for the transport system, (ii) oxidative energy metabolism, and (iii) some specific enzymes of the glucose-6-phosphate metabolism. Deprivation of glucose was shown to deprive the PGI mutant of UDP hexose, whereas the glucose-fed mutant contained high levels. The parental strain preserved the UDP hexose with or without glucose feeding. Cycloheximide added to the mutant showed two different types of effects. If added at the onset of glucose starvation, the up-regulation of the transport system was scarcely affected. If cycloheximide was added to the mutant at the onset of glucose refeeding, it prevented the development of the glucose-mediated transport curb. In the mutant, the glucose-mediated curb is not derived from energy metabolism but is solely dependent on certain enzymes of glucose-6-phosphate metabolism. The interference of this curb by cycloheximide requires evidently a reassessment, including that of the role of the UDP hexose pathway in regulation of the hexose transport system.
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PMID:Further clues concerning the vectors essential to regulation of hexose transport, as studied in fibroblast cultures from a metabolic mutant. 658


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