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)

Inosine is a potent primary stimulus of insulin secretion from isolated mouse islets. The inosine-induced insulin secretion was totally depressed during starvation, but was completely restored by the addition of 5 mM-caffeine to the medium and partially restored by the addition of 5 mM-glucose. Mannoheptulose (3 mg/ml) potentiated the effect of 10 mM-inosine in islets from fed mice. The mechanism of the stimulatory effect of inosine was further investigated, and it was demonstrated that pancreatic islets contain a nucleoside phosphorylase capable of converting inosine into hypoxanthine and ribose 1-phosphate. Inosine at 10 mM concentration increased the lactate production and the content of ATP, glucose 6-phosphate (fructose 1,6-diphosphate + triose phosphates) and cyclic AMP in islets from fed mice. In islets from starved mice inosine-induced lactate production was decreased and no change in the concentration of cyclic AMP could be demonstrated, whereas the concentration of ATP and glucose 6-phosphate rose. Inosine (10 mM) induced a higher concentration of (fructose 1,6-diphosphate + triose phosphates) in islets from starved mice than in islets from fed mice suggesting that in starvation the activities of glyceraldehyde 3-phosphate dehydrogenase or other enzymes below this step in glycolysis are decreased. Formation of glucose from inosine was negligible. Inosine had no direct effect on adenylate cyclase activity in islet homogenates. The observed changes in insulin secretion and islet metabolism mimic what is seen when glucose and glyceraldehyde stimulate insulin secretion, and as neither ribose nor hypoxanthine-stimulated insulin release, the results are interpreted as supporting the substrate-site hypothesis for glucose-induced insulin secretion according to which glucose has to be metabolized in the beta-cells before secretion is initiated.
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PMID:Inosine-stimulated insulin release and metabolism of inosine in isolated mouse pancreatic islets. 18 35

Cultures of Physarum polycephalum incubated with caffeine or theophylline for over 100 min prior to mitosis exhibited mitotic delay proportional to the time of treatment before 100 min. Starved cultures exhibited mitotic delay at times of starvation longer than 180 min and slight stimulation from 100-180 min. Dibutyryl cAMP appeared to accelerate reconstruction of the nucleus following mitosis.
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PMID:Timing of mitosis in Physarum polycephalum: effects of agents affecting cyclic AMP concentrations. 18 79

Caffeine, at doses which enhance the killing action of ultraviolet light, inhibits both de novo synthesis and the utilization of exogenous purines in cultured CHO-K1, a Chinese hamster ovary cell line. The decrease in synthesis was measured as inhibition by caffeine of the accumulation of phosphoribosylformylglycineamide or of phosphoribosylaminoimidazolecarboxamide, the fourth and ninth intermediates, respectively, in the de novo biosynthetic pathway. The effect is dose dependent, with a caffeine concentration of 7.5 mM producing a 90% reduction in 15 min. Interference with utilization of exogenous purines was seen as a substantial decrease in the conversion of [14C]hypoxanthine, [14C]adenine, or [14C]guanine into their respective di- and triphosphates in the presence of caffeine. Purine deprivation either by starvation of purine-requiring mutants or by treatment of parental cells with methylmercaptopurine ribonucleoside, a known inhibitor of purine synthesis, results in a partial sensitization to killing by ultraviolet light which can be maximized by the addition of caffeine. Thus, one of the ways by which antimetabolites and caffeine act to enhance ultraviolet light killing may be by interference with the supply of purine nucleotides needed for repair.
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PMID:Effects of caffeine on purine metabolism and ultraviolet light-induced lethality in cultured mammalian cells. 49 24

Some aspects of the inhibitory effect of caffeine on conjugation transfer of R-factors described by the authors earlier were studied. The effect of the above substance on the donor and recipient competence was tested in experiments with cultivation of the parent strains for 18 hours in the presence of caffeine. For this purpose the effect of caffeine on reduction of the donor and recipient cell competence after starvation in a physiological solution was investigated. It was shown that caffeine markedly decreased the donor competence of strain 15-3Mdrd of E. coli in the experiments of both types. Caffeine also inhibited reduction of the recipient competence of strain C600 of E. coli after starvation without its changing on 18-hour treatment. For the study of the caffeine effect on formation of the conjugation pairs experiments were carried out with dilution of the conjugation mixture after definite intervals which practically stopped formation of new conjugation pairs and eliminated further effect of caffeine on conjugation. Under such conditions transfer of R-factors may occur in the conjugation pairs after elimination of caffeine by dilution, if they were formed in the presence of caffeine before the mixture dilution. The experiments showed that caffeine inhibited not the formation of the conjugation pairs but the genetic transfer of R-factors. In addition, it was found that the substance insignificantly inhibited the process of phenotypic manifestation of the resistance markers. Inhibition of conjugation R-transfer by caffeine was associated with its eliminating effect, since the concentrations used did not induce elimination of the resistance markers in R+ strains.
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PMID:[Caffeine as an inhibitor of the conjugation transfer of R-factors. A study of certain aspects of the mechanism of action of caffeine on the conjugation transfer of R-factors]. 109 37

When the excision proficient strain E. coli WP2 Hcr+ trp- was grown to stationary phase by glucose starvation in M-9 minimal medium before UV -irradiation, the ability of nutrient broth enrichment of minimal medium to enhance trp- leads to Trp+ reversion was greatly reduced. Less than 50% of the Trp+ revertants were found to be ochre suppressors. However, in the WWP2 Hcr- strain, 75-86% of the tested revertants were ochre suppressors. This indicates that, under the cultural conditions employed, many potential suppressor mutations were removed by excision repair in the presence of broth enrichment. Broth enhancement of reversion also occurred in the Hcr- strain, which indicates that a less error-prone mode of recombination repair functions under minimal growth conditions. An Hcr+ strr derivative of WP2 Hcr+ was more resistant than its strs parent to the lethal effect of UV light and showed a lower UV-induced Trp+ reversion frequency. The percentage of Trp+ revertants that were due to ochre suppressors was markedly reduced in the strr strain. The Hcr- strr strain also had a lower UV-induced Trp+ reversion frequency than its strs parent. The excision repair inhibitor caffeine had little effect at lower UV doses on increasing Trp+ reversion in both Hcr+ strains. Acriflavine, however, was effective at lower UV doses in enhancing reversiin of the Hcr+ strains and the degree of enhancement increased with the dose. Acriflavine appeared to specifically enhance the number of ochre suppressing Trp+ revertants. In both Hcr- strains (strs and strr) caffeine (500 mug/ml) had no effect on survival but reduced the UV-induced Trp+ reversion frequency acting as an antimutagen. In contrast, acriflavine (2 mug/ml) decreased survival and increased the Trp+ reversion frequency of the Hcr- strains. The data on spontaneous Trp+ reversion frequencies show that the Hcr+ strs strain had a higher spontaneous reversion frequency than the Hcr- strs strain on all plating media. Further, caffeine was shown to reduce spontaneous Trp+ reversion in both Hcr+ and Hcr- strains while acriflavine increased the spontaneous reversion frequencies of both strains.
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PMID:The effect of streptomycin resistance, caffeine and acriflavine on ultraviolet light-induced reversion to tryptophan independence in strains of Escherichia coli B/r. 110 29

The addition of glucose to the medium of Tetrahymena thermophila results in a 7-fold repression of galactokinase (EC 2.7.1.6; ATP:D-galactose-1-phosphotransferase). The presence of millimolar amounts of the catecholamines dopa, dopamine, norepinephrine, and epinephrine or the hormone glucagon also results in the repression of galactokinase in the absence of glucose. The addition of millimolar amounts of adrenergic agonists (isoproterenol, tyramine, 2-amino-6,7-dihydroxytetrahydronaphthalene) results in significant repression of galactokinase in the absence of glucose; concentrations of 2-amino-6,7-dihydroxytetrahydronaphthalene less than or equal to 10(-4) M result in a derepression of galactokinase specific activity. Addition of adrenergic antagonists (propranolol, dichloroisoproterenol) have no effect on galactokinase activity at concentrations less than 10(-4) M but do arrest cell growth at greater concentrations. The addition of the cAMP analogs caffeine or theophylline in millimolar amounts results in repression of galactokinase activity; however, cell growth is greatly slowed or completely arrested at these concentrations. Analysis of the repression response of several mutants demonstrates that mutants deficient in catecholamine biosynthesis are altered in their regulation of galactokinase. Measurements of intracellular cAMP levels for 0-24 h following the addition of several of the above compounds to exponentially growing cells did not demonstrate any change over this period. Measurement of intracellular cAMP levels for 24 h following the addition of glucose or galactose to exponentially growing wild-type and mutant cell strains did not demonstrate any difference in cAMP concentrations over this period although a wide range of galactokinase activity was exhibited. Starvation of wild-type cells prior to the addition of glucose in minimal medium without added carbohydrate resulted in a significant increase in cAMP following the addition of glucose. This increase is demonstrated to be dependent upon the ability of the cells to resume division after the arrest of growth and is not correlated with galactokinase regulation. These results support the conclusion that cAMP is not involved in the repression of galactokinase gene expression initiated by glucose or hormone-like effectors and demonstrate the participation of an adrenergic control system in galactokinase regulation which is subordinate to the regulation by glucose. A possible model is discussed.
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PMID:Regulation of galactokinase gene expression in Tetrahymena thermophila. I. Intracellular catecholamine control of galactokinase expression. 241 Apr 18

Dictyostelium discoideum amebae chemotax toward folate during vegetative growth and toward extracellular cAMP during the aggregation phase that follows starvation. Stimulation of starving amebae with extracellular cAMP leads to both actin polymerization and pseudopod extension (Hall et al., 1988, J. Cell. Biochem. 37, 285-299). We have identified an actin nucleation activity (NA) from starving amebae that is regulated by cAMP receptors and controls actin polymerization (Hall et al., 1989, J. Cell Biol., in press). We show here that NA from vegetative cells is also regulated by chemotactic receptors for folate. Our studies indicate that NA is an essential effector in control of the actin cytoskeleton by chemotactic receptors. Guided by a recently proposed model for signal transduction from the cAMP receptor (Snaar-Jagalska et al., 1988, Dev. Genet. 9, 215-225), we investigated which of three signaling pathways activates the NA effector. Treatment of whole cells with a commercial pertussis toxin preparation (PT) inhibited cAMP-stimulated NA. However, endotoxin contamination of the PT appears to account for this effect. The synag7 mutation and caffeine treatment do not inhibit activation of NA by cAMP. Thus, neither activation of adenylate cyclase nor a G protein sensitive to PT treatment of whole cells is necessary for the NA response. Actin nucleation activity stimulated with folate is normal in vegetative fgdA cells. However, cAMP suppresses rather than activates NA in starving fgdA cells. This indicates that the components of the actin nucleation effector are present and that a pathway regulating the inhibitor(s) of nucleation remains functional in starving fgdA cells. The locus of the fgdA defect, a G protein implicated in phospholipase C activation, is directly or indirectly responsible for transduction of the stimulatory chemotactic signal from cAMP receptors to the nucleation effector in Dictyostelium.
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PMID:Transduction of the chemotactic signal to the actin cytoskeleton of Dictyostelium discoideum. 251 Oct 51

We have analyzed the effects of the cAMP relay inhibitor, caffeine, and the receptor antagonist, adenosine, on the regulation of the cell-surface cAMP receptor in suspension-starved Dictyostelium discoideum cells by measuring ammonium sulfate-stabilized binding of [3-H]cAMP to intact cells. When cells were starved in fast (230 r.p.m.) shaken suspension in 10 mM Na+/5 mM K+ phosphate buffer, pH 6.5, plus 1 mM CaCl2 and 2.5 mM MgCl2, and assayed for specific cAMP binding, receptor accumulation peaked at approximately 6 hours, reaching a maximum of 1.5 pmol cAMP bound/10(7) cells (saturation binding). Neither caffeine nor adenosine inhibited the accumulation of cAMP receptors. Similar results were obtained in caffeine-treated, slow shaken (90 r.p.m.) suspension cultures. These results suggest that starvation alone is sufficient stimulus to induce the cAMP receptor. We have also tested the effects of different buffer ionic compositions on the accumulation of cAMP receptors. Elevation of the monovalent ion concentration to 30-40 mM was found to significantly inhibit the induction of cAMP receptors.
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PMID:The effect of caffeine, adenosine, and buffer ionic composition on the induction of cell-surface cAMP binding during starvation of Dictyostelium discoideum. 285 21

Diet clearly influences neurotransmission. This can be important in grossly undernourished children. It can also be important in children in whom normal homeostatic mechanisms governing food intake are bypassed. Subtle differences in behavior can occur with physiologic variation in food intake. Components of foods can also be used as drugs. Starvation can impair neuronal maturation and can have lasting effects upon behavior and intellectual performance. The extent of starvation's impact upon the brain depends upon whether undernutrition occurred during a critical phase in brain development. Short-term fasting has small, but significant, effects upon intellectual performance. Even when gross malnutrition is not present, subtle changes in diet may modulate brain function. Tryptophan, tyrosine, and choline in the diet are used as precursors for neuronal synthesis of serotonin, dopamine and norepinephrine, and acetylcholine, respectively. It is likely that the brain's sensitivity to certain components of the diet exists to permit monitoring of food intake by the central nervous system. Tryptophan, tyrosine, and choline may be useful in treatment of humans with sleep disorders, pain depression, mania, hypertension, shock, or dyskinesias. Other components of the diet that may affect behavior include food additives, sugar, and caffeine. Food additives may exacerbate hyperactive symptoms in a small proportion of children with attention deficit disorder. Given that there is little potential for harm and that there is a subpopulation that may respond, a trial of a diet that contains no food additives may be a valid diagnostic approach for children with attention deficit disorder who do not respond to stimulant therapy or for children for whom stimulant therapy is not desired. Refined sugar has been blamed for many behavioral abnormalities. Subtle effects of carbohydrate upon behavior have been reported, but the existing data do not support the hypothesis that sucrose or fructose exert special effects upon neurotransmission. Caffeine is easily detected as a stimulant by humans, but it has little effect upon cognitive function. Administration of large doses of vitamins has no beneficial effect in most humans with schizophrenia, attention deficit disorder, autism, Down's syndrome, or drug addiction. Large doses of niacinamide may even be harmful, as they may cause hepatic damage.
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PMID:Dietary influences on neurotransmission. 302 51

We examined two sets of genes expressed early in the developmental cycle of Dictyostelium discoideum that appear to be regulated by cyclic AMP (cAMP). The transcripts of both sets of genes were not detectable in vegetative cells. During normal development on filter pads, RNA complementary to these genes could be detected at about 2 h, peaked around 6 to 8 h, and decreased gradually thereafter. Expression of these genes upon starvation in shaking culture was stimulated by pulsing the cells with nanomolar levels of cAMP, a condition that mimics the in vivo pulsing during normal aggregation. Expression was inhibited by caffeine or by continuous levels of cAMP, a condition found later in development when in vivo expression of these genes decreased. The inhibition of caffeine could be overcome by pulsing cells with cAMP. These results suggest that the expression is mediated via the cell surface cAMP receptor, but does not require a rise in intracellular cAMP. mRNA from a gene of the second class was induced upon starvation, peaked by 2.5 h of development, and then declined. In contrast to the other genes, its expression was maintained by continuous levels of cAMP and repressed by cAMP pulses. These and other results on a number of classes of developmentally regulated genes indicates that changing levels of cAMP, acting via the cell surface cAMP receptor, are involved in controlling these groups of genes. We also examined the structure and partial sequence of the cAMP pulse-induced genes. The two tandemly duplicated M3 genes were almost continuously homologous over the sequenced portion of the protein-coding region except for a region near the N-terminal end. The two M3 genes had regions of homology in the 5' flanking sequence and showed slight homology to the same regions in gene D2, another cAMP pulse-induced gene. D2 showed extremely significant homology over its entire sequenced length to an acetylcholinesterase. The results presented here and by others suggest that expression of many early genes in D. discoideum is regulated via the cell surface cAMP receptor. We expect that many of these genes may play essential roles in early Dictyostelium development and could code for elements of the cAMP signal transduction pathway involved in aggregation.
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PMID:Cyclic AMP regulation of early gene expression in Dictyostelium discoideum: mediation via the cell surface cyclic AMP receptor. 303 75


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