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)

Regulation of T4-specific mRNA synthesis was studied during leucine starvation of a leucine-requiring stringent Escherichia coli B strain. This was done by imposing starvation prior to T4 infection and then letting RNA synthesis proceed for different time periods. Rifampin or streptolydigin was added to stop further RNA synthesis, and protein synthesis was restored by addition of leucine. Samples were withdrawn at different times, and the enzyme-forming capacities found that, during conditions which elicit the stringent response in uninfected bacteria, immediate early mRNA is not stringently regulated. This conclusion contradicts the earlier conclusion of others, obtained by measuring incorporation of radioactive uracil; this is explained by the observation of Edlin and Neuhard (1967), confirmed and extended by us to the T4-infected cell, that the incorporation of uracil into RNA of a stringent strain is virtually blocked by amino acid starvation, whereas that of adenine continues at 30 to 50% of the rate seen in the presence of the required amino acid.
J Virol 1975 Sep
PMID:Regulation of early mRNA synthesis after bacteriophage T4 infection of Escherichia coli. 109 29

The inhibition of Salmonella typhimurium by 1,2,4-triazole appears to be mediated through an effect on L-cysteine biosynthesis. O-Acetylserine sulfhydrylase A, the final enzyme in the L-cysteine biosynthetic pathway, was found to catalyze a reaction (triazolylase) between O-acetyl-L-serine and 1,2,4-triazole, giving 1,2,4-triazole-1-alanine as a product. In wild type S. typhimurium grown on 4 mM 1,2,4-triazole, 97% of the total O-acetyl-L-serine synthesized in vivo is incorporated into 1,2,4-triazole-1-alanine. 1,2,4-triazole also significantly lowers the levels of several of the enzymes necessary for sulfate reduction. This effect is presumably due to the ability of the inhibitor to lower intracellular concentrations of O-acetyl-L-serine, an inducer of these enzymes. Inhibition of growth is probably caused by L-cysteine starvation, arising from the decreased availability of the L-cysteine precursors, sulfide and O-acetyl-L-serine. Two 1,2,4-triazole-resistant strains bearing mutations in cysK, the structural gene for O-acetylserine sulfhydrylase A, incorporate only small quantities of O-acetyl-L-serine into 1,2,4-triazole-1-alanine in vivo. In vitro studies, using purified preparations of O-acetylserine sulfhydrylase A, revealed greater losses of triazolylase activity than sulfhydrylase activity in the enzymes from both cysK mutants. Resistance to 1,2,4-triazole apparently can arise from mutations leading to a preferential loss of triazolylase activity or from mutations which diminish both activities to the extent that high concentrations of O-acetyl-L-serine and sulfide accumulate behind the sulfhydrylase reaction.
J Biol Chem 1975 Sep 25
PMID:Studies on the mechanism of inhibition of Salmonella typhimurium by 1,2,4-triazole. 110 Jun 24

The synthesis of ribosomal proteins during pyrimidine starvation was investigated. A progressive turn-off of protein synthesis, with a decay half-time of about 5 min, was observed when Escherichia coli cells were starved of uridine. By means of double-labelling, the syntheses of different ribosomal proteins were shown to be turned off unequally during the starvation. Comparison of the turn-off patterns for some proteins and the known polycistronic organization of the structural genes for these proteins suggests that a major cause of the unequal turn-off was the degradation of mRNA molecules for the ribosomal proteins from the 5'-end toward the 3'-end.
Biochem J 1975 Sep
PMID:Regulation of synthesis of ribosomal proteins during pyrimidine starvation in Escherichia coli. 110 74

Although there exists some indirect evidence that circulating ketone bodies might inhibit their own production rate, the direct demonstration of this homeostatic feed-back phenomenon is still lacking. The present work aims at demonstrating the operation of this control mechanism in human fasting ketosis. Six obese subjects, who fasted 2-23 days, were given a primed constant i.v. infusion of 3- 14C-acetoacetate for 4 hr. After a control period of 2 hr, unlabeled sodium acetoacetate was administered as a primed constant i.v. infusion at the rate of 0.688-1.960 mmol/min until the end of the study. During both periods, the rates of inflow of ketones were estimated from the specific activity of total ketones measured under near isotopic steady state conditions. During the control period, total ketone concentration amounted to 3.98-9.65 mumol/ml and production rates of total ketones ranged between 1.450 and 2.053 mmol/min. The levels of free fatty acids, glycerol, glucose, and insulin averaged respecitvely 1.30 mumol/ml, 0.11 mumol/ml, 74 mg/100 ml, and 5.2 muU/ml. The administration of exogenous ketones during the second phase of the study induced a 47%-92% increase in total ketone levels. During this period, the endogenous production of ketones (calculated as the difference between total inflow rate and acetoacetate infusion rate) amounted only to 67%-90% of control values. Among other factors, this inhibition of ketogenesis was probably partially related to the direct antilipolytic effect of infused ketones. Indeed, there was a concomitant fall in FFA and in glycerol levels averaging respectively 13.5% and 17.3%, without significant changes in peripheral insulin concentrations. Our results demonstrate that during fasting, circulating ketone bodies exert an inhibitory influence on the rate of ketogenesis. This mechanism might play an important role in preventing the development of uncontrolled hyperketonemia during starvation.
Metabolism 1975 Sep
PMID:Inhibition of ketogenesis by ketone bodies in fasting humans. 115 76

Experiments were conducted to determine whether the rate of entry of arginine into liver varies with changes in dietary protein or in the protein-catabolic state of the animal. It was first established by liver perfusion with [14C]ureidocitrulline that release of arginine by liver is sufficiently small that it can be ignored and that disappearance of arginine from a perfusion medium can be used to measure entry rate. Disappearance rates of arginine were then determined for rats that had been starved of fed either a stock control diet, a 15% casein diet, a 90% casein diet, or which had been injected with cortisol. There was no difference in arginine uptake between the control and 15% casein groups. The high protein group showed a threefold increase in rate of entry of arginine into liver as compared with the control group. Cortisol treatment and 48 hours of starvation also caused a threefold increase in arginine uptake. Cortisol treatment combined with high protein adaptation resulted in a sevenfold increase over controls. It was concluded that rate of entry of arginine into rat liver varies with nutritional and endocrine states.
J Nutr 1975 Sep
PMID:Effects of protein content of diet and cortisol treatment on uptake of arginine by rat liver. 115 37

In subjects of ideal weight (7 males and 7 females) total whole blood ketones and breath acetone were determined during a 6 day fast, and in obese subjects (8 males, 18 females) during 6-28 days of fasting. Development of starvation ketosis was significantly slower in overweight than in normal weight subjects. Breath acetone concentration was up to blood ketone levels of 4 mMol/1 a linear function of the blood ketone concentration, beyond that level, however, an additional exponential component became apparent. The highest acetone elimination found was 4.46 mg/min, corresponding to 6.4 g acetone and 11.2 g acetoacetic acid in 24 hours. Hence the decarboxylation of acetoacetic acid to acetone may be an additional mechanism for the lowering of ketoacidosis in starvation.
Res Exp Med (Berl) 1975 Sep 24
PMID:[Breath acetone and ketonemia in normal- and overweight subjects during total fasting (author's transl)]. 116 85

In many eucaryotic systems protein synthesis is coupled to ribosomal RNA synthesis such that shut-down of the former causes inhibition of the latter. We have investigated this stringency phenomenon in HeLa cells. The protein synthesis inhibitors cycloheximide and puromycin cause inactivation of both processes but valine starvation totally inhibits only the processing of 45-S RNA. DNA-dependent RNA polymerases from A, B and C (or I, II and III respectively) were extracted, separated partially by DEAE-cellulose chromatography and their activity levels determined. These do not decrease significantly during inhibition of protein synthesis. To find out whether or not form A is bound to its template under these conditions, proteins were removed from chromatin with the detergent sarkosyl. This does not affect bound RNA polymerase. Inhibition of protein synthesis caused up to 50% reduction in endogenous alpha-amanitin-insensitive chromatin-RNA-synthesising activity. This reduced level of activity was not affected by sarkosyl treatment. Levels in normal cells were stimulated. This result indicates that the form A RNA polymerase is not bound to its template when protein synthesis is inhibited.
Eur J Biochem 1975 Sep 01
PMID:Studies on the control of ribosomal RNA synthesis in HeLa cells. 117 42

This study was designed to explore the relationship of estrogen, human chorionic gonadotropin (HCG), and food availability to endocytosis in developing oocytes. When estrogen alone is administered to an animal, large amounts of vitellogenin are synthesized by the liver and secreted into the circulatory system, where it accumulates. Under these conditions there is no evidence of endocytosis at the surface of the oocytes. Other studies have shown that following HCG injection into estrogen-treated animals, vitellogenin is removed from the circulation and the oocyte surface is highly contoured and displays endocytotic activity. Food deprivation has much the same effect on oocyte endocytosis as does estrogen. When animals are given HCG and subsequently starved for 20 days, developing oocytes show little endocytotic activity. We conclude that HCG acts to promote or stimulate endocytosis in developing oocytes while estrogen and/or starvation inhibits this process.
Cell Tissue Res 1975 Sep 17
PMID:Oogenesis in Xenopus laevis (Daudin). IV. Effects of gonadotropin, estrogen and starvation on endocytosis in developing oocytes. 118 Oct 38

Phosphatidylethanolamine in freshly drawn human erythrocytes is trinitrophenylated by 2,4,6-trinitrobenzene sulfonic acid only slowly and to a maximum of 32%. After different preincubation procedures at 37 degrees C in saline media in the absence of glucose (24 h without additive, 1-5 h with 8 mM hexanol or 1-4 h with the SH reagent, 5 mM tetrathionate) the rate of subsequent trinitrophenylation of phosphatidylethanolamine, in the absence of the additives, is greatly enhanced and the amount of phospholipid reacting increased. Glucose or inosine prevent these effects, inhibitors of glycosis abolish this protection. The results indicate that in fresh as well as in glycolysing incubated erythrocytes phosphatidylethanolamine in the outer layer of the membrane lipid is shielded by a protein. Conformational changes of this protein induced by metabolic starvation and perturbing agents expose the phospholipid head group to 2, 4, 6-trinitrobenzene sulfonic acid. In addition, a "flip-flop" of phosphatidylethanolamine from the inner to the outer layer may also contribute to the effects observed.
Biochim Biophys Acta 1975 Sep 02
PMID:Experimental alteration of phospholipid-protein interactions within the human erythrocyte membrane. Dependence on glycolytic metabolism. 118 48

The authors present the results of experimental-morphological study of the intestine and other internal organs of guinea pigs subjected and not subjected to starvation infected with a dysentery culture against the background of antiepithelial serum. A marked form of the infectious process with erosive-ulcerative affection of the cecum mostly developed in 70% of the former and in 58.8% of the latter animals.
Zh Mikrobiol Epidemiol Immunobiol 1975 Sep
PMID:[Morphological characteristics of an experimental dysenteric infection reproduced against a background of reduced intestinal mucosal resistance]. 119 88


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