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)

Transcription of the cobinamide biosynthetic genes (the CobI operon) was induced under three different physiological conditions: anaerobiosis (anaerobic respiration or fermentation), aerobic respiration at low oxygen levels, and aerobic respiration with a partial block of the electron transport chain. After a shift to inducing conditions, there was a time lag of approximately 50 min before the onset of CobI induction. Under conditions of anaerobic respiration, the level of CobI transcription was dependent on the nature of both the electron donor (carbon and energy source) and the acceptor. Cells grown with electron acceptors with a lower midpoint potential showed higher CobI expression levels. The highest level of CobI transcription observed was obtained with glycerol as the carbon source and fumarate as the electron acceptor. The high induction seen with glycerol was reduced by mutational blocks in the glycerol catabolic pathway, suggesting that glycerol does not serve as a gratuitous inducer but must be metabolized to stimulate CobI transcription. In the presence of oxygen, CobI operon expression was induced 6- to 20-fold by the following: inhibition of cytochrome o oxidase with cyanide, mutational blockage of ubiquinone biosynthesis, and starvation of mutant cells for heme. We suggest that the CobI operon is induced in response to a reducing environment within the cell and not by the absence of oxygen per se.
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PMID:Redox regulation of the genes for cobinamide biosynthesis in Salmonella typhimurium. 268 49

To evaluate the contribution of catecholamines to the fasting-induced lipid mobilization prolonged or acute blockade of beta-adrenergic receptors with propranolol was applied in dogs during 72 hrs of food withdrawal. Propranolol given orally in a dose of 15 mg twice daily throughout the whole period of fasting failed to modify the increases in the plasma FFA and glycerol concentrations. The acute beta-adrenergic blockade due to i.v. injection of propranolol (0.5 mg/kg b.w.) caused marked decreases in the plasma glycerol concentration both in the dogs fasting for 24 h and 72 hrs, whereas the effects of propranolol on the plasma FFA concentration was found only in the early stage of fasting. Plasma catecholamine concentrations were enhanced significantly by the 72 hrs food withdrawal and neither prolonged nor acute propranolol administration modified significantly this effect. The fasting-induced decreases in the serum insulin concentration were more pronounced in dogs treated with propranolol. Results of this study indicate that catecholamines are involved in the control of lipolysis during short term starvation. However, under these conditions beta-adrenergic blockade did not impair FFA mobilization most probably due to an enhanced contribution of other hormones to the control of this process.
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PMID:Effect of beta-adrenergic blockade on lipid mobilization induced by fasting in dogs. 285 49

The effects of adrenaline, noradrenaline, and of the alpha 2- and beta-selective agonists clonidine and isoproterenol were studied in fifteen obese subjects before and after 4 weeks of caloric restriction (300 cal day-1). Basal glycerol release averaged 1.4 mumol (10(6) cells)-1 (180 min)-1 before starvation and 2.8 mumol (10(6) cells)-1 (180 min)-1 during starvation (P less than or equal to 0.1). Before starvation adrenaline and noradrenaline caused a 2-3-fold increase of glycerol release. This lipolytic effect disappeared during starvation. An inhibitory effect of adrenaline was observed instead which was maximal at an adrenaline concentration of 1 mumol 1(-1) (P less than or equal to 0.05). The dose-response relationships of the alpha 2- and beta-selective agents clonidine and isoproterenol were not appreciably changed by caloric restriction. The increase of basal lipolytic rate and the reversal of adrenaline action seen during caloric restriction could be mimicked by removal of endogenous adenosine using adenosine deaminase (1.6 microgram ml-1). In addition, inclusion of N6-phenylisopropyladenosine (1 mumol 1(-1)) into the medium reverted the adrenaline-induced inhibition seen during caloric restriction. The results suggest that local modulators such as adenosine are of primary importance for the apparent change of responsiveness to adrenaline and noradrenaline seen during starvation of human fat cells in vitro.
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PMID:Adrenergic regulation of lipolysis in abdominal adipocytes of obese subjects during caloric restriction: reversal of catecholamine action caused by relief of endogenous inhibition. 285 98

Inositol-starved Saccharomyces uvarum cells hydrolyse exogenous glycerophosphodiesters to glycerol 3-phosphate and the corresponding alcohol. Glycerophosphodiesterase activity is highest with glycerophosphoinositol as the substrate, followed by glycerophosphoethanolamine and glycerophosphocholine; the artificial substrate for phosphodiesterases, bis-p-nitrophenylphosphate,is hydrolysed at a similar rate as compared with glycerophosphoinositol. Competition experiments suggest that distinct phosphodiesterases are involved in the hydrolysis of the respective substrates. An Mg2+-dependent glycerophosphate phosphohydrolase with a pH-optimum around neutral cleaves glycerol 3-phosphate to glycerol and orthophosphate. The latter is taken up into cells without first entering the pool of orthophosphate present in the growth medium. Accessibility to substrates with whole cells, adhesion of enzymes to spheroplasts, and solubilization of enzymes by treatment of whole cells with Triton X-100 under mild conditions suggest that phosphodiesterases and glycerol-3-phosphate phosphohydrolase are loosely associated with the outer side of the yeast plasma membrane. Enzyme activities are only marginal in inositol-supplemented cells, but are derepressed not only by inositol deficiency, but also by starvation of orthophosphate.
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PMID:Utilization of exogenous glycerophosphodiesters and glycerol 3-phosphate by inositol-starved yeast, Saccharomyces uvarum. 298 39

Plasma insulin, glucagon, glucose, free fatty acids and glycerol, hepatic cyclic AMP and glycogen, and liver phosphoenolpyruvate carboxykinase (PEPCK), fructose 1,6-bisphosphatase (FBPase), glucose 6-phosphatase (G6Pase) and alanine amino transferase (AAT) activities were examined in adult rats during the first 24 h of either starvation or consumption of a high protein, carbohydrate-free (HP) diet. Under both nutritional conditions, plasma insulin fell within 12 h and remained constant thereafter. Glucagon increased 12 h after the start of the experiment and peaked between 18-24 h. The insulin: glucagon ratio was lower during the last 12 h of the experiment. In both experimental groups, liver cyclic AMP increased progressively and peaked between 15-24 h, but it increase was higher on HP diet than on starvation. Whereas plasma glucose remained low on starvation for 24 h, it returned to normal on consumption of the HP diet. In both groups, liver glycogen fell within 12 h and remained low until the end of experiment. FBPase, G6Pase and AAT did not change on starvation, while they increased toward the end of 1 d HP consumption. During starvation or consumption of the HP diet, PEPCK increased progressively and peaked between 15-24 h, but the increase was greater with the HP diet than with starvation. These findings suggest that in the first 24 hours, the adaptative response of hepatic gluconeogenesis is higher with a HP diet than upon starvation.
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PMID:Comparison between starvation and consumption of a high protein diet: plasma insulin and glucagon and hepatic activities of gluconeogenic enzymes during the first 24 hours. 300 46

Chicks of king penguin (Aptenodytes patagonica), while only 3-4 months old, tolerate 4-6 months of fasting when they are abandoned by their parents during the subantarctic winter. The body mass of nine chicks, which were followed during this natural winter fast, was 13.1 kg at capture and 3.4 kg after 150 days of fasting, a 74% decrease. The longer phase II (129 days) was marked by lipid mobilization and protein sparing, as indicated by a continuous increase in plasma levels of free fatty acids, glycerol, and beta-hydroxybutyrate, whereas plasma alanine, uric acid, and urea remained stable at low values. In phase III, by contrast, plasma concentrations of lipid-derived metabolites decreased, while plasma alanine, uric acid, and urea increased markedly, indicating an increase in protein utilization. Plasma insulin concentration did not significantly change during either phase II or phase III. Plasma glucagon remained constant during phase II and at the beginning of phase III but increased 2.6 times afterward. Plasma corticosterone increased only slightly during the first 4 months of the fast but reached very high values at the end of phase II and the beginning of phase III (4.7 times basal values); moreover, it further increased 3.1 times before phase III was stopped. Altogether, these data accord with the idea that the outstanding resistance of king penguin chicks to starvation is due to the ability to extensively prolong the situation of protein sparing, which seems to require the maintenance of low plasma concentrations of corticosterone and insulin for up to 4 months.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Plasma hormone levels in relation to lipid and protein metabolism during prolonged fasting in king penguin chicks. 306 Mar 95

The heat shock response of Myxococcus xanthus was investigated and characterized. When shifted from 28 to 40 degrees C, log-phase cells rapidly ceased growth, exhibited a 50% reduction in CFU, and initiated the synthesis of heat shock proteins (HTPs). Heat-shocked log-phase M. xanthus cells labeled with [35S]methionine were found to produce 18 major HTPs. The HTPs, analyzed by sodium dodecyl sulfate-polyacrylamide gel electrophoresis and fluorography, were characterized with regard to molecular mass, subcellular location (periplasm, membrane, or cytoplasm), and temperature required for expression. Most HTPs were expressed at 36 degrees C, the optimum growth temperature of M. xanthus. Cells preincubated at 36 degrees C for 1 h before being shifted to 40 degrees C demonstrated increased thermotolerance compared with cells shifted directly from 28 to 40 degrees C. The HTPs produced by heat-shocked starvation-induced fruiting cells and glycerol-induced sporulating cells were also analyzed and characterized. Thirteen HTPs were detected in fruiting cells shifted from 28 to 40 degrees C. Six of these HTPs were not seen in vegetative M. xanthus cells. Log-phase cells induced to sporulate by the addition of glycerol produced 17 HTPs after being shifted to 40 degrees C. These HTPs were found to be a mixture of HTPs detected in heat-shocked log-phase cells and heat-shocked fruiting cells.
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PMID:Heat shock proteins of vegetative and fruiting Myxococcus xanthus cells. 309 68

The effect of heat shock on Myxococcus xanthus was investigated during both glycerol- and starvation-induced development. Cells heat shocked at 40 degrees C for 1 h prior to a development-inducing signal displayed an accelerated rate of myxospore formation at 30 degrees C. Additionally, M. xanthus cells heat shocked prior to glycerol induction formed a greater total number of myxospores when sporulation was complete than did control cells maintained at 30 degrees C. However, in starvation-induced fruiting cells the total number of myxospores in control and heat-shocked populations was about equal when fruiting body and myxospore formation was complete. When extended heat shock (3 h) was applied to cells prior to development, no acceleration of myxospore formation was observed. Heat shock elicited the premature expression of many developmentally regulated proteins. Cell fractionation and analysis by sodium dodecyl sulfate-polyacrylamide gel electrophoresis and fluorography revealed the subcellular location and molecular weights of the 18 glycerol-induced and 9 starvation-induced developmental proteins. Comparison with previously identified M. xanthus heat shock proteins showed that nine of the developmental proteins found in glycerol-induced cells and three of the developmental proteins found in starvation-induced cells were heat shock proteins. Furthermore, heat shock increased the activity of alkaline phosphatase, a developmentally regulated enzyme, in vegetative cells, glycerol-induced cells, and starvation-induced cells.
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PMID:Acceleration of starvation- and glycerol-induced myxospore formation by prior heat shock in Myxococcus xanthus. 314 80

Hepatic lipid synthesis was measured in rats in vivo with 3H2O, and the appearance of label in triacylglycerol and its constituent fatty acid and glycerol moieties was determined. In rats treated with Triton WR1339, the amount of newly synthesized fatty acid secreted as very-low-density lipoprotein (VLDL) triacylglycerol was greater during the dark phase of the diurnal cycle than during the light phase (11.3 versus 4.8 mumol of 3H2O/3 h per g of liver respectively). However, the total mass of VLDL triacylglycerol secreted remained constant, as did the amount of label in the secreted triacylglycerol glycerol. Newly synthesized fatty acids comprised only a small proportion of the total VLDL triacylglycerol fatty acids (TGFA) at both times (dark phase, 7.7%; light phase, 2.4%). Starvation for 24 h resulted in a small increase in the secretion of VLDL triacylglycerol. However, the contribution from newly synthesized fatty acids was decreased. Similar effects were observed in streptozotocin-diabetic animals. During the light and dark phases of the cycle, similar quantities of newly synthesized TGFA entered the hepatic cytosol, and these amounts were much smaller than those secreted as VLDL triacylglycerol. The mass of cytosolic triacylglycerol showed a diurnal variation, with a greater concentration during the light phase than in the dark. In diabetes, the mass of triacylglycerol was increased in the cytosol, as was the incorporation of labelled acylglycerol glycerol. Diabetes also abolished the diurnal variation in the quantity of cytosolic triacylglycerol. In each group of animals the specific radioactivity of the microsomal triacylglycerol was similar to that of the respective newly secreted plasma VLDL. The specific radioactivity of the cytosolic triacylglycerol was only 15.8% (dark phase) or 16.8% (light phase) that of the microsomal triacylglycerol. This increased to 35.5% in the starved animals and 40.2% in the diabetic animals.
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PMID:Secretion and storage of newly synthesized hepatic triacylglycerol fatty acids in vivo in different nutritional states and in diabetes. 321 32

The mechanism that induces maternal hypertriglyceridemia in late normal pregnancy, and its physiologic significance are reviewed as a model of the effects of sex steroids on lipoprotein metabolism. In the pregnant rat, maternal carcass fat content progressively increases up to day 19 of gestation, then declines at day 21. The decline may be explained by the augmented lipolytic activity in adipose tissue that is seen in late pregnancy in the rat. This change causes maternal circulating free fatty acids and glycerol levels to rise. Although the liver is the main receptor organ for these metabolites, liver triglyceride content is reduced. Circulating triglycerides and very-low-density lipoprotein (VLDL)-triglyceride levels are highly augmented in the pregnant rat, indicating that liver-synthesized triglycerides are rapidly released into the circulation. Similar increments in circulating VLDL-triglycerides are seen in pregnant women during the third trimester of gestation. This increase is coincident with a decrease in plasma postheparin lipoprotein lipase activity, indicating a reduced removal of circulating triglycerides by maternal tissues or a redistribution in their use among the different tissues. During late gestation in the rat, tissue lipoprotein lipase activity varies in different directions; it decreases in adipose tissue, the liver, and to a smaller extent the heart, but increases in placental and mammary gland tissue. These changes play an important role in the fate of circulating triglycerides, which are diverted from uptake by adipose tissue to uptake by the mammary gland for milk synthesis, and probably by the placenta for hydrolysis and transfer of released nonesterified fatty acids to the fetus. After 24 hours of starvation, lipoprotein lipase activity in the liver greatly increases in the rat in late pregnancy; this change is not seen in virgin animals. This alteration is similar to that seen in liver triglyceride content and plasma ketone body concentration in the fasted pregnant rat. In the fasting condition during late gestation, heightened lipoprotein lipase activity is the proposed mechanism through which the liver becomes an acceptor of circulating triglycerides, allowing their use as ketogenic substrates, so that both maternal and fetal tissues may indirectly benefit from maternal hypertriglyceridemia. Changes in the magnitude and direction of lipoprotein lipase activity in different tissues during gestation actively contribute both to the development of hypertriglyceridemia and to the metabolic fate of circulating triglycerides.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Role of lipoprotein lipase activity on lipoprotein metabolism and the fate of circulating triglycerides in pregnancy. 328 29


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