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)

The rate of protein degradation in cultured Chinese hamster ovary cells increases in response to histidine starvation. Using cell lines with defective histidyl-tRNA synthetase, or histidinol (a competitive inhibitor of the enzyme), we have previously demonstrated a functional connection between the increase in degradation and the amino acylation of this tRNA (Scornik, O. A., Ledbetter, M. L. S., and Malter, J. S. (1980) J. Biol. Chem. 255, 6322-6329). A correlation is shown here between the steady state level of histidyl-tRNA and the regulatory response. Cells were incubated for 15 min in the presence of L-[3H]histidine, at a concentration at which greater than 90% of histidine for protein synthesis derives from the medium. The level of histidyl-tRNA was measured by its radioactivity after purification by phenol extraction, ethanol precipitation, and mild alkaline hydrolysis. Protein degradation in each condition was determined by the release of acid-soluble radioactivity from cells labeled for 24 h with L-[1-14C]leucine. The steady state level of histidyl-tRNA was altered by either histidinol (which slows down its production) or cycloheximide (which interferes with its utilization). Cycloheximide counteracts the effects of histidinol both on the level of histidyl-tRNA and on the rate of protein degradation. Both effects can be obtained, however, even in the presence of cycloheximide, if higher concentrations of histidinol are used. The results indicate that this regulatory mechanism does not recognize the rate of amino acylation per se but rather, the steady state level of its product, amino acyl-tRNA.
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PMID:Faster protein degradation in response to decreases steady state levels of amino acylation of tRNAHis in Chinese hamster ovary cells. 654 56

As was shown using various reagents (Ag+, Cd2+) and solvents (ethanol, methanol), Thiobacillus ferrooxidans cells accumulate colloidal sulfur when they grow in the medium 9K containing elemental sulfur. Colloidal sulfur is accumulated in the periplasmic space, in large, bipolarly arranged spherical structures and in simple invaginates of the cytoplasmic membrane. T. ferrooxidans cells accumulate the sulfur at a highest rate during the stationary phase of growth and can use it as a source of energy under the conditions of starvation. The factors causing sulfur accumulation in T. ferrooxidans cells are discussed.
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PMID:[Nature of the sulfur-containing component and its function in Thiobacillus ferrooxidans]. 664 91

Vitamin D deficiency was induced in lactating rats and their pups by placing female rats on a vitamin D-deficient diet immediately after mating. Evidence of vitamin D deficiency included undetectable plasma levels of 25-hydroxyvitamin D3 in the dams, maternal hypocalcemia, the lack of pup growth, and pup hypocalcemia following starvation. This method of producing vitamin D-deficient pups was then used to determine whether the failure of vitamin D-deficient pups to grow properly results from a maternal or neonatal defect. Vitamin D-deficient dams and pups were injected with either vitamin D3 or the ethanol vehicle, and pup growth was monitored over the subsequent 6 days. Providing vitamin D3 to the pups directly had no effect on their growth, but administering vitamin D3 to the dams resulted in a tripling of the pup growth rate. The failure of vitamin D3 to promote pup growth when given directly to the pups was not the result of their inability to metabolize the vitamin because these pups converted [3H]-vitamin D3 to 25(OH)D3, 24,25(OH)2D3, and 1,25(OH)2D3 as determined by comigration with standards on both straight and reverse phase high-performance liquid chromatography systems. These results demonstrate that a maternal defect is responsible for the growth failure observed in vitamin D-deficient rat pups.
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PMID:A maternal defect is responsible for growth failure in vitamin D-deficient rat pups. 670 50

The effects of ethanol and starvation on ketone body production and utilization were investigated. In the first experiment, adult C57BL/6J mice were divided into four groups: (i) control (fed); (ii) starvation (up to 31 h); (iii) ethanol (acute 5 g/kg i.p.); (iv) ethanol (ETOH) + starvation. Plasma ketone body (KB) concentrations in control mice remained constant at approx. 0.37 mM. The levels of KBs in starved mice began to increase at about 7 h and rose to a peak of 2.5 mM at about 24 h, then fell to 1.8 mM at 31 h. The levels in mice treated with ETOH began to rise soon after injection, reached 1.5 mM at 10 h, and returned to control levels by 15 h. Although there was no difference in elevated levels of KBs between two groups of mice treated with ETOH plus starvation and ETOH alone at 7-10 h, the level continued to rise steadily to 2.0 mM through 31 h in the former group. At 10 h post ETOH, mice either fed ad lib. or fasted had increased hepatic capacity to synthesize acetoacetate (AcAc) from palmitate; this effect was prolonged and enhanced by continued fasting for 24 h. In the brain, the rate of AcAc oxidation was twice that for beta-hydroxybutyrate (beta OHB) and glucose. Neither ETOH nor starvation affected energy production from KB and glucose. AcAc was also utilized for fatty acid synthesis and the rate of synthesis was stimulated by ETOH at 10 h after injection. The rate of lipogenesis from beta OHB accounted for less than 10% of that from AcAc. Together these experiments demonstrate that ETOH increases both hepatic ketone production and plasma KB levels for at least 10 h. ETOH alone led to elevated KB levels long before the rise due to starvation. In brain, at 10 h, an increased capacity to utilize AcAc for lipogenesis was found. The results indicate that ETOH through the production of KBs could provide an important source of energy and lipid precursors for the brain of mice.
Drug Alcohol Depend 1984 Mar
PMID:Temporal changes in plasma levels and metabolism of ketone bodies by liver and brain after ethanol and/or starvation in C57BL/6J mice. 672 14

Three experiments were conducted for the purpose of determining the effect of feeding isoenergetic diets with and without fish meal or its fractions on hepatic lipid deposition in estrogenized chicks. The chicks were fasted for 48 hr before being fed the experimental diets and were injected with estradiol three times during the experiment. After 4 days, hepatic lipid content was determined. In the first experiment, the quantity of hepatic lipid deposited per unit of liver and per 100 g body weight was significantly less for chicks fed 10% fish meal and an ethanol extract of fish meal equivalent to 10% than for chicks fed an unsupplemented corn-soy diet. In a second experiment a significant reduction in hepatic lipids deposited per 100 g body weight was observed with 10% fish meal but only a numerical reduction with ethanol extracts of fish meal equivalent to 10 or 20% and the ash of ethanol extract equivalent to 20%. In a third experiment a highly significant reduction in hepatic lipid deposition was observed in birds refed a diet containing fish meal, alfalfa, and torula yeast but feeding this before the starvation-refeeding period did not affect liver lipids. These results show that fish meal contains hepatic lipid lowering activity in refed estrogenized chicks and suggest that the activity may be extracted with ethanol.
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PMID:Effect of fractions of fish meal and hepatic lipid deposition in estrogenized chicks. 672 89

The product of the permeability x vascular surface area (PA) of the blood-brain barrier to [14C]sucrose has been measured in rats maintained for 3 weeks in a chamber, the air supply to which carried a controlled concentration of ethanol vapour. No statistically significant difference was found between the permeability measurements in rats inhaling ethanol vapour for 3 weeks and non-alcohol exposed rats. The PA value was found to be significantly increased (115%) in rats given the same ethanol exposure when additionally subject to starvation during the last 3 days of this treatment. If the ethanol supply was also withdrawn at the same time as the food, a similar significant increase (116%) in PA value was found. In the absence of any ethanol exposure, 3 days' starvation did not significantly alter the measured PA value. Finally, when rats are given 200 mg/kg disulfiram every second day during a 2-week period of ethanol inhalation, the PA value was not significantly altered, although the concentration of acetaldehyde in the blood was up to 129 microM. The results indicate that while ethanol or acetaldehyde alone do not cause a weakening in the blood-brain barrier, the additional stress of food withdrawal after alcohol exposure does reduce barrier function, and this could be significant in human binge drinking.
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PMID:Weakening of the blood-brain barrier by alcohol-related stresses in the rat. 720 7

An anaerobic marine spirochete (strain MA-2) fermented glucose and formed ethanol, acetic acid, CO(2), and H(2) as end products. The organism required carbohydrates as growth substrates. Amino acids did not support the growth of strain MA-2. However, when the spirochete was grown in media containing branched-chain amino acids and glucose, significant quantities of 4- and 5-carbon branched-chain volatile fatty acids were formed in addition to products of glucose fermentation. Smaller quantities of branched-chain alcohols were also formed under these conditions. The spirochete converted l-valine, l-isoleucine, and l-leucine to isobutyric, 2-methylbutyric, and isovaleric acids, respectively. CO(2) formation accompanied each of these conversions. Spirochete MA-2 did not require branched-chain amino acids for growth, but these compounds could serve as sole sources of nitrogen for the organism. In addition, the survival of starving cells (no growth substrate available) of spirochete MA-2 was prolonged significantly when l-valine, l-isoleucine, and l-leucine were present in starvation media. Starving cells fermented these amino acids, forming adenosine 5'-triphosphate and branched-chain fatty acids. Our findings indicate that energy derived from amino acid fermentation allows the spirochete to survive periods of growth substrate starvation. Apparently, dissimilation of branched-chain amino acids can provide this bacterium with maintenance energy for cell functions not related to growth. In its natural environment spirochete MA-2 may catabolize branched-chain amino acids as a strategy for survival when growth substrates are not available.
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PMID:Branched-chain amino acid fermentation by a marine spirochete: strategy for starvation survival. 728 22

The effects of 1.0, 3.0 and 5.0 g/kg of ethanol on blood glucose levels and body temperature were examined in rats submitted to either acute food deprivation (24 or 48 hr), chronic starvation, or to both chronic plus acute food deprivation. The results show that: (a) 3.0 and 5.0 g/kg produced either an increase or a decrease of glucose levels depending on the state of fasting; (b) rats not deprived of food presented hyperglycemia while being hypothermic; (c) a marked hypothermia was present when no substantial alterations in glycemia were observed; and (d) in cases where hypoglycemia and hypothermia occurred, the fall in body temperature paralleled or preceded the decrease in glucose levels.
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PMID:Blood glucose and body temperature alterations induced by ethanol in rats submitted to different levels of food deprivation. 729 Dec 58

Selenomonas ruminantium accumulated large quantities of intracellular polysaccharide when grown in simple defined medium in a chemostat, particularly at low dilution rate under NH3 limitation when the carbohydrate content of the cells was greater than 40% of the dry weight. This polysaccharide was used as a source of energy under conditions of energy starvation. Abundant, densely staining cytoplasmic granules were observed by electron microscopy in sections stained by the periodic acid-thiocarbohydrazide-osmium technique. The polysaccharide was extracted in 30% KOH followed by precipitation with 60% ethanol and was found to be a glucose homopolymer. Sepharose 4B gel filtration and iodine-complex spectroscopy showed that the polysaccharide was of the glycogen type with a molecular weight of 5 X 10(5) to greater than 20 X 10(5) and an average chain length of 12 glucose residues.
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PMID:Cytoplasmic reserve polysaccharide of Selenomonas ruminantium. 738 59

Triacylglcerol metabolism was studied in isolated rat hepatocytes using a fully enzymatic method to masure cellular glyceride-glycerol. With this method 40 and 50 MUmol triacylglycerol were found per g cellular protein in liver cells from fed and starved rats, respectively, comparable to values obtained after organic solvent extraction and alkaline hydrolysis of neutral lipids. Carbohydrate refeeding of animals increased triacylglycerol levels in hepatocytes to 80 mumol. Upon incubation without fatty acids a 15% decrease in cellular triacylglycerol was found in 60 min. When 1mM oleate or palmitate were added cellular triacylglycerol increased. The rates of net triacylglycerol increased. The rates of net triacylglycerol synthesis were not significantly different with oleate and palmitate. Starvation reduced the rates from both fatty acids, whereas carbohydrate refeeding led to a marked increase in net triacylglycerol synthesis. Besides 20mM glucose, 5mM L-lactate and 5mM fructose stimulated triacylglycerol synthesis from fatty acids. THe stimulatory effect of lactate was higher in hepatocytes from starved animals, so that the differences in triacylglycerol synthesis between liver cells from fed and starved rats were abolished. Fatty acids taken up and not recovered in newly formed triacylglycerol were released as ketone bodies. When radioactive lectate was offered to cells from starved rats, label incorporated into neutral lipids was exclusively recovered from the glycerol moiety of triacylglycerols. 5mM ethanol which alone increased fatty acid esterification, reduced the stimulatory effect of lactate but increased the effect of fructose on net triacylglycerol formation. These findings indicate that esterification rate in liver cells from starved rats can be limited by availability of alpha-glycerophosphate, which is provided by glyceroneogenesis. The possible physiological significance of these findings is discussed with regard to liver cell heterogeneity and nutritional adaptation of liver triacylglycerol formation.
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PMID:Regulation of net triacylglycerol synthesis by metabolic substrates in isolated rat liver cells. 740 49


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