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 inhibition of phospholipid synthesis engendered by starving glycerol 3-phosphate (G3P) auxotrophs of Escherichia coli (plsB or gpsA) for G3P is incomplete; 5 to 10% of the normal rate of phospholipid synthesis remains, even after prolonged starvation. We report that G3P starvation of a strain having lesions in both the gpsA and plsB genes resulted in essentially complete (greater than 98.5%) inhibition of phospholipid synthesis, indicating that all de novo glycerolipid synthesis in E. coli proceeds by acylation of G3P.
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PMID:Acylation of glycerol 3-phosphate is the sole pathway of de novo phospholipid synthesis in Escherichia coli. 329 13

The influence of prolonged energy restriction (1250 kJ for 4 weeks) on insulin's antilipolytic action was investigated in abdominal adipocytes of obese subjects. An attempt was made to discriminate between dietary influences per se and indirect influences caused by changes in the concentration or action of adenosine. Prolonged energy restriction resulted in about a 3.5-fold increase in basal lipolytic rate which was associated with a corresponding increase in maximal response to insulin. Both these effects could be mimicked by adenosine deaminase (1.6 micrograms/ml) which increased glycerol release of adipocytes from fed donors to levels normally seen during starvation suggesting that the improvement of lipolytic responsiveness to insulin during energy restriction was an apparent one only, due to the fact that glycerol release was increased. To identify dietary influences that selectively affect insulin action the effects of insulin were compared with those of other antilipolytic agents in the presence of adenosine deaminase. Maximally effective concentrations of prostaglandin E2, clonidine and N6-phenylisopropyladenosine almost completely suppressed glycerol release before and during starvation. The extent of inhibition produced by these latter compounds was therefore related to basal activity by the same linear relationship in all experimental settings. By contrast insulin only partially depressed glycerol release and the relationships between basal activity and response to maximal concentrations of insulin were significantly different before and during starvation (P less than or equal to 0.01) in the presence of adenosine deaminase indicating that starvation selectively influences insulin action via mechanisms that are unrelated to the effects of other antilipolytic compounds. It is concluded that the main effect of energy restriction on insulin's antilipolytic action is an apparent one which is secondary increased lipolytic activity. Direct dietary effects on insulin action became apparent upon removal of endogenous adenosine. These tend to limit the maximal response to insulin and may be due to changes at the post-binding level but could also reflect an intrinsic property of insulin's antilipolytic action.
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PMID:Antilipolytic action of insulin in abdominal adipocytes of obese subjects before and during energy restriction. Influence of adenosine deaminase. 330 11

In synchronized culture of Escherichia coli, the specific arrest of phospholipid synthesis (brought about by glycerol starvation in an appropriate mutant) did not affect the rate of ongoing DNA synthesis but prevented the initiation of new rounds. The initiation block did not depend on cell age at the time of glycerol removal, which could be before, during, or after the doubling in the rate of phospholipid synthesis (DROPS) and as little as 10 min before the expected initiation. We conclude that the initiation of DNA replication is not triggered by the preceding DROPS but requires active phospholipid synthesis. Conversely, when DNA replication initiation was specifically blocked in a synchronized culture of a dnaC(Ts) mutant, two additional DROPS were observed, after which phospholipid synthesis continued at a constant rate for at least 60 min. Similarly, when DNA elongation was blocked by thymine starvation of a synchronized culture, one additional DROPS was observed, followed by linear phospholipid accumulation. Control experiments showed that specific inhibition of cell division by ampicillin, heat shock, or induction of the SOS response did not affect phospholipid synthesis, suggesting that the arrest of DROPS observed was due to the DNA replication block. The data are compatible with models in which the DROPS is triggered by an event associated with replication termination or chromosome segregation.
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PMID:DNA replication initiation, doubling of rate of phospholipid synthesis, and cell division in Escherichia coli. 330 9

Derangements of posttraumatic glucose metabolism have long been recognized, with observed changes implicating abnormal action of insulin on target tissues. Insulin is important as well in fat metabolism, and "resistance" to insulin's effects on lipid metabolism after injury has been demonstrated. Although fat-derived fuels are the body's major energy source during starvation and after injury, most studies of posttraumatic insulin "resistance" have focused on carbohydrate metabolism. This study investigated adipose tissue response to insulin in vitro in rats subjected to starvation and/or trauma. Relationships between various parameters, including adipocyte size and weight, plasma glucose, insulin, and glycerol, and basal and insulin-suppressed lipolytic rates, were also studied. Results observed include a decrease in adipocyte size and an increase in basal lipolysis in both starved and traumatized rats, with both decreased sensitivity (T greater than S) and responsiveness (S greater than T) to insulin. These results support the concept that adipocytes of injured animals retain the ability to respond to insulin but lipolytic rates at maximal suppression are still quite high as compared to fed controls. Only minor differences were observed between starved animals and those with starvation and superimposed trauma.
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PMID:Adipose tissue response to insulin following injury. 332 55

The formation of the oligosaccharide-lipid intermediates of the dolichol pathway by the bovine retina was investigated. Intact retinas were incubated in vitro for various periods of time in the presence of a variety of radioactive sugars (2-[3H]mannose, 6-[3H]glucose, 1-[3H]galactose, 1-[14C]glucosamine) using incubation conditions which have been shown previously to support the glycosylation of rhodopsin. The oligosaccharide-lipids were isolated and partially purified by DEAE cellulose chromatography. After mild acid hydrolysis and reduction, the oligosaccharides were analysed by HPLC. Further identification was obtained by chemical means and after digestion of the oligosaccharides with alpha-mannosidase and endohexosaminidase H. The full array of oligosaccharide-lipids which have been observed in other tissues were detected in the bovine retina, although some striking differences were seen in their relative distribution. Although short-term incubations (up to 15 min) indicated that the major species was the fully glucosylated oligosaccharide-lipid (Glc3Man9GlcNAc2), with longer incubation times the non-glucose-containing intermediate, Man9GlcNAc2, became the predominant species. Since glycerol was the carbon source for these incubations, the possibility was investigated that glucose starvation may have been the basis for this phenomenon, as has been reported in other tissues. It was established that this was not the case. Experiments carried out in the presence of castanospermine and bromoconduritol indicated that alpha-glucosidase activity in the retina may have resulted in the accumulation of the unglucosylated oligosaccharide-lipids. The formation of oligosaccharide-lipid intermediates by cells of the retinal pigment epithelium from the embryonic chick, maintained in cell culture, was also examined. In contrast to the bovine retina, the major species present were the glucose-containing intermediates, similar to other tissues.
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PMID:The dolichol pathway in the retina: oligosaccharide-lipid biosynthesis. 338 23

Fatty acid metabolism was examined in Escherichia coli plsB mutants that were conditionally defective in sn-glycerol-3-phosphate acyltransferase activity. The fatty acids synthesized when acyl transfer to glycerol-3-phosphate was inhibited were preferentially transferred to phosphatidylglycerol. A comparison of the ratio of phospholipid species labeled with 32Pi and [3H]acetate in the presence and absence of glycerol-3-phosphate indicated that [3H]acetate incorporation into phosphatidylglycerol was due to fatty acid turnover. A significant contraction of the acetyl coenzyme A pool after glycerol-3-phosphate starvation of the plsB mutant precluded the quantitative assessment of the rate of phosphatidylglycerol fatty acid labeling. Fatty acid chain length in membrane phospholipids increased as the concentration of the glycerol-3-phosphate growth supplement decreased, and after the abrupt cessation of phospholipid biosynthesis abnormally long chain fatty acids were excreted into the growth medium. These data suggest that the acyl moieties of phosphatidylglycerol are metabolically active, and that competition between fatty acid elongation and acyl transfer is an important determinant of the acyl chain length in membrane phospholipids.
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PMID:Fatty acid metabolism in sn-glycerol-3-phosphate acyltransferase (plsB) mutants. 354 64

Fed and 48-h starved rats were infused on day 21.5 of gestation for 20 min through the left uterine artery with [U-14C-]-D-glucose, [U-14C]-glycerol, or [U-14C]-L-alanine. The mother and fetuses from both uterine horns were processed separately for radioactivity measurements in plasma and liver. Differences in radioactivity values between fetuses from the left and the right sides are used as indexes of placental transference of the infused tracers prior to their distribution and transformation in the maternal circulation. After infusion of [U-14C]-D-glucose, [U-14C]-glycerol, or [U-14C]-L-alanine, plasma radioactivity values and specific activities corresponding to the respective infused tracer appeared much higher in fetuses from the left than the right uterine side. Plasma 14C-lactate values also were higher in the left than the right fetuses indicating that fetoplacental structures produced lactate from those placentally transferred 14C-metabolites. No difference in plasma 14C-glucose between left and right uterine horn fetuses was observed after maternal infusion with either [U-14C]-glycerol or [U-14C]-L-alanine, either in fed or 48-h starved rats. In the mother both [U-14C]-glycerol and [U-14C]-L-alanine were efficiently converted to 14C-glucose, and this process was significantly enhanced with starvation. 14C-fatty acids present in fetal liver after maternal infusions with either [U-14C]-D-glucose or [U-14C]-glycerol were decreased by starvation whereas no fatty acid synthesis from [U-14C]-L-alanine was detected.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Lactate production and absence of gluconeogenesis from placental transferred substrates in fetuses from fed and 48-H starved rats. 362 73

Treatment of the eukaryotic organism Tetrahymena with various types of DNA-damaging agents has been reported to cause a 35-fold induction of a mitochondrial DNA polymerase. We here report that the enzyme can be induced in large-scale cultures by exposure of the cells to thymine starvation and/or intercalating agents. The induced DNA polymerase has been purified to near homogeneity, with a specific activity of approx. 300,000 units/mg protein. The relative molecular mass of the active form of the enzyme is approx. 100,000, as determined by glycerol gradient sedimentation. The subunit structure has been analysed by SDS polyacrylamide gel electrophoresis of the highly purified preparation and by immunoprecipitation with a monoclonal antibody directed to the DNA polymerase. A polypeptide of Mr 47,000 has been observed to be a subunit of the enzyme. This corresponds to the size of the subunits suggested for mitochondrial DNA polymerase from chicken embryos and mouse myeloma cells.
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PMID:Purification and characterization of an inducible mitochondrial DNA polymerase from Tetrahymena thermophila. 381 2

Gluconeogenesis from dihydroxyacetone (DHA), glycerol, lactate, pyruvate or alanine was studied in the absence or in the presence of glucagon in hepatocytes isolated from starved rats or from rats fed a high protein diet for 2-48 h. In both groups, gluconeogenesis from DHA, glycerol, lactate and pyruvate exhibited similar changes over 48 h; the rates of glucose production increased progressively until 24 h and then plateaued. During the early phase (2-11 h), gluconeogenesis from DHA and glycerol were higher than gluconeogenesis from lactate and pyruvate. During the first 24 h of the experiment, gluconeogenesis from alanine displays a kinetic similar to that from lactate or pyruvate. After feeding a high protein diet for 24 to 48 h, gluconeogenesis from alanine was slightly higher than that in starved rats and paralleled the increase in alanine aminotransferase activity. Glucagon stimulated gluconeogenesis from DHA up to 48 h, but with glycerol this effect occurred only during the early phase (2-11 h). Glucagon stimulated gluconeogenesis from lactate, pyruvate or alanine by 1.35-fold throughout the experimental period. These findings suggest that the development of gluconeogenesis during starvation or after feeding a high protein diet displays different kinetics, depending on the substrate used and on the level of entry in the gluconeogenic pathway: triose phosphates or pyruvate.
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PMID:Development of gluconeogenesis from various precursors in isolated rat hepatocytes during starvation or after feeding a high protein, carbohydrate-free diet. 381 63

The basal blood glycerol concentration was determined and the rate of glycerol turnover was assessed by a nonradioactive infusion technique in six healthy nonobese adults after an overnight fast and again after four days of total starvation. Simultaneously, estimates of total energy expenditure and net fat oxidation were made from measurements of oxygen consumption, carbon dioxide production, and urinary nitrogen excretion. The data were combined to provide quantitative estimates of the activity of the triglyceride/fatty acid cycle. The basal concentration of glycerol in venous blood rose from a mean value of 54 +/- 8 mumol/L (SEM) before starvation to 154 +/- 5 mumol/L on day 4 of starvation. Glycerol turnover rates correlated well with the basal blood glycerol concentration (r = .95) and increased from a mean value of 115 +/- 17 mumol/min before starvation (equivalent to mobilization of about 3.95 kJ triglyceride/min) to 304 +/- 20 mumol/min (equivalent to mobilization of about 18.41 kJ/min). The estimated rate of net fat oxidation was 3.00 +/- 0.47 kJ/min before starvation and 4.00 +/- 0.14 kJ/min on day +4 of starvation. The rate of triglyceride energy recycling or rate of deposition of triglyceride energy into fat stores was calculated from the difference in the rate of fat energy mobilization and the rate of energy released during net fat oxidation. The values were found to be 0.94 +/- 0.26 kJ/min before starvation and 6.29 +/- 0.54 kJ/min on day +4 of starvation.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:The energy cost of triglyceride-fatty acid recycling in nonobese subjects after an overnight fast and four days of starvation. 382 5


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