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

The antilipolytic effects of N6-phenylisopropyladenosine and of prostaglandin E2 were studied with adipocytes of obese volunteers before and after 4 weeks of severe energy restriction [1250 kJ (300 cal)/day] in the presence and absence of adenosine deaminase (1.6 micrograms/ml, corresponding to 320 m-units/ml). The studies were undertaken to define more clearly the role that local modulators might play in adaptation of lipid mobilization to starvation in humans. Starvation was associated with an approx. 3-fold increase in non-stimulated lipolysis. Removal of endogenous adenosine resulted in a similar increase in basal glycerol release under both conditions, averaging 2 and 2.2 mumol/180 min per 10(6) cells respectively. The sensitivity of the cells to N6-phenylisopropyladenosine and to prostaglandin E2 was not changed by starvation in the presence of adenosine deaminase. These results are discussed in terms of the possible role that local regulators might play during dietary adaption in human fat-cells in vitro.
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PMID:Antilipolytic effects of N6-phenylisopropyladenosine and prostaglandin E2 in fat-cells of obese volunteers before and during energy restriction. 386 51

Intraperitoneal injection of 3-mercaptopicolinate into 24 h-food-deprived 27-week-old female control (GSD/GSD) rats lowered the concentration of circulating glucose by 66%, but glycerol and lactate concentrations were increased up to 3- and 4-fold respectively. In phosphorylase b kinase-deficient (gsd/gsd) rats the corresponding changes for blood glucose, lactate and glycerol were half those observed in the controls. Although the concentration of liver glycogen (approx. 12%, w/w) in the gsd/gsd rats was not altered during food deprivation, total hepatic glycogen was decreased by 17%. It is suggested that the gradual breakdown of the extensive hepatic glycogen stores during starvation assists in the maintenance of normoglycaemia in the gsd/gsd rat.
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PMID:Effects in vivo of food deprivation and 3-mercaptopicolinate in the glycogen-storage-disease (gsd/gsd) rat. 386 52

Natural-abundance high-resolution 13C NMR spectra (linewidth, 10 Hz) of the hyphal fungus Aspergillus nidulans have been obtained after growth on glycolytic or gluconeogenic carbon sources. Various polyols, some tricarboxylic acid-cycle intermediates and amino acids, and some phospholipids and fatty acyl compounds are present. The polyols found are mannitol, arabitol, erythritol, and glycerol. The nature of the carbon source has a pronounced effect on the pool sizes of the various polyols. All are present when the fungus is grown on sucrose or sucrose/acetate under strongly aerobic conditions. When grown on acetate, both arabitol and glycerol levels are low, whereas on glycerol erythritol is also hardly detectable. The effect of oxygen is most outspoken in glycolytically grown cultures. Limited oxygenation leads to low levels of arabitol and glycerol. Strong oxygenation changes the ratio of erythritol to mannitol, favoring the C4 polyol. An increase in oxygen supply leads to (i) stimulation of the fluxes through the pentose phosphate pathway and glycolysis, (ii) an overflow of reduced metabolites both at the pentose phosphate pathway level (erythritol and arabitol) and at the C3 level of the glycolytic pathway (glycerol), and (iii) the usual accumulation of mannitol. Upon starvation, glycerol, the other three polyols, and the tricarboxylic acid-cycle intermediates and their associated amino acids disappear in this order. As in yeast, gluconeogenic substrates lead to the synthesis of trehalose, which also occurs when mycelium is grown on acetate/sucrose under limiting aeration. A transient formation of trehalose has been observed upon incubation of starved mycelium, cultured on different substrates, with [13C]glucose.
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PMID:13C NMR studies of carbon metabolism in the hyphal fungus Aspergillus nidulans. 388 52

Starvation, diabetes and insulin did not alter the concentration of casein kinases in rat liver cytosol. However, the Km for casein of casein kinase 2 from diabetic rats was about 2-fold lower than that from control animals. Administration of insulin to control rats did not alter this parameter, but increased the Km for casein of casein kinase 2 in diabetic rats. Starvation did not affect the kinetic constants of casein kinases. The effect of diabetes on casein kinase 2 persisted after partial purification of the enzyme by glycerol-density-gradient centrifugation and affected also its activity on other protein substrates such as phosvitin, high-mobility-group protein 14 and glycogen synthase. The results indicate that rat liver cytosol casein kinase 2 is under physiological control.
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PMID:Effect of starvation, diabetes and insulin on the casein kinase 2 from rat liver cytosol. 388 88

In Escherichia coli BB26-36, the inhibition of net phospholipid synthesis during glycerol starvation affected cell duplication in a manner that was similar in some respects to that observed during the inhibition of protein synthesis. Ongoing rounds of chromosome replication continued, and cells in the D period divided. The initiation of new rounds of chromosome replication and division of cells in the C period were inhibited. Unlike the inhibition of protein synthesis, however, the accumulation of initiation potential in dnaA and dnaC mutants at the nonpermissive temperature was not affected by the inhibition of phospholipid synthesis. Furthermore, proteins synthesized during the inhibition of phospholipid synthesis can be utilized later for division. The results are consistent with a dual requirement for protein and phospholipid synthesis for both the inauguration of new rounds of chromosome replication and the initiation of septum formation. Once initiated, both processes progress to completion independent of continuous phospholipid and protein synthesis.
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PMID:Duplication of Escherichia coli during inhibition of net phospholipid synthesis. 388 97

Previous attempts to account for the labelling in vivo of liver metabolites associated with the citrate cycle and gluconeogenesis have foundered because proper allowance was not made for the heterogeneity of the liver. In the basal state (anaesthetized after 24h starvation) this heterogeneity is minimal, and we show that labelling by [14C]bicarbonate can be interpreted unambiguously. [14C]Bicarbonate was infused to an isotopic steady state, and measurements were made of specific radioactivities of blood bicarbonate, alanine, glycerol and lactate, of liver alanine and lactate, and of individual carbon atoms in blood glucose and liver aspartate, citrate and malate. (Existing methods for several of these measurements were extensively modified.) The results were combined with published rates of gluconeogenesis, uptake of gluconeogenic precursors by the liver, and citrate-cycle flux, all measured under similar conditions, and with estimates of other rates made from published data. To interpret the results, three ancillary measurements were made: the rate of CO2 exchange by phosphoenolpyruvate carboxykinase (PEPCK; EC 4.1.1.32) under conditions that simulated those in vivo; the 14C isotope effect in the pyruvate carboxylase (EC 6.4.1.1) reaction (14C/12C = 0.992 +/- 0.008; S.E.M., n = 8); the ratio of labelling by [2-14C]- to that by [1-14C]-pyruvate of liver glutamate 1.5 min after injection. This ratio, 3.38, is a measure of the disequilibrium in the mitochondria between malate and oxaloacetate. The data were analysed with due regard to experimental variance, uncertainties in values of fluxes measured in vitro, hepatic heterogeneity and renal glucose output. The following conclusions were reached. The results could not be explained if CO2 fixation was confined to pyruvate carboxylase and there was only one, well-mixed, pool of oxaloacetate in the mitochondria. Addition of the other carboxylation reactions, those of PEPCK, isocitrate dehydrogenase (EC 1.1.1.42) and malic enzyme (EC 1.1.1.40), was not enough. Incomplete mixing of mitochondrial oxaloacetate had to be assumed, i.e. that there was metabolic channelling of oxaloacetate formed from pyruvate towards gluconeogenesis. There was some evidence that malate exchange across the mitochondrial membrane might also be channelled, with incomplete mixing with that in the citrate cycle. Calculated rates of exchange of CO2 by PEPCK were in agreement with those measured in vitro, with little or no activation by Fe2+ ions.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:[14C]bicarbonate fixation into glucose and other metabolites in the liver of the starved rat under halothane anaesthesia. Metabolic channelling of mitochondrial oxaloacetate. 392 30

While malnutrition attending cancer cachexia may be associated with variable losses of body fat, lipid metabolism has been only minimally studied. To clarify potential aberrations of lipid metabolism in weight losing cancer patients, the whole body rate of lipolysis was determined in 9 cancer patients in the postabsorptive state and compared to that in 5 normal subjects. A primed-three stage infusion of glycerol was used to measure plasma glycerol clearance and turnover. A positive correlation between glycerol turnover and plasma concentration was demonstrated in both cancer patients (r = 0.72) and in normal subjects (r = 0.81). Glycerol turnover rate in cancer patients (2.05 +/- 0.14 mumol X kg-1 X min-1) was not different from that in normals (2.31 +/- 0.50); while glycerol clearance in cancer patients (1.72 +/- 0.13 L/min) was significantly lower (P less than 0.025) by 32% than that in normals. This study demonstrates that the whole body lipolytic rate in cancer patients is not different from healthy normals. As a consequence, the loss of body fat in patients with cancer cachexia may be due to a reduced rate of lipogenesis rather than augmented lipolysis as is observed in nonmalignant malnutrition, starvation, or injury.
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PMID:Cancer cachexia and the rate of whole body lipolysis in man. 395 2

The effects of cimetidine on plasma secretin were studied during prolonged fasting in order to determine whether gastric acid output influences secretin release under these circumstances. Twenty healthy volunteers starved for 36 h and were refed with oral glucose. They were given placebo or cimetidine (1.6 g daily) for 24 h before and during the starvation period. After 12 h fasting plasma secretin like immunoreactivity (SLI) was lower (P less than 0.02) in the cimetidine group than in the placebo group. After 36 h plasma SLI was higher (P less than 0.001) in both groups compared to the 12 h value but there was no statistically significant difference between the 2 groups. Refeeding caused prompt suppression of plasma SLI in both groups. Plasma gastrin was lower (P less than 0.001) after 36 h than 12 h in the placebo group only, but there was no significant difference between the groups. Blood glycerol (P less than 0.01) and 3 hydroxybutyrate (P less than 0.02) concentrations were higher after 36 h than after 12 h fasting in both groups. During fasting, sufficient to cause mobilisation of fat and ketosis, cimetidine failed to suppress plasma SLI. This may be due to inadequate suppression of gastric acid output or to some alternative stimulus to secretin release during fasting.
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PMID:Cimetidine fails to suppress the rise in plasma secretin during fasting. 399 16

Addition of 5% xylitol to growing cultures of Streptococcus mutans OMZ 176 reduced the amount of extractable glycerol-phosphate polymers in these cells compared to S. mutans cultures grown in medium with 5% glucose added. The glycerol-phosphate polymers were extracted from the cells by hot phenol-water-extraction, and separated by column chromatography. Lipoteichoic acid (LTA) was identified by indirect haemagglutination tests and lipid analysis. The amount of LTA extracted from the cells or present in the medium was not significantly different. It is suggested that the accumulation of intracellular xylitol-phosphate observed in a previous study causes an effect similar to glucose starvation, which is known to affect the composition of the cell wall.
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PMID:Addition of xylitol to the growth medium of Streptococcus mutans OMZ 176--effect on the synthesis of extractable glycerol-phosphate polymers. 401 41

Glucose and cycloheximide activated biosynthesis of phospholipids and, especially, of triacylglycerols involving 14C-acetate in rat liver tissue in vivo. Starvation did not affect the glycerolipid biosynthesis but decreased markedly the cholesterol production. In liver tissue of starved rats cycloheximide activated synthesis of glycerolipids and inhibited the cholesterol synthesis. Administration of glucose into the animals under conditions of their satiation augmented the fatty acid synthesis; the activating effect of cycloheximide was more distinct as compared with glucose. In satiated animals the most part of the label was incorporated into glycerolipid fatty acids after glucose and cycloheximide administration. Starvation inhibited synthesis of fatty acids with simultaneous activation of the glycerolipid glycerol production; cycloheximide activated still further the glyceroneogenesis. Both glucose and cycloheximide activated biosynthesis of palmitic and oleic acids of glycerolipids and inhibited the arachidonic acid synthesis. Similarity in the effect of glucose and cycloheximide on the glycerolipid biosynthesis might occur due to stimulation of glyceroneogenesis and to augmented production of alpha-glycerophosphate, which in turn increased the fatty acid esterification.
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PMID:[The effect of glucose and cycloheximide on glycerolipid biosynthesis in the rat liver]. 409 Mar 84


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