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Query: UMLS:C0038187 (starvation)
 24,951 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A 29-year-old woman with short bowel syndrome and prolonged starvation developed hyperchloremic metabolic acidosis after initiation of hyoeralimentation with a casein hydrolysate solution. The acidosis was not due to bicarbonate loss but was associated with diminished ability of the kidney to increase urinary acid excretion, particularly titratable acidity. Supplemental parenteral bicarbonate administration was necessary for two weeks until urinary acid excretion rose to normal.
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PMID:Metabolic acidosis after hyperalimentation with casein hydrolysate. Occurrence in a starved patient. 2 2

Experimental models of chronic and acute peptic ulcerations were produced in the albino rats by means of prolonged starvation and indomethacin administration. In the case of acute indomethacin-induced peptic ulceration, the effects of anticholinergic drugs on the ulcers produced were also studied. Starving the rats for a period of seven days produced gastric ulceration in all the rats used while indomethacin produced gastric ulceration within five hours in all the rats used. Severe ulceration of the degree found in human peptic ulcer disease was produced only by chronic starvation. Anticholinergic drugs ameliorated indomethacin-induced gastric ulceration, partly at least, by reducing intra-gastric acidity.
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PMID:Comparative studies on starvation - and indomethacin - induced ulcerations in albino rats. 3 60

Out of different azapyrimidines tested for their ability to affect metabolism of orotic acid in the liver of rats kept on food only 5-azacytidine resulted in the enhanced incorporation of orotate into liver RNA following 24 hr pretreatment. Similar effect was observed also in cycloheximide-treated animals. No stimulation of orotic acid utilization following 5-azacytidine or cycloheximidine treatment was observed in the liver of starved animals. Both drugs (but not other pyrimidine analogues tested) depressed markedly gastric secretion in rats and caused decreased evacuation of the stomach. The decreased secretion of pepsin and lower gastric acidity resulting in drug-simulated starvation of the treated animals are discussed in relation to the enhanced uptake of orotic acid into liver RNA.
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PMID:Lower gastric secretion and higher incorporation of orotic acid into liver RNA in rats treated with 5-azacytidine and cycloheximide. 7 86

Abomasal secretion has been collected from Grosskopftype pouches prepared in five adult Karrakul ewes. Feeding caused a marked increase in volume, acidity and pepsin activity, whereas these factors were reduced by starvation. Both insulin-induced hypoglycaemia and electrical stimulation of the vagal nerve supply to the pouch increased the volume, total acid and pepsin secretion. It is concluded that vagal activity is an important factor in the control of abomasal secretion in sheep.
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PMID:Neural and chemical control of abomasal secretion in sheep. 38

The restraint model and other models for the production of experimental stress ulcers have been reviewed. The mechanism of experimental stress ulcers appears to depend on an interaction between the presence of acid, changes in mucosal circulation, an increase in the excretion of glycoproteins in the mucus, and a decrease in mitotic activity of the mucosal lining of the stomach. Factors enhancing ulceration are cold, starvation, increased acidity, burns, reflux of bile, endotoxin, adrenalectomy, and hemorrhage. Factors inhibiting ulceration are vagotomy, anticholinergics, elemental diets, vitamin A, antacids, prevention of bile reflux, corticosteroids, epinephrine and norepinephrine, serotonin antagonists, and immediate replacement of blood loss with low molecular weight dextran. The role of sepsis is unclear and more work is needed in this area. Ulcers from intracranial injury are usually associated with the hypersecretion of gastric acid. Stimulation of the hypothalamus, directly or indirectly, with resultant vagal stimulation is thought to be the responsible mechanism for the increase in acid.
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PMID:Experimental stress ulcers: a review. 110 3

Eighty-eight children (mean age 5.6 yr, range 1-14 yr) about to undergo elective outpatient surgery were randomly assigned to four groups. All children were given phenolsulfonphthalein (PSP) orally 2-3 h before the scheduled time of surgery as a marker dye to assess gastric emptying. Immediately after receiving PSP they were given: group A--liquids, up to 5 ml/kg + placebo (glucose water 0.2 ml/kg); group B--liquids, up to 5 ml/kg + ranitidine 2 mg/kg in glucose water 0.2 ml/kg; group C--placebo only; group D--ranitidine only. Gastric contents were aspirated after induction of anesthesia. Mean volume (range) in ml/kg of aspirated gastric fluid in each group was: group A--0.34 (0-1.0); group B--0.17 (0.07); group C--0.25 (0-1.1); group D--0.16 (0-0.6). The pH mean (range) value was: group A--1.83 (0.9-3.6); group B--4.76 (2.0-7.7); group C--2.10 (1.2-4.1); group D--3.97 (1.3-7.3). PSP could not be detected in the gastric samples from children in whom the ingestion-sampling interval was more than 2.25 h. In comparison with prolonged starvation, administration of oral liquids without ranitidine 2-3 h preoperatively did not produce a significant increase in mean volume of gastric aspirate, and there was no increase in the number of patients with gastric aspirate greater than 0.4 ml/kg. Administration of ranitidine with or without fluids resulted in a decrease in both volume and acidity of gastric contents.
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PMID:Effect of oral liquids and ranitidine on gastric fluid volume and pH in children undergoing outpatient surgery. 231 45

A study was undertaken on the antiulcer effect of some active ingredients present in the lipid part of the fruits of M. azedarach administered p.o. to male rats. Acute gastric ulcers were induced by gipsing the rats for 22 hr preceded by 24 hr starvation to obtain the maximum stress. The free HCl, total HCl and total acidity were also measured. The total lipid (TLP), 1.0, 2.5 and 5.0 g/kg, reduced the ulcer index by 25-41.8% and 50-58% when given daily for 5 and 10 days, respectively. The saponifiable fraction (SP), 0.85, 2.0 and 4.0 g/kg, given for 10 days reduced the ulcer index by 41.8-50%, while the nonsaponifiable (NSP), 0.075, 0.150 and 0.50 g/kg, for 10 days reduced it by 50-83.5%. The 70% ethanol extract of the defatted residue showed no antiulcer effect. Analysis of the gastric juice showed a significant decrease in free HCl (P less than 0.001) induced by TLP; the total HCl and total acidity were reduced only at 5 g/kg. The results revealed the antiulcer effect of the lipid components of M. azedarach fruits which is mainly due to the phytosterol fraction.
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PMID:Effect of Melia azedarach fruits on gipsing-restraint stress-induced ulcers in rats. 654 33

Acidification power, defined as the sum of the spontaneous pH change determined after suspending yeast cells in water and the substrate-induced pH change after addition of glucose to the resulting suspension, reflects the level of cellular energy sources. Its use as an indicator of metabolic state of the cells was tested during a 120-h aerobic starvation. Its changes coincided with changes in cell viability, initial rate of endogenous oxygen consumption rate, cell ATP, extra- and intracellular buffering capacity, and the ability of cell-free extract to produce acidity by glucose fermentation. It was used as a sensitive marker of metabolic changes occurring during starvation, on treatment with glycolytic and respiratory inhibitors, and at elevated temperature.
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PMID:Acidification power: indicator of metabolic activity and autolytic changes in Saccharomyces cerevisiae. 675 71

It is now generally recognized that cell growth conditions in nature are often suboptimal compared to controlled conditions provided in the laboratory. Natural stresses like starvation and acidity are generated by cell growth itself. Other stresses like temperature or osmotic shock, or oxygen, are imposed by the environment. It is now clear that defense mechanisms to withstand different stresses must be present in all organisms. The exploration of stress responses in lactic acid bacteria has just begun. Several stress response genes have been revealed through homologies with known genes in other organisms. While stress response genes appear to be highly conserved, however, their regulation may not be. Thus, search of the regulation of stress response in lactic acid bacteria may reveal new regulatory circuits. The first part of this report addresses the available information on stress response in Lactococcus lactis. Acid stress response may be particularly important in lactic acid bacteria, whose growth and transition to stationary phase is accompanied by the production of lactic acid, which results in acidification of the media, arrest of cell multiplication, and possible cell death. The second part of this report will focus on progress made in acid stress response, particularly in L. lactis and on factors which may affect its regulation. Acid tolerance is presently under study in L. lactis. Our results with strain MG1363 show that it survives a lethal challenge at pH 4.0 if adapted briefly (5 to 15 minutes) at a pH between 4.5 and 6.5. Adaptation requires protein synthesis, indicating that acid conditions induce expression of newly synthesized genes. These results show that L. lactis possesses an inducible response to acid stress in exponential phase. To identify possible regulatory genes involved in acid stress response, we determined low pH conditions in which MG1363 is unable to grow, and selected at 37 degrees C for transposition insertional mutants which were able to survive. About thirty mutants resistant to low pH conditions were characterized. The interrupted genes were identified by sequence homology with known genes. One insertion interrupts ahrC, the putative regulator of arginine metabolism; possibly, increased arginine catabolism in the mutant produces metabolites which increase the pH. Several other mutations putatively map at some step in the pathway of (p)ppGpp synthesis. Our results suggest that the stringent response pathway, which is involved in starvation and stationary phase survival, may also be implicated in acid pH tolerance.
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PMID:Lactococcus lactis and stress. 887 9

The aggravation of acid-induced gastric damage and its prevention by glucose, ascorbate or glutathione precursors was studied in fed and food-deprived rats. The stomachs of fed rats and those starved for 1, 3 or 5 d were vagotomized just before irrigating for 3 h with solutions containing 0-150 mmol HCI/L. Mucosal glutathione, mucus, lipid peroxides and acid back-diffusion were measured. Stomach ulcers were evaluated by morphological and histological examination. The preventive effects of glucose, ascorbate and a mixture of L-glutamine, L-glycine and L-cysteine were evaluated in the stomachs of rats that were starved for 5 d, vagotomized, then perfused for 3 h with 100 mmol HCI/L. Greater acid back-diffusion and ulcer formation, and lower glutathione and mucus levels in starved rats were dependent on the duration of starvation and luminal acidity. Increased acid back-diffusion and decreased glutathione and mucus production were negatively correlated (r < -0.80, P < 0.05) with ulcer formation. A significant enhancement in mucosal lipid peroxide concentration and serious damage of forestomach and corpus mucosal cells were observed in starved rats exposed to 100 mmol HCI/L. These ulcerogenic factors were effectively inhibited in acid-perfused stomachs of food-deprived rats by daily intraperitoneal injection of the amino acid mixture (150 mg/kg) or by an average daily consumption via drinking water of glucose (10 g) or ascorbate (1.2 g). Starvation aggravated acid-induced gastric damage and was associated with greater acid back-diffusion and oxygen radical generation, and lower mucosal glutathione and mucus production.
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PMID:Acid-induced gastric damage in rats is aggravated by starvation and prevented by several nutrients. 910 15


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