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At least 1,351 records · Page 75Linked to original sources
PubMed1981

Hexose transport in human adipocytes: factors influencing the response to insulin and kinetics of methylglucose and glucose transport.

Optimal experimental conditions were defined for measuring the initial uptake rate of the non-metabolizable sugar analogue 3-O-methylglucose in non-stimulated and insulin-stimulated human adipocytes. The permeability of the adipocyte plasma membrane for tracer methylglucose (100 mumol/l) was 2.9 X 10(-7) cm X s-1 at 37 degrees C and slightly lower at 20 degrees C. At 37 degrees C and pH 7.4 insulin (5 nmol/l) increased the permeability about twofold (range 1.5 to fivefold) with half maximal effect at about 100 pmol/l). At pH 7.0 the dose response curve for the insulin effect on the uptake rate of methylglucose was shifted about 2.5-fold to the right. The permeability to L-glucose due to simple diffusion was estimated as 3.0 X 10(-10) cm X s-1 suggesting that uptake of methylglucose occurs almost exclusively by facilitated diffusion. The Km for methylglucose equilibrium exchange in insulin stimulated cells was about 4.8 mmol/l. The initial uptake of tracer methylglucose in insulin-stimulated cells was inhibited by unlabelled methylglucose and by D-glucose with inhibition constants of about 3.8 and 7.7 mmol/l respectively. Uptake of tracer 2-deoxyglucose (50 mumol/l) in insulin-stimulated adipocytes was linear from 10 s to 5 min whereas the rate of uptake in the presence of 3 mmol/l of D-glucose was markedly decreased suggesting that deoxyglucose uptake after a few minutes is mainly limited by hexokinase in the presence of glucose.

Adipose Tissue↗
PubMed1976

Glycolysis and glycogen metabolism after inhibition of hexose monophosphate pathway in C6-GLIAL cells.

1. 6-Aminonicotinamide (0.01 mg/ml) leads to a strong accumulation of 6-PG in C6 glial cells after 24h. 2. The accumulated 6-PG is dephosphorylated to gluconate which easily permeates the cell membrane. Extracellular gluconate is formed at a rate of 12% of the total glucose consumption. 3. 6-PG as competitive inhibitor of the PG1 caused a reduction of the glycolytic flux of about 40%. 4. The reduced glycolytic flux lowers the ATP concentration under anaerobic conditions to 75% of the controls. 5. The glycogen content after 6-AN is increased by 50%, probably by the activation of the glycogen synthetase due to the higher Glc 6-P concentration. 6. The fibroblast-like morphology of the C6 cell line has typically changed under 6-aminonicotinamide.

6-Aminonicotinamide↗
PubMed1977

Glucose metabolism in C-1300 neuroblastoma cells after inhibition of hexose monophosphate pathway.

1. Application of 6-AN (0.01 mg/ml) leads to a strong accumulation of 6-PG in C-1300 neuroblastoma cells which, however, only amounts to one third of that found in C-6 glial cells. 2. In C-1300 neuroblastoma cells dephosphorylation of the accumulated 6-PG causes a rise of the intracellular gluconate to eight times the value found for 6-PG. It is four times higher than the gluconate content observed in C-6 glial cells. 3. Although 6-PG is a competitive inhibitor of PGI it causes no reduction of glycolytic flux and ATP content in stationary phase C-1300 neuroblastoma cells in contrast to the strong reduction of glycolytic flux and ATP content observed in C-glial cells. 4. The intracellular Glc-6-P and Fru-6-P content of C-1300 neuroblastoma cells increases by four to five times after treatment with 6-AN. Both this increase and the decrease of Fru-1,6-P2 content point to an inhibition of the phosphofructokinase. 5. In contrast to C-6 glial cells no morphological changes could be observed in C-1300 neuroblastoma cells up to 24 h after administration of 6-AN.

6-Aminonicotinamide↗
PubMed1994

Hexose diphosphates and phosphofructokinase in rat brain during development.

Fructose 2,6-diphosphate and glucose 1,6-diphosphate concentrations were determined during late gestation and over the course of suckling in rat brain cortex and cerebellum. Cortex fructose 2,6-diphosphate concentration was greatest in neonatal animals and gradually declined thereafter by 25% to reach the adult level at 15 days of age. In contrast, the glucose 1,6-diphosphate concentration increased 4-fold over the same period to reach its highest level by postnatal day 15. Neither cerebellar fructose 2,6-diphosphate nor glucose 1,6-diphosphate concentrations varied significantly. Six day cortex 6-phosphofructo-1-kinase was less sensitive to inhibition by citrate than the enzyme obtained from 15 day pups, and fructose 2,6-diphosphate was better than glucose 1,6-diphosphate at relieving the inhibition imposed by citrate at either age. It is suggested that the rise in cerebral glucose use which occurs during suckling cannot be attributed to either changes in the concentrations of fructose 2,6-diphosphate or glucose 1,6-diphosphate, or the age-related differential sensitivity of 6-phosphofructo-1-kinase toward these effectors.

Animals↗
PubMed1983

Possible role of calmodulin in stimulation of hexose transport by 12-O-tetradecanoylphorbol-13-acetate, a tumor promoter.

12-O-tetradecanoylphorbol-13-acetate (TPA), a potent tumor promoter stimulated the rate of 2-deoxy-D-glucose (2DG) transport. Three different kinds of calmodulin antagonists inhibited the TPA-stimulated 2DG transport, the mechanism of which was examined in kinetic analysis. These results indicate that the expression of the effect of TPA may depend on Ca2+-calmodulin system.

Animals↗
PubMed1981

Independent control of selected insulin-sensitive cell membrane and intracellular functions-the linkage of cell membrane and intracellular events controlled by insulin. III. The influence of trypsin on cell membrane hexose transport and on glycogen synthase and mitochondrial pyruvate dehydrogenase activation.

Brief treatment of rat adipocytes with low concentration of trypsin activated both cell membrane and intracellular insulin-sensitive functions in marked contrast H2O2 (1), increase in pH, and oxidized glutathione (papers I and II). Glucose oxidation was activated maximally by trypsin in 30 s and preceded maximal activation of glycogen synthase, which occurred in 60s. Trypsin action to activate glycogen synthase was further enhanced by insulin. Mitochondrial pyruvate dehydrogenase was also rapidly activated by trypsin. With both insulin and trypsin action, mediator generation was directly demonstrated by glycogen synthase phosphoprotein phosphatase activation. Trypsin is thus the most insulin-like of these four agents studied since it acts by the formation of chemical mediator peptide(s) which are similar but not identical to those produced by insulin.

Adipose Tissue↗