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

Starvation of strains of Escherichia coli which are glycerol auxotrophs and are also defective in beta oxidation results in the accumulation of large amounts of free fatty acid (Cronan, J. E., Jr., Weisberg, L. W., and Allen, R. G. (1975) J. Biol. Chem. 250, 5835-5840). We now report that the ratio of saturated to unsaturated species appearing in the free fatty acid fraction depends on the incubation temperature at the time of synthesis of these acids. This result indicates that fatty acid synthesis is one site of the thermal control of phospholipid fatty acid composition. We also report experiments on the incorporation of exogenously supplied fatty acids into membrane phospholipids. The effect of temperature on this incorporation supports the hypothesis that a second site of thermal regulation acts at the level of phosphatidic acid synthesis.
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PMID:Thermal regulation of the membrane lipid composition of Escherichia coli. Evidence for the direct control of fatty acid synthesis. 109 1

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.
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PMID:Inhibition of ketogenesis by ketone bodies in fasting humans. 115 76

Addition of serum to incubated adipose tissue resulted in excess of free fatty acids and/or glycerol released. It was propranolol-resistant and in many but not all experiments greater after using serum of fasting (FS) rats than that of fed rats (CS). The increment of free fatty acids and/or glycerol released due to the presence of FS was not potentiated by theophylline; however the effect of both CS and FS was potentiated by heparin. The postheparin serum lacked the property of CS or FS. By the interaction with serum, adipose tissue could be substituted by lipoprotein lipase isolated either from this tissue or from bovine milk. It is suggested that the difference between CS and FS might be caused by a qualitative alteration of the lipoprotein pattern resulting in easier availability of serum lipids to the extraadipose tissues during starvation.
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PMID:Enhanced lipolysis during interaction of serum and adipose tissue: its mechanism and effect of starvation. 123 48

The role of glucagon in regulating peripheral tissue metabolism in man was assessed in the present studies. To do this, glucagon was infused for two hours into the brachial artery to produce a high but physiologic increment in the glucagon content of arterial blood supplying ipsilateral tissues. Metabolic effects on muscle and on subcutaneous adipose tissue plus skin were sought in seven overnight-fasting subjects and seven subjects starved briefly (60 hours). In the overnight-fasted group the infusion increased bassl glucagon concentration by 1,216 pg./ml. but was without effect on forearm tissue metabolism of glucose, lactate,glycerol, or amino acids. Starvation significantly reduced basal insulin (11.0 to 7.4 muU./ml.) and increased endogenous glucagon (116 to 134 pg./ml.). Basally, there was substantial ketone utilization and a decrease in glucose consumption by both muscle and subcutaneous adipose tissue plus skin. The glucagon infusion increased basal glucagon by 784 pg./ml. Muscle balances of glucose, lactate, acetoacetate, amino acids, and glycerol were unaffected. The metabolism of glucose, lactate, acetoacetate, glycerol, and free fatty acids by subcutaneous adipose tissue plus skin was also unchanged. It is concluded that physiologic increments of glucagon lasting two hours are without effect on forearm tissues in overnight-fasted and briefly starved man.
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PMID:Metabolism of forearm tissues in man. Studies with glucagon. 124 74

Plasma lipid and hormone levels have been measured during 72 hours total starvation in nine healthy subjects, to assess the relative importance of hormones and substrates in human triglyceride metabolism. Plasma free fatty acid and glycerol concentrations rose steadily on each day of starvation. Plasma triglyceride concentrations rose on the second and third days, from a control level of 649 +/- 67 mg/1 to a maximum of 1001 +/- 66 mg/1. Plasma cholesterol concentrations remained unchanged while glucose concentrations fell and insulin did not change. Plasma glucagon (C-GLI) levels doubled while secretin levels, reported previously, rose threefold. It is suggested that during acute starvation the rise in triglyceride concentration results from the increased availability of free fatty acids, and that elevated secretin and glucagon levels enhance lipolysis and hence provide substrates for triglyceride synthesis.
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PMID:Triglyceride metabolism in acute starvation: the role of secretin and glucagon. 126 85

Newborn Long-Evans rats were undernourished by maternal deprivation so that by 20 days of age their body and brain weights were about 45 and 80%, respectively, of the values obtained for control (well-nourished) values. Proteins from myelin of undernourished and control rats were separated by polyacrylamide gel electrophoresis in buffers containing sodium dodecyl sulfate. At 15 and 20 days of age the proportion of basic and proteolipid protein was reduced in the starved animals relative to controls, indicative of a delay in maturation. However, by 30 days of age the composition of myelin from starved and control animals appeared similar. At all ages the yield of myelin from brains of starved rats was less than 25% of that obtained from control animals. A series of isotope labeling experiments, using a double label design, was carried out to compare relative rates of incorporation of radioactive amino acids into individual proteins of various brain subcellular fractions. In 20-day-old rats the incorporation of [3H] OR [14C] leucine or glycine into myelin proteins, relative to incorporation into proteins of other subcellular fractions, is preferentially depressed (about 60%) in starved animals. Synthesis of all the myelin proteins was depressed, supporting the hypothesis that the high molecular weight proteins isolated with myelin are true myelin constituents. Similar experiments were conducted using [3H]-and [14C] acetate, choline, or glycerol as precursors of lipids. Incorporation of isotope into lipids of myelin, relative to lipids of other subcellular fractions, was also depressed by about 60% in starved animals. In several experiments we studied synthesis during rehabilitation (ad libitum feeding) following 20 days of postnatal starvation. After 6 days of rehabilitation, incorporation of radioactive precursors into myelin, relative to other subcellular fractions, was still depressed. This result was true for both proteins and lipids, and was interpreted as evicence against the initiation of a process leading to a net recovery of myelin (i.e., an irreversible deficit of myelin synthesis is induced by this regime of nutritional deprivation).
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PMID:Myelin synthesis during postnatal nutritional deprivation and subsequent rehabilitation. 126 27

1. Administration of tumour necrosis factor (cachectin) and of interleukin-1-alpha increased the plasma level of nonesterified fatty acids in fed rats, and in the case of interleukin-1-alpha the blood glycerol level was also increased, suggesting stimulation of adipose tissue lipolysis. There were parallel increases in the plasma level of triacylglycerols. Neither cytokine had significant effects on blood or liver total ketone body (acetoacetate plus 3-hydroxybutyrate) concentrations. 2. In starved rats, the higher plasma non-esterified fatty acid concentration was not increased further by the cytokines. The plasma triacylglycerol level was increased, although the absolute change was less than in fed rats. The ketonaemia associated with starvation tended to be increased by the cytokines, but this was only significant in the case of interleukin-1-alpha. Parallel changes occurred in hepatic ketone bodies. 3. It is concluded that tumour necrosis factor-alpha and interleukin-1-alpha are not responsible for the hypoketonaemia associated with sepsis or other inflammatory states.
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PMID:Acute administration of tumour necrosis factor-alpha or interleukin-1-alpha does not mimic the hypoketonaemia associated with sepsis and inflammatory stress in the rat. 131 59

1. We describe a method for the selective labelling of hepatic fatty acids in the rat in vivo. It relies on (i) the rapid and preferential uptake of cholesteryl ester from chylomicron and/or very-low-density-lipoprotein remnants by the liver [Holder, Zammit & Robinson (1990) Biochem. J. 272, 735-741] (without prior exchange of the ester to other lipoproteins in the plasma), and (ii) the very short half-life of the cholesteryl ester in the liver. The 14C-labelled fatty acid moiety generated by cholesteryl ester hydrolysis was shown to be utilized by the liver for glycerolipid synthesis in a very similar pattern to that demonstrated for exogenous fatty acids by isolated cultured hepatocytes in previous studies. 2. Starvation (24 h) was shown to decrease the proportion of fatty acid utilized for glycerolipid synthesis, but to result in a proportionately smaller effect on incorporation into phospholipid. This was accompanied by a decrease in the fraction of synthesized triacylglycerol that was secreted by the liver. 3. Streptozotocin-diabetes did not affect the phospholipid/triacylglycerol ratio, but resulted in a small, but significant, decline in the fraction of triacylglycerol secreted by the liver. 4. In both starved and diabetic animals fatty acid esterification to the glycerol moiety constituted a smaller proportion of the total disposal of label. 5. These findings appear to validate the present method for the selective labelling of liver fatty acids in vivo in a non-invasive manner. Other possible uses for the method are suggested.
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PMID:Selective labelling of hepatic fatty acids in vivo. Studies on the synthesis and secretion of glycerolipids in the rat. 156 62

Key enzymes related to lipogenesis in the liver are induced by a high glucose diet or insulin and suppressed by starvation, diabetes, or glucagon. Most of these enzymes are also induced by dietary fructose, even in diabetic liver. This regulation occurs at the posttranscriptional level as well as at the transcriptional level. We studied extensively the molecular mechanism of induction of L-type pyruvate kinase (LPK). The transcription of the LPK gene in the liver was stimulated by insulin and inhibited by glucagon. This insulin action required ongoing protein synthesis and metabolism of glucose and was enhanced by glucocorticoid. On the other hand, the mechanism of induction of the LPK by dietary fructose depended on plasma insulin levels. Dietary fructose stimulated transcription of the LPK gene in normal rats, whereas it acted mainly at the posttranscriptional level in diabetic rats. These fructose effects were attributable to a common metabolite of fructose and glycerol. The induction of LPK mRNA by dietary glucose was impaired in the liver of Wistar fatty rats, a model of obese non-insulin-dependent diabetes mellitus, but fructose-induced accumulation of the mRNA was not. Studies on transgenic mice indicated that the 5'-flanking region up to -3 kb of the LPK gene contained all cis-acting elements necessary for tissue-specific expression of LPK and its stimulation by diets and insulin. Further analysis using a transient expression assay revealed the presence of three cis-acting elements necessary for expression of LPK in hepatocytes in the region up to -170 kb. However, these elements alone were not sufficient for dietary and hormonal regulation of this enzyme when analyzed in transgenic mice.
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PMID:Molecular mechanism of induction of key enzymes related to lipogenesis. 157 84

Enrichment procedures, such as those utilizing inositol-less death, have proven to be extremely powerful for increasing the efficiency of identification of spontaneous mutants in a variety of procaryotic and eucaryotic organisms. We characterized inositol-less death in several widely used strains of the inositol-requiring yeast Schizosaccharomyces pombe and determined conditions under which this phenomenon can be used to enrich for mutants. Conflicting reports in the literature on the effects of inositol starvation upon viability of S. pombe had cast doubt on the suitability of using inositol-less death in a mutant enrichment procedure for this organism. We determined that inositol-less death was strain dependent, with differences in viability of up to 5 orders of magnitude observed between the most-sensitive strain, 972, and the least-sensitive strain, SP837. Inositol-less death was also dependent upon the cell concentration at the time of initiation of starvation. While inositol-less death occurred at all four temperatures tested, the kinetics of death was slower at 16 degrees C than at 23, 30, or 37 degrees C. Inositol-less death was observed during growth in fermentable and nonfermentable carbon sources, although loss of viability in glycerol-ethanol was significantly slower than that in glucose, sucrose, or raffinose. The feasibility of exploiting inositol-less death to enrich for spontaneous mutants was demonstrated by the identification of amino acid auxotrophs, nucleotide auxotrophs, carbon source utilization mutants, and temperature-sensitive mutants. By varying starvation conditions, some mutants were recovered at frequencies as high as 5.7 x 10(-2), orders of magnitude higher than the spontaneous mutation rate.
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PMID:Mutant enrichment of Schizosaccharomyces pombe by inositol-less death. 159 22


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