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PubMed1991

Reduced absolute rate of myo-inositol biosynthesis of cultured bovine retinal capillary pericytes in high glucose.

De novo biosynthesis of myo-inositol (MI) by permeabilized cultured bovine retinal capillary pericytes (BRCP) and feline retinal pigment epithelial cells (FRPE), grown in different concentrations of glucose, were studied. After incubation with a physiological concentration of [14C]glucose 6-phosphate (G6P), the radioactive G6P derivatives were quantitated by a single HPLC column. Based on the determined specific activity of [14C]G6P, activities of inositol 1-phosphate synthase (MI synthase) were calculated. The activity of MI synthase was reduced 48% by growing BRCP in a high-glucose medium (20 mM) in comparison with that in the normal medium (glucose 5 mM). In contrast, the de novo MI biosynthesis by FRPE was not changed with increasing concentrations of glucose in the medium. As compared with MI uptake previously studied, the synthesized MI contributes a substantial proportion of cellular MI pool in BRCP. Therefore, in BRCP growing in high glucose the reduced MI biosynthesis aggravates the low MI content resulting from the inhibited MI uptake, and thus leads to altered inositol phospholipid metabolism.

Animals↗
PubMed1969

The distribution of glucose and [14C]glucose between erythrocytes and plasma in the rat.

1. Of the glucose in rat blood 79.8+/-3.3% (s.d.) was in the plasma. The variance was mostly due to differences between rats. 2. The concentration of glucose in erythrocyte water was 51+/-8% (s.d.) of that in plasma water. 3. The ratio (specific radioactivity in plasma)/(specific radioactivity in whole blood), i.e. the P/B ratio, was estimated for glucose at intervals after intravenous injection of [U-(14)C]glucose and [U-(14)C]fructose. The ratio differed from unity by more than the standard error of a single determination of the specific radioactivity of blood or plasma glucose except from 10 to 17min. after injection of [(14)C]glucose and from 22 to 30min. after injection of [(14)C]fructose. At all other times specific radioactivities in blood had to be corrected to give specific radioactivities in plasma. How to do so is described. 4. The P/B ratios were accounted for by a turnover of glucose in erythrocytes of 0.14mumole/min./ml. of erythrocytes. 5. Metabolism of glucose in rat erythrocytes is unlikely to be a major source of lactate.

Animals↗
PubMed1975

Glucosamine-labelled envelope proteins of Escherichia coli K-12. I. Electrophoretic studies and partial fractionation of phenol-soluble proteins.

Hydrophobic envelope proteins were extracted by phenol from a glucosamine- and leucine-requiring mutant of Escherichia coli K-12 (E-110). Three protein fractions labelled with D-[1-14C]glucosamine and L-[4,5-3H]leucine were obtained by electrophoretic separation. Envelopes were isolated from cells labelled with D-[1-14C]glucosamine--HCL and acid hydrolyzed. At least 68% of the radioactivity was recovered as glucosamine and glucose with no random distribution of label. Fingerprinting of pronase digests of glucosamine-labelled proteins showed four radioactive spots associated with peptides. The glycoproteins were pronase- and trypsin-sensitive and had apparent molecular weights of 11 000 (fast mobility), 35 000 (intermediate mobility) and 62 000 (slow mobility) as estimated by sodium dodecyl sulfate-polyacrylamide disc electrophoresis. The two heavier fractions were labelled with meso-diamino[1,7-14C2]pimelic acid, while orth[32P]phosphate was not incorporated into any fraction. The glucosamine radioactivity of the fast fraction underwent rapid changes upon a chase with non-radioactive glucosamine. Using a Sephadex LH-20 column, the radioactive proteins were separated from the phenol and subsequently fractionated on a DEAE-cellulose column. The DEAE-cellulose fractions were distinct from each other in the number and composition of protein bands, when analyzed by sodium dodecyl sulfate-polyacrylamide disc electrophoresis. Radioactive bands with intermediate and fast electrophoretic mobilities were found in separate DEAE-cellulose fractions.

Bacterial Proteins↗
PubMed2000

In vivo measurements of control coefficients for hexokinase and glucose-6-phosphate dehydrogenase in Xenopus laevis oocytes.

Hexokinase and glucose-6-phosphate dehydrogenase activities were increased in Xenopus laevis oocytes by microinjection of commercial pure enzymes. The effect of increased fractional activities on glycogen synthesis or on the production of 14CO(2) (the oxidative portion of the pentose phosphate pathway) was investigated by microinjection of [1-(14)C]glucose and measurements of the radioactivity in glycogen and CO(2). Control coefficients calculated from the data show that hexokinase plays an important role in the control of glycogen synthesis (control coefficient=0.7) but its influence on the control of the pentose phosphate pathway is almost nil (control coefficient=-0.01). Glucose-6-phosphate dehydrogenase injections did not affect the production of 14CO(2) by the pentose phosphate pathway, indicating that other factors control the operation of this pathway. In addition, an almost null control of this enzyme on glycogen synthesis flux was observed.

Animals↗
PubMed1981

Control of glycogen metabolism by insulin in isolated hepatocytes.

Isolated rat hepatocytes incubated in a simple bicarbonate buffer, previously shown to display enhanced rates of fatty acid biosynthesis upon a brief exposure to insulin, were used to study acute effects of this hormone on glycogen metabolism. In hepatocytes prepared from fed rats insulin does not increase glycogen deposition as measured chemically, but the incorporation of labelled glucose is markedly accelerated. The rate of disappearance of radioactivity from glycogen, prelabelled with D[U-14C]glucose, is lowered by insulin. In hepatocytes from starved rats insulin promotes net glycogen synthesis. All metabolic parameters studied are affected by glucagon in manner opposite to that of insulin.

Animals↗
PubMed1975

Studies on the nutrition of marine flatfish. The metabolism of glucose by plaice (Pleuronectes platessa) and the effect of dietary energy source on protein utilization in plaice.

1. The effects of dietary energy level and dietary energy source on protein utilization by plaice (Pleuronectes platessa) were examined by giving diets containing 400 g crude protein/kg to nine groups of fish. Five of these diets contained only lipid as a source of energy (in addition to protein) and their energy contents were varied by increasing the lipid level in a step-wise manner from 56 to 176 g/kg. The remaining four diets contained both lipid and carbohydrate (glucose plus dextrin) together as energy sources: two levels of carbohydrate (100 and 200 g/kg) being used at each of two (56 and 86 g/kg) lipid levels. 2. Weight gains of plaice given the diets containing only lipid as an energy source did not differ significantly from each other. Weight gains of plaice given diets containing carbohydrate as well as protein and lipid were superior to those given diets lacking carbohydrate. 3. Values obtained for protein efficiency ratio (PER) and net protein utilization (NPU) increased with increasing dietary energy level in both those fish given the diets containing carbohydrate and those given diets lacking it. Both PER and NPU values were greater for plaice given diets containing carbohydrate than for fish diets without carbohydrate even when the total energy content of the diets was approximately the same. 4. Liver glycogen levels were significantly higher in plaice given diets containing 200 g carbohydrate/kg than in plaice given diets without carbohydrate. Blood glucose levels and hepatic hexokinase (EC 2-7-1-1) levels were not significantly different in plaice given these diets. No glucokinase (EC 2-7-2-2) was detected in plaice given either diet. 5. The metabolic fate of glucose carbon in plaice was investigated by injecting the fish intraperitoneally with [U-14C] glucose and examining, 18 h afterwards the distribution of radioactivity in different biochemical fractions from the fish. 6. Glucose was respired much less rapidly in the carnivorous plaice, irrespective of dietary treatment, than in omnivorous mammals (mouse and rat). The rate of production of 14CO2 from (U-14C) glucose by plaice given diets containing carbohydrate was not significantly greater than that by plaice given diets lacking carbohydrate. 7. More glucose was incorporated into liver glycogen when plaice were given carbohydrate in their food than when it was absent. Otherwise no differences were apparent in the fate of glucose C by plaice which could be related to the diets used. 8. No mortalities occurred nor was any histopathology observed in the plaice as a consequence of the inclusion of carbohydrate in the food.

Animal Nutritional Physiological Phenomena↗
PubMed1988

Quantification of carbon fluxes through the tricarboxylic acid cycle in early germinating lettuce embryos.

A method involving labeling to isotopic steady state and modeling of the tricarboxylic acid cycle has been used to identify the respiratory substrates in lettuce embryos during the early steps of germination. We have compared the specific radioactivities of aspartate and glutamate and of glutamate C-1 and C-5 after labeling with different substrates. Labeling with [U-14C]acetate and 14CO2 was used to verify the validity of the model for this study; the relative labeling of aspartate and glutamate was that expected from the normal operation of the tricarboxylic acid cycle. After labeling with 14CO2, the label distribution in the glutamate molecule (95% of the label at glutamate C-1) was consistent with an input of carbon via the phosphoenolpyruvate carboxylase reaction, and the relative specific radioactivities of aspartate and glutamate permitted the quantification of the apparent rate of the fumarase reaction. CO2 and intermediates related to the tricarboxylic acid cycle were labeled with [U-14C]acetate, [1-14C] hexanoate, or [U-14C]palmitic acid. The ratios of specific radioactivities of asparate to glutamate and of glutamate C-1 to C-5 indicated that the fatty acids were degraded to acetyl units, suggesting the operation of beta-oxidation, and that the acety-CoA was incorporated directly into citrate. Short-term labeling with [1-14C]hexanoate showed that citrate and glutamate were labeled earlier than malate and aspartate, showing that this fatty acid was metabolized through the tricarboxylic acid cycle rather than the glyoxylate cycle. This was in agreement with the flux into gluconeogenesis compared to efflux as respiratory CO2. The fraction of labeled substrate incorporated into carbohydrates was only about 5% of that converted to CO2; the carbon flux into gluconeogenesis was determined after labeling with 14CO2 and [1-14C]hexanoate from the specific radioactivity of aspartate C-1 and the amount of label incorporated into the carbohydrate fraction. It was only 7.4% of the efflux of respiratory CO2. The labeling of alanine indicates a low activity of either a malic enzyme or the sequence phosphoenolpyruvate carboxykinase/pyruvate kinase. After labeling with [U-14C]glucose, the ratios of specific radioactivities indicated that the labeled carbohydrates contributed less than 10% to the flux of acetyl-CoA. The model indicated that the glycolytic flux is partitioned one-third to pyruvate and two-thirds to oxalacetate and is therefore mainly anaplerotic. The possible role of fatty acids as the main source of acetyl-CoA for respiration is discussed.

Acetates↗
PubMed1991

Glycero-3-phosphate is a precursor of glucose but not of glycero-3-phosphocholine in rat liver.

The previous claims by others of a novel choline transfer reaction involving CDP-choline and leading to the conversion of [U-14C]glycero-3-phosphate to glycero-3-phosphocholine in liver sub-cellular fractions could not be confirmed. Apparent labelling of glycero-3-phosphocholine, isolated by paper chromatography, was, in fact, explained by contamination by other radioactive metabolites, especially D-glucose. A synergistic effect on gluconeogenesis from [U-14C]glycero-3-phosphate was obtained by incubating well-washed mitochondria with washed microsomes.

Animals↗
PubMed1978

Calcium and pancreatic beta-cell function. 2. Mobilisation of glucose-sensitive 45Ca from perifused islets rich in beta-cells.

beta-Cell-rich pancreatic islets were microdissected from ob/ob-mice and loaded with 45Ca in the presence of 3 or 20 mM glucose. Subsequent measurements of the effluxes of radioactivity in a perifusion apparatus revealed that the slowly exchangeable 45Ca taken up in response to glucose was also preferentially mobilised by this compound. Glucose stimulation of 45Ca efflux was abolished after omission of calcium from the perifusion medium but persisted when insulin release was inhibited by prolonged starvation, addition of L-epinephrine or lowering of temperature. The presence of a stimulated efflux of radioactivity even under conditions of inhibited insulin release indicates that sources other than beta-granules ejected by exocytosis contribute to the additional 45Ca released after raising the glucose concentration of the perifusion medium. It is suggested that the beta-cell depolarisation as such may account for part of the 45Ca mobilised by glucose.

Animals↗
PubMed1982

Glucose turnover, gluconeogenesis from glycerol, and estimation of net glucose cycling in cancer patients.

A double isotope method was used in patients with progressive malignancy and in control patients to measure: glucose turnover, conversion rate of carbon skeleton of glycerol into glucose, and the interorgan cycling of glucose carbons (Cori-cycle plus alanine-glucose cycle). [U-14C]glycerol and [6-3H]glucose were given intravenously as a single dose injection. The time course of the specific radioactivities of [6-3H] and [U-14C]glucose was followed in blood. The pool size and the turnover rate of glucose were increased in the cancer group as compared with the control patients. The net recycling of glucose carbons was not increased in the cancer group, despite the increased turnover of glucose. The alterations in the metabolism of glucose did not correlate with the plasma levels of insulin or thyroid hormones (T4, T3, rT3) neither in the entire cancer group nor in those cancer patients who were repeatedly investigated at different intervals of time. The turnover rate of glucose in the cancer patients correlated inversely to their body weight index. The gluconeogenesis rate, given as the fractional conversion rate of the injected radioactive dose of [14C]glycerol, or as mol glucose . kg body weight-1 . day-1, was increased in the cancer group, but still contributed only 3% of the glucose turnover rate in both cancer and control patients. We conclude that an increased gluconeogenesis from glycerol is not significant in terms of energy expenditure in patients with progressive malignancy, as has previously been concluded for the gluconeogenesis from alanine. It seems that increased turnover of glucose may contribute to inappropriately high energy expenditure in cancer patients.

Adult↗
PubMed1992

The influence of biological and technical factors on the variability of global and regional brain metabolism of 2-[18F]fluoro-2-deoxy-D-glucose.

This study investigated the influence of biological and technical factors on variations of global and regional cerebral metabolic rate of glucose (CMRglc) measured with 2-[18F]fluoro-2-deoxy-D-glucose ([18F]FDG). Twelve male volunteers (22-40 years) were investigated on three or four occasions for a total of 42 studies. We calculated the variance/covariance of the following parameters: CMRglc, six parameters of the blood clearance of [18F]FDG, hour of injection, peak time of blood radioactivity, and six components of the operational equation (nonradioactive blood glucose concentration, brain radioactivity, two integrals, numerator, and denominator). There was correlation among these six components, except for nonradioactive blood glucose. However, the correlation between the CMRglc and the individual components of the operational equation was poor. The inter- and intrapersonal CMRglc coefficients of variations were 13.8 and 7.1%, respectively. In contrast, coefficients of variations of the numerator and denominator of the operational equation were 34.6 and 32.6%, respectively, and were always in the same direction. No correlation was found between CMRglc and the technical factors in the numerator and denominator of the operational equation. Factor analysis disclosed that a single factor was responsible for 70% of the variance. This factor included caudate, putamen, thalamus, frontal cortex, temporal cortex, and cingulate gyrus. These structures are involved with multiple complex functions, from autonomic motor control to behavior and emotions. The intrinsic metabolic variability of these structures, along with the basal metabolic processes that are continuously going on in the brain, may be the best explanation for the variance encountered in our investigation.

Adult↗
PubMed1988

Transport and metabolism of D-glucose in human adipocytes. Studies of the dependence on medium glucose and insulin concentrations.

Uptake and metabolism of the physiologically labelled D-glucose (D-[U-14C]glucose) has been characterized in human adipocytes at several unlabelled D-glucose concentrations in the absence and presence of insulin. Following a 90 min incubation, about 80% of the intracellular radioactivity was incorporated into total lipids at tracer glucose concentration, as well as at higher glucose concentrations in basal and insulin-stimulated cells, whereas 20% was recovered as hydrophilic metabolites. The only 14C-labelled metabolite escaping the cells in detectable amounts was CO2, which accounted about 4%. At trace glucose concentrations (5 mumol/l), the rate of glucose uptake was linear with time. Comparative studies of initial glucose uptake after 10 s and tracer D-glucose conversion to total lipids after 90 min showed high coefficients of correlation between basal rates (r = 0.87), maximal response above basal level to insulin (r = 0.92) and insulin sensitivity (r = 0.78). Thus, under these conditions glucose transport is rate-limiting for net glucose uptake, and measurements over long time intervals of rates for total cell-associated radioactivity or lipogenesis may serve as reliable estimates of initial glucose influx rates. However, the conversion rate of tracer glucose to metabolites decreased progressively with the glucose concentration and with an apparent Km of about 0.2 mmol/l. The three metabolic pathways exhibited similar percentage decreases in their activities, suggesting that a common enzymatic step is rate-limiting. In comparison, the Km for initial D-glucose uptake rate was about 7 mmol/l. Hence, the capacity for total glucose metabolism comprised only a small fraction of the glucose transport capacity at medium glucose concentrations above tracer concentrations. Both basal, half-maximal and maximal insulin-stimulated rates of adipocyte glucose utilization were dependent on the glucose concentration. Thus, comparing lipogenesis at tracer and at 0.5 mmol/l medium glucose concentration, it was shown that the higher medium glucose concentration was associated with a 60% lowering of the basal rate, a 35% reduction in the percentage response above baseline to maximal insulin stimulation and a 4-fold increase in the insulin sensitivity. Obviously, these findings reflect some intracellular step(s) being rate-limiting at medium glucose levels above tracer values.

Adipose Tissue↗
PubMed1975

Effect of carbon source during growth on sensitivity of Pseudomonas fluorescens to actinomycin D.

Sensitivity to actinomycin D(AD) varies in Pseudomonas fluorescens cells grown in glucose or succinate minimal salts medium. Growth is inhibited in succinate minimal medium by much lower concentrations of AD than in glucose minimal medium. Uptake of selected radioactive metabolites is inhibited by AD in cells incubated for 2 h in succinate medium containing AD but glucose-grown cells were not sensitive. EDTA treatment promotes increased sensitivity to AD in succinate-grown cells but does not alter sensitivity in glucose-grown cells. Succinate-grown cells bound 2-3 times as much 3H-AD as glucose-grown cells. Glucose-grown cells had much higher lipopolysaccharide levels in the envelope than succinate-grown cells. It is proposed that the lipopolysaccharide masks the binding sites and, therefore, is responsible for the difference in binding of AD by the glucose- and succinate-grown cells. The availability of the binding sites is also reflected in the sensitivity of the cells to the antibiotic.

Alanine↗
PubMed1988

Effects of a cafeteria diet and starvation of global 14C(U)-glucose disposal.

The label distribution in control and cafeteria-diet fed rats, either in basal conditions or after 24 hours of food deprivation, 10 minutes after the i.v. injection of carrier-free D-14C-(U)-glucose, has been studied. The radioactivity recovered in the different fractions of liver, kidney, heart, striated muscle and white adipose tissue showed comparable patterns of change with starvation in both dietary groups. Most of the radioactivity was found in the free amino acid fraction as well as in proteins, with significant proportions also in lipid and liver glycogen. However, most of the label was lost due to its oxidation, remaining in the combined indicated tissues 10-20% of the injected label. On the whole, cafeteria rats consumed more glucose than controls, the lowest oxidation corresponding to the starved-control group. The amount of glucose oxidized by cafeteria rats was actually comparable to that of fed controls. The availability of other energetic sources--i.e. lipid--allows for an increased glucose utilization in cafeteria rats, even in the starved state.

Adipose Tissue↗
PubMed2006

Glycosylation is altered by ethanol in rat hippocampal cultured neurons.

AIMS: Glycoproteins, such as adhesion molecules and growth factors, participate in the regulation of nervous system development. Ethanol affects the synthesis, intracellular transport, distribution, and secretion of N-glycoproteins in different cell types, including astrocytes and hepatocytes, suggesting alterations in the glycosylation process. We analysed the effect of exposure to low doses of ethanol (30 mm, 7 days) on glycosylation in cultured hippocampal neurons. METHODS: Neurons were incubated for short (5 min) and long (90 min) periods with the radioactively labelled carbohydrate precursors 2-deoxy-glucose, N-acetyl-D-mannosamine and mannose. The uptake and metabolism of these precursors, as well as the radioactivity distribution in protein gels, were analysed. The levels of the glucose transporters GLUT1 and GLUT3 were also determined. RESULTS: Ethanol exposure reduces the synthesis of proteins, DNA and RNA and decreased the uptake of mannose, but not of 2-deoxy-glucose and N-acetyl-D-mannosamine, and it increased the protein levels of both glucose transporters. Moreover, it altered the carbohydrate moiety of several proteins. Finally, alcohol treatment results in an increment of cell surface glycoconjugates containing terminal non-reduced mannose. CONCLUSIONS: Alcohol-induced alterations in glycosylation of proteins in neurons could be a key mechanism involved in the teratogenic effects of alcohol exposure on brain development.

Animals↗
PubMed1991

Modeling the dependence of hexose distribution volumes in brain on plasma glucose concentration: implications for estimation of the local 2-deoxyglucose lumped constant.

The steady-state distribution volumes of glucose, 3-O-methylglucose, and 2-deoxyglucose (2DG) are known to change as the concentration of glucose in plasma ranges from hypo- to hyperglycemic values. Model estimates of the three distribution volumes were compared with distribution volume values experimentally measured in the brains of conscious rats as the concentration of glucose in plasma was varied from 2 to 28 mM. The dependence on plasma glucose concentration of the 2DG lumped constant, the factor that relates the phosphorylation rate of 2DG to the net rate of glucose utilization at unit specific radioactivity in the plasma, had been determined previously in separate series of experiments. The model was extended to incorporate this dependence of the lumped constant. In the model both the transport and the phosphorylation barriers were assumed to be single and saturable. The values of their respective half-saturation concentrations and the ratio of the two maximum velocities for glucose were assumed to be invariant over the entire range of plasma glucose concentration. Good agreement between measured and estimated values for the distribution volumes and the lumped constant was attained over the full range of plasma glucose concentration. The model estimates reflected the progressive transport limitation of the brain glucose content as plasma glucose levels were reduced to hypoglycemic values. The results also indicated that these changes should be evident in the time course of 2DG in brain following administration by bolus or continuous infusion, and thus that indexes of local lumped constant change could be derived from the time course data.

3-O-Methylglucose↗
PubMed1984

Inhibition by corticosterone of calcium inflow and insulin release in rat pancreatic islets.

Corticosterone (0.6 mumol/l) inhibited both 45Ca outflow and insulin release evoked by glucose, the combination of leucine and glutamine, 2-ketoisocaproate, gliclazide or the association of gliclazide and a tumour-promoting phorbol ester in rat pancreatic islets perifused at normal extracellular Ca2+ concentration (1.0 mmol/l). In all cases, the inhibitory action of corticosterone reached statistical significance within 10-22 min of exposure to this steroid and failed to be rapidly reversible. Corticosterone failed to affect basal 45Ca outflow and insulin release. The steroid also failed to affect the inhibitory action of glucose upon 45Ca outflow, as judged from either the glucose-induced early fall in effluent radioactivity from islets maintained at normal extracellular Ca2+ concentration or the steady-state values for 45Ca outflow from glucose-stimulated but Ca2+-deprived islets. Corticosterone caused a modest increase in 86Rb outflow from islets perifused in the presence of glucose (16.7 mmol/l). It is concluded that corticosterone impairs Ca2+ inflow into the islet cells and, by doing so, causes a progressive inhibition of insulin release. The pancreatic B cell might thus serve as a further model for the study of the rapid biological response to steroids, as presumably mediated by alteration in the biophysical properties of the plasma membrane.

Animals↗