Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0038187 (starvation)
 24,951 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The effect of starvation on liver weight and the specific activity of hepatic tryptophan dioxygenase (EC 1.13.1.12) in prepubertal male rats (Vom Ife strain) maintained in several stages of fasting was studied. The specific activity of hepatic tryptophan dioxygenase was significant after 24 h of fasting. It then fell to a nadir at 96 h before a secondary but significant peak after 120 h. During refeeding after a 120 h fast the specific activity was initially lower than controls after 96 h. The liver weight was significantly lower than controls throughout the fasting period although it was higher at 96 h. On refeeding the liver weight attained control values after 96 h. There appears to be some adaptive change with respect to liver weight and the specific activity of tryptophan dioxygenase at 96 h during fasting, and on refeeding after a severe fast.
 ...
PMID:Changes in rat liver weight and specific activity of hepatic tryptophan dioxygenase in different stages of fasting. 209 Mar 91

The effect of tryptophan and uracil starvation on the viability of the transformant B. subtilis BSA 170 trp- ura- and its parent strains Bacillus subtilis PB 168 trp -C and Bacillus subtilis PB 3308 ura- was examined. These studies were performed at the conditions for competence development, during 16 hours. Our results showed that B. subtilis BSA 170 was resistant to tryptophan-less death during all the assay and was also resistant to uracil-less death during three hours. After this time, viability measurements revealed less colony forming units per milliliter, and decrease of the culture absorbances. The uracil-less death required the presence of tryptophan suggesting that protein synthesis is needed. The parental strains exhibit similar behavior. Bacillus subtilis PB 168 was resistant to tryptophan-less death and B. subtilis PB 3308 showed decrease of the viability after uracil starvation comparable to that of the transformant strain.
 ...
PMID:[Viability of Bacillus subtilis auxotrophs in the absence of their essential metabolites]. 212 39

Recent pharmacological studies have more precisely characterised the nature of the inhibitory effect of brain serotonin (5-hydroxytryptamine) on feeding behaviour. Thus, the brain sites and receptors involved have been identified, and a possible physiological role of endogenous serotonin in controlling natural patterns of eating and nutrient selection has been defined. The medial hypothalamus is believed to be a critical location in the mediation of serotonin's action. Specifically, the paraventricular and ventromedial nuclei are known to be involved in controlling energy balance, while the suprachiasmatic nucleus determines circadian patterns of eating. Serotonergic stimulation of these 3 nuclei with exogenous serotonin or drugs that release endogenous serotonin, preferentially reduces carbohydrate intake in naturally feeding animals through satiety mechanisms involved in the termination of feeding. This phenomenon is mediated by serotonin and possibly serotonin receptors, in contrast to serotonin autoreceptors which potentiate feeding possibly by inhibiting serotonin release. The activity of serotonergic function in the medial hypothalamus exhibits a circadian rhythm which is characterised by a peak at the beginning of the active cycle when the motivation to eat is strongest and is triggered by deficits in energy stores. At this time, carbohydrate is found to be the naturally preferred macronutrient, and it appears that serotonin becomes most activated under these conditions to terminate the carbohydrate-rich meal, possibly by activating satiety neurons localised in the medial hypothalamus. In this process, serotonin may interact antagonistically with noradrenaline (norepinephrine) and its alpha 2-noradrenergic receptors that normally function to enhance carbohydrate intake at the onset of the natural feeding cycle. Moreover, while inducing satiety for carbohydrate, serotonin may also play a role in switching the animal's preference towards protein. The regulation of this macronutrient is closely linked to that of carbohydrate, and it is normally preferred in the second meal of the natural feeding cycle. Most of the pharmacological evidence to date generally supports the hypothesis that disturbances in serotonin function occur in eating disorders. Decreases in plasma tryptophan, urinary 5-hydroxyindoleacetic acid (5-HIAA), platelet serotonin binding and basal cerebrospinal fluid 5-HIAA in anorexia nervosa normalise upon weight restoration and appear to be starvation effects. These alterations in serotonergic function may however perpetuate the symptomatology of anorexia nervosa once the illness is set in motion. Some drugs which in part affect serotonergic function facilitate weight gain in conjunction with an integrated psychotherapeutic and behavioural programme. Patients with bulimia nervosa, regardless of the presence of anorexia nervosa or major depression, who have been relatively weight stable and free of binge/vomit episodes for at least 3 weeks, have significantly blunted prolactin responses to the serotonin agonists. These findings indicate that post-synaptic responsiveness in hypothalamic-pituitary serotonergic pathways is reduced in bulimia. Similar alterations in other serotonin pathways at or above the level of the hypothalamus may contribute to binge eating and other behavioural symptoms in bulimic patients. The clinical response to several psychotropic agents known to potentiate serotonergic transmission further substantiates a serotonin dysregulation hypothesis of bulimia nervosa.(ABSTRACT TRUNCATED AT 400 WORDS)
 ...
PMID:The role of serotonin in eating disorders. 219 74

Recent reports have called into question the widespread belief "that mutations arise continuously and without any consideration for their utility" (in the words of J. Cairns) and have suggested that some mutations (which Cairns called "directed" mutations) may occur as specific responses to environmental challenges, i.e., they may occur more often when advantageous than when neutral. In this paper it is shown that point mutations in the trp operon reverted to trp+ more frequently under conditions of prolonged tryptophan deprivation when the reversions were advantageous, than in the presence of tryptophan when the reversions were neutral. The overall mutation rate, as determined from the rates of mutation to valine resistance and to constitutive expression of the lac operon, did not increase during tryptophan starvation. The trp reversion rate did not increase when the cells were starved for cysteine for a similar period, indicating that the increased reversion rate was specific to conditions where the reversions were advantageous. Two artifactual explanations for the observations, delayed growth of some preexisting revertants and cryptic growth by some cells at the expense of dying cells within aged colonies, were tested and rejected as unlikely. The trp+ reversions that occurred while trp- colonies aged in the absence of tryptophan were shown to be time-dependent rather than replication-dependent, and it is suggested that they occur by mechanisms different from those that have been studied in growing cells. A heuristic model for the molecular basis of such mutations is proposed and evidence consistent with that model is discussed. It is suggested that the results in this and previous studies can be explained on the basis of underlying random mechanisms that act during prolonged periods of physiological stress, and that "directed" mutations are not necessarily the basis of those observations.
 ...
PMID:Spontaneous point mutations that occur more often when advantageous than when neutral. 222 88

Male Long-Evans rats were given 50 micrograms/kg 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) intraperitoneally and after 1, 4, 28 or 76 hr, noradrenaline, dopamine, dihydroxyphenylacetic acid (DOPAC), homovanillic acid (HVA), 5-hydroxytryptamine (5-HT), 5-hydroxyindoleacetic acid (5-HIAA), tryptophan and histamine were measured in the brain (dissected into ten parts) as well as in the pituitary gland. Several slight but significant changes were observed, e.g. in the hypothalamus where HVA and 5-HIAA were decreased after 4 hr, noradrenaline was decreased after 76 hr and histamine increased after 28 hr. Several late changes were also found, conspicuously tryptophan was increased in most brain areas after 76 hr and in some cases earlier; these changes may be due to starvation after hypophagia rather than TCDD directly. The results demonstrate that TCDD causes changes in brain neurotransmitter systems, but the changes are minor and it is not likely that aminergic systems are the key mediators in TCDD-induced hypophagia.
 ...
PMID:Changes in rat brain monoamines, monoamine metabolites and histamine after a single administration of 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD). 225 84

Starvation of Mouse hepatoma cells for essential amino acids or glucose results in the mono-ADP-ribosylation of the 78 kDa glucose-regulated protein, GRP78. Here we show that the ADP-ribosylated and non-ADP-ribosylated forms of GRP78 are interconvertible during tryptophan starvation and refeeding. In addition, the ADP-ribosylation of GRP78 was shown to be reversible even during nutritional stress. The overexpressed pool of non-ADP-ribosylated GRP78 synthesized during tunicamycin treatment was available for ADP-ribosylation during subsequent amino acid starvation, especially in the absence of tunicamycin. The reversible ADP-ribosylation of GRP78 could be part of a metabolic control mechanism in operation during nutritional stress.
 ...
PMID:Reversible ADP-ribosylation of the 78 kDa glucose-regulated protein. 226 6

We present an analysis of the expression of the trpE gene and the trpFBA operon in the dimorphic bacterium Caulobacter crescentus. The catalytic activity of component I of anthranilate synthase, the product of the trpE gene, was efficiently inhibited by tryptophan, the end product of the pathway, which suggests that tryptophan biosynthesis is likely controlled at the pathway level in C. crescentus. However, trpFBA mRNA levels and trpE enzyme levels did not vary significantly in wild-type C. crescentus in response to the presence of tryptophan in the growth medium or to growth in minimal versus rich medium. This lack of regulation of the trpE, trpF, trpB, and trpA genes is consistent with the idea that oligotrophic bacteria, such as C. crescentus, do not utilize regulatory mechanisms that greatly alter the biosynthetic capabilities in exponentially growing cells. In contrast, mRNA levels from the 5'-untranslated region and the upstream gene (usg) coding region increased dramatically in C. crescentus trpD or hisB auxotrophs starved for tryptophan or histidine, respectively. Surprisingly, concomitant increases in mRNA levels were not detected from the trpF, trpB, or trpA coding regions downstream in the operon. Thus, severe starvation of C. crescentus for amino acids appears to elicit a strong, general transcriptional response that is not observed in bacteria growing exponentially in medium lacking amino acids.
 ...
PMID:Regulation of tryptophan biosynthesis in Caulobacter crescentus. 244 92

Starvation of a mouse hepatoma cell line, Hepa, for any essential amino acid results in the mono-ADP-ribosylation of an 80-kDa protein, P80. The ADP-ribose acceptor and its putative precursor were identified in two-dimensional gel patterns and isolated by electroelution. Amino-terminal sequence analysis showed they were the 78-kDa glucose-regulated protein, GRP78. Starvation of Hepa cells for tryptophan or glucose stimulated the relative rate of synthesis, and the ADP-ribosylation of GRP78. Inhibition of N-linked glycosylation by treatment with tunicamycin, 2-deoxy-D-glucose or glucosamine stimulated the synthesis of non-ADP-ribosylated GRP78 up to sixfold with relatively little effect on its ADP-ribosylation. Both forms were identified in mouse liver, lung, heart, kidney, spleen and brain.
 ...
PMID:ADP-ribosylation of the 78-kDa glucose-regulated protein during nutritional stress. 251 84

Adult rats were submitted to a 4-day starvation period or maintained on a 50% carbohydrate-restricted diet for 8 consecutive days to obtain a body weight loss of 20-30%. Serum dopamine-beta-hydroxylase (DBH) activity and amino acids content were measured as well as brain tryptophan and tyrosine levels. Moreover, brain serotonin (5-HT), 5-hydroxyindoleacetic acid (5-HIAA), noradrenaline (NA), and dopamine (DA) contents were assayed in five brain areas. In 4-day starved and 8-day carbohydrate-restricted rats, the serum tyrosine and total tryptophan contents as well as tyrosine to the sum of six neutral amino acids ratios were lowered. Moreover, in these groups, free tryptophan to the sum of six neutral amino acids ratio remained normal and serum DBH activity increased. In the brain, to a decreased tyrosine content observed in 4-day starved and 8-day carbohydrate-restricted rats corresponded a high DA to NA ratio in the hypothalamus, thalamus, and raphe nuclei, thus suggesting a low DA utilization whereas a low DA to NA ratio was found in the neostriatum. On the other hand, brain tryptophan content was decreased in 4-day starved rats and increased in 8-day carbohydrate-restricted rats. In the former group, a high 5-HT to 5-HIAA ratio characteristic of a low 5-HT utilization was found in the hypothalamus and neostriatum whereas in the latter group a significant decrease in this ratio was only observed in the thalamus. These results suggest that the biochemical response to starvation vs carbohydrate restriction can be differentiated on neurochemical and neuroanatomical bases.
 ...
PMID:Comparative effects of carbohydrate restriction vs starvation on biochemical parameters related to neurotransmitters in rat. 256 2

This study describes the isolation and characterization of a mutant (strain GP122) of Salmonella typhimurium with a partial deficiency of phosphoribosylpyrophosphate (PRPP) synthetase activity. This strain was isolated in a purE deoD gpt purin auxotroph by a procedure designed to select guanosine-utilizing mutants. Strain GP122 had roughly 15% of the PRPP synthetase activity and 25% of the PRPP pool of its parent strain. The mutant exhibited many of the predicted consequences of a decreased PRPP pool and a defective PRPP synthetase enzyme, including: poor growth on purine bases; decreased accumulation of 5-aminoimidazole ribonucleotide (the substrate of the blocked purE reaction) under conditions of purine starvation; excretion of anthranilic acid when grown in medium lacking tryptophan; increased resistance to inhibition by 5-fluorouracil; derepressed levels of aspartate transcarbamylase and orotate phosphoribosyltransferase, enzymes involved in the pyrimidine de novo biosynthetic pathway; growth stimulation by PRPP-sparing compounds (e.g. guanosine, histidine); poor growth in low phosphate medium; and increased heat lability of the defective enzyme. This mutant strain also had increased levels of guanosine 5'-monophosphate reductase. This genetic lesion, designated prs, was mapped by conjugation and phage P22-mediated transduction at 35 units on the Salmonella linkage map.
 ...
PMID:Characterization of a Salmonella typhimurium mutant defective in phosphoribosylpyrophosphate synthetase. 258 45


<< Previous 1 2 3 4 5 6 7 8 9 10 Next >>