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PubMed1975

Rapid determination of (carbon-14) glucose specific radioactivity for in vivo glucose kinetics.

Specific radioactivity of blood glucose was determined by use of a Dowex-1 anion-exchange column after (carbon-14) glucose was infused for in vivo kinetics. The first 20-ml eluate of protein-free blood filtrate from the column was discarded; then 10 ml was collected, lyophilized, and counted in a liquid-scintillation counter. Glucose concentration was determined and specific radioactivity calculated. Kinetic results were comparable to those obtained with the more laborious glucose-pentaacetate procedure.

Acetates↗
PubMed1980

Glucose metabolism and recycling of radioactively labelled glucose in the Zucker genetically obese rat (fa/fa).

1. The glucose metabolism of conscious lean and obese rats of the Zucker strain was studied by using doubly labelled glucose ([6-3H,U-14C]glucose) given by intravenous injection as a single dose. Fed animals were used, allowing the study to be made in conditions favouring active lipogenesis. 2. At any given prior food intake (consumption during preceding 24 h), the irreversible glucose replacement rate, R0, was considerably higher in the growing obese rat (4-6 months old) when both of these variables were scaled in terms of the total body water of the animals. 3. When scaled in a similar way, the minimal mass of glucose (Mmin.) was also larger in the obese rats. The mean transit time, t, through the pool did not differ significantly between the two groups, but there was a tendency for this to be shorter in obese rats. 4. There was no difference in the proportion of 14C (derived from metabolized labelled glucose) that recycled as [14C]-glucose after passing through the pyruvate pool in the two groups of rats if the rate of recycling of radioactivity (Rc) was expressed as a percentage of R0.

Animals↗
PubMed2006

Biosynthesis of radiolabeled cellodextrins by the Clostridium thermocellum cellobiose and cellodextrin phosphorylases for measurement of intracellular sugars.

The Clostridium thermocellum cellobiose and cellodextrin phosphorylases (glucosyl transferases) in the cell extract were used to synthesize radiolabeled cellodextrins with a degree of polymerization (DP=2-6) from nonradioactive glucose-1-phosphate and radioactive glucose. Chain lengths of synthesized cellodextrin were controlled by the absence or presence of dithiothreitol and by reaction conditions. All cellodextrins have the sole radioactive glucose unit located at the reducing ends. Mixed cellodextrins (G2-G6) were separated efficiently by size-exclusion chromatography or less efficiently by thin-layer chromatography. A new rapid sampling device was developed using disposable syringes containing an ultracold methanol-quenching buffer. It was simple, less costly, and especially convenient for anaerobic fermentation. After an impulse feed of radiolabeled cellobiose, the intracellular sugar levels were measured after a series of operations-sampling, extracting, concentrating, separating, and reading. Results showed that the largest amount of radioactivity was cellobiose with lesser amounts of glucose, cellotriose, and cellotetraose, and an average DP of intracellular cellodextrins was ca. 2.

Anaerobiosis↗
PubMed1977

Turnover and recycling of glucose in man during prolonged fasting.

The effect of prolonged (3-5 wk) fasting on tracer-determined glucose turnover and of recycling radioactive glucose has been examined. We followed the specific activity of plasma glucose after the simultaneous administration of 1-14C-glucose and 3-3H-glucose. The rate of glucose turnover decreased during prolonged fasting. Recycling of radioactive glucose was estimated by two different techniques: (1) the appearance of 14C in positions 2 to 6 glucose was measured; (2) the difference in the slopes of specific activity decline for 1-14C-glucose and for 3-3H-glucose was calculated. The two methods of estimating the radioactive recycling gave results similar to each other. The amount of glucose recycled did not change during prolonged fasting. However, in view of the decline in glucose production during fasting, the proportion of glucose production which was represented by recycling increased. Based on weight and urinary nitrogen loss an estimate of the glucose production from amino acids and glycerol was obtained. The difference between the rate of glucose production from the contribution of amino acids and glycerol and that estimated by radioisotopic techniques was much larger than the measured rate of recycling. This finding suggests that either a large exchange of 12C with 14C occurred in some glycolytic intermediates or that a hitherto unknown source of carbon for glucose production appeared during prolonged fasting.

Adult↗
PubMed2000

Stimulatory effect of caffeic acid on alpha1A-adrenoceptors to increase glucose uptake into cultured C2C12 cells.

In an attempt to understand the antihyperglycemic action of caffeic acid, the myoblast C2C12 cells were employed to investigate the glucose uptake in the present study. Caffeic acid enhanced the uptake of radioactive glucose into C2C12 cells in a concentration-dependent manner. Similar effect of phenylephrine on the uptake of radioactive glucose was also observed in C2C12 cells. Prazosin attenuated the action of caffeic acid in a way parallel to the blockade of phenylephrine. Effect of caffeic acid on alpha1-adrenoceptors was further supported by the displacement of [3H]prazosin binding in C2C12 cells. Moreover, the glucose uptake-increasing action of phenylephrine in C2C12 cells was inhibited by the antagonists of alpha1A-adrenoceptors, both tamsulosin and WB 4101, but not by the antagonist of alpha1B-adrenoceptors, chlorethylclonidine (CEC). The presence of alpha1A-adrenoceptors in C2C12 cells can thus be considered. Similar inhibition of the action of caffeic acid was also obtained in C2C12 cells co-incubating these antagonists. An activation of alpha1A-adrenoceptors seems responsible for the action of caffeic acid in C2C12 cells. In the presence of U73312, the specific inhibitor of phospholipase C, caffeic acid-stimulated uptake of radioactive glucose into C2C12 cells was reduced in a concentration-dependent manner and it was not affected by U73343, the negative control of U73312. Moreover, chelerythrine and GF 109203X diminished the action of caffeic acid at concentrations sufficient to inhibit protein kinase C. Therefore, the obtained data suggest that an activation of alpha1A-adrenoceptors in C2C12 cells by caffeic acid may increase the glucose uptake via phospholipase C-protein kinase C pathway.

Adrenergic alpha-Agonists↗
PubMed2002

Activation of muscarinic M1 receptors by acetylcholine to increase glucose uptake into cultured C2C12 cells.

Regulation of glucose metabolism by cholinergic nervous activation has been demonstrated. In an attempt to evaluate the role of cholinergic receptor subtype in this regulation of glucose metabolism, we employed cultured myoblast C2C12 cells to investigate the glucose uptake in the present study. Acetylcholine (ACh) enhanced the uptake of radioactive glucose into C2C12 cells at the concentration range of 0.001 to 1.0 micromol/l. This effect was suppressed by the muscarinic antagonist atropine. Effect of ACh on muscarinic receptors was further supported by the blockade of scopolamine, another classical antagonist. Thus, activation of muscarinic receptors to enhance the radioactive glucose uptake into C2C12 cells can be considered. Moreover, pirenzepine, the antagonist of muscarinic M1 receptors, competitively antagonized the action of ACh in C2C12 cells. However, methoctramine at concentration sufficient to inhibit the muscarinic M2 receptors failed to produce similar effect. Similarly, 4-DAMP at effective concentration to block muscarinic M3 receptors lacked the influence. An activation of muscarinic M1 receptors seems responsible for the action of ACh in C2C12 cells. Pharmacological inhibition of phospholipase C by U73312 resulted in a concentration-dependent decrease in ACh-stimulated uptake of radioactive glucose into C2C12 cells. However, treatment with U73343, the inactive congener, failed to block the action of ACh. Moreover, both chelerythrine and GF 109203X diminished the action of ACh at concentrations sufficient to inhibit protein kinase C. Therefore, the obtained data suggest that increase of the glucose uptake evoked by ACh is mainly due to the activation of muscarinic M1 receptors in cultured myoblast C2C12 cells.

Acetylcholine↗
PubMed2004

Activation of alpha1A-adrenoceptor by andrographolide to increase glucose uptake in cultured myoblast C2C12 cells.

We investigated the mechanism of the plasma glucose lowering action of andrographolide, using radioactive glucose uptake into cultured myoblast C2C12 cells as the indicator. In C2C12 cells, andrographolide increased the radioactive glucose uptake in a concentration-dependent manner that was abolished by pretreatment with prazosin. Activation of alpha1-adrenoceptors by andrographolide was further indicated by the displacement of the [3H]prazosin binding in C2C12 cells. The alpha1A-adrenoceptor appears to have caused the displacement, because RS17053 abolished this andrographolide-stimulated glucose uptake at concentrations sufficient to block the alpha1A-adrenoceptor. Inhibition of phospholipase C (PLC) with U73312 concentration-dependently decreased under the action of andrographolide in C2C12 cells. This inhibition of glucose uptake by U73122 was specific because the inactive congener, U73343, failed to influence the action of andrographolide. Moreover, both chelerythrine and GF 109203X diminished the action of andrographolide at concentrations sufficient to inhibit protein kinase C (PKC). Our data suggest that an activation of alpha1A-AR by andrographolide in C2C12 cells may increase the glucose uptake via the PLC-PKC pathway.

Adrenergic alpha-Antagonists↗
PubMed2002

Plasma glucose-lowering effect of beta-endorphin in streptozotocin-induced diabetic rats.

The effect of beta-endorphin on plasma glucose levels was investigated in streptozotocin-induced diabetic rats (STZ-diabetic rats). A dose-dependent lowering of plasma glucose was observed in the fasting STZ-diabetic rat fifteen minutes after intravenous injection of beta-endorphin. The plasma glucose-lowering effect of beta-endorphin was abolished by pretreatment with naloxone or naloxonazine at doses sufficient to block opioid mu-receptors. Also, unlike wild-type diabetic mice, beta-endorphin failed to induce its plasma glucose-lowering effect in the opioid mu-receptor knock-out diabetic mice. In isolated soleus muscle, beta-endorphin enhanced the uptake of radioactive glucose in a concentration-dependent manner. Stimulatory effects of beta-endorphin on glycogen synthesis were also seen in hepatocytes isolated from STZ-diabetic rats. The blockade of these actions by naloxone and naloxonazine indicated the mediation of opioid mu-receptors. In the presence of U73312, the specific inhibitor of phospholipase C (PLC), the uptake of radioactive glucose into isolated soleus muscle induced by beta-endorphin was reduced in a concentration-dependent manner, but it was not affected by U73343, the negative control of U73312. Moreover, chelerythrine and GF 109203X diminished the stimulatory action of beta-endorphin on the uptake of radioactive glucose at a concentration sufficient to inhibit protein kinase C (PKC). The data obtained suggest that activating opioid mu-receptors by beta-endorphin may increase glucose utilization in peripheral tissues via the PLC-PKC pathway to lower plasma glucose in diabetic rats lacking insulin.

Animals↗
PubMed1980

Measurement of free glucose turnover in brain.

A method has been developed for the measurement of the turnover rate constant or the half-life of the free glucose content of brain. It is based on an equation derived by the mathematical analysis of a kinetic model of the equilibration of the specific activity of the free glucose in brain with that of the plasma during an infusion of radioactive glucose. The method requires the measurement of the time course of the specific activity of glucose in the arterial plasma during an intravenous infusion of radioactive glucose for a period of 1 to 4 min and the specific activity of the free glucose in brain at the termination of the infusion. The turnover rate constant, or the half-life, is then calculated from these data by means of the operational equation of the method. The technique has been applied to conscious and anesthetized rats. In conscious rats the half-life of the free glucose content of brain was found to be 1.6 +/- 0.5 min (mean +/- S.D.) when the animals were killed by decapitation and 1.2 +/- 0.2 min (mean +/- S.D.) when they were killed by microwave irradiation; this difference is not statistically significant. In anesthetized rats, the half-life was found to be 2.6 +/- 0.8 min (mean +/- S.D.) in those killed by decapitation and 1.8 +/- 0.3 min (mean +/- S.D.) in those killed by microwave irradiation; this difference is statistically significant. The half-life of the glucose content of brain was found to be significantly prolonged during anesthesia and to be significantly and positively correlated with the plasma glucose concentration (r = 0.78; p < 0.001).

Animals↗
PubMed2001

Stimulatory effect of isoferulic acid on alpha1A-adrenoceptor to increase glucose uptake into cultured myoblast C2C12 cell of mice.

In an attempt to elucidate the effect of isoferulic acid on alpha1-adrenoceptor (AR), the myoblast C2C12 cells of mice were employed to investigate the change of glucose uptake in the present study. Isoferulic acid enhanced the uptake of radioactive glucose into C2C12 cells in a concentration-dependent manner, which were abolished by pretreatment with prazosin. Effect of isoferulic acid on alpha1-AR was further characterized using the displacement of [3H]YM617 binding in C2C12 cells. The radioactive glucose uptake increasing action of isoferulic acid was abolished by tamsulosin or WB 4101 at concentration sufficient to block alpha1A-adrenoceptor (alpha1A-AR) but it was not modified by chlorethylclonidine (CEC) at the concentration sufficient to abolish alpha1B-AR. An activation of alpha1A-AR by isoferulic acid in C2C12 cells can thus be considered. Pharmacological inhibition of phospholipase C (PLC) by U73312 resulted in a concentration-dependent reduction of isoferulic acid-stimulated glucose uptake in C2C12 cells. This inhibition by U73112 was specific because the inactive congener, U73343, failed to modify the action of isoferulic acid. Also, chelerythrine and GF 109203X diminished the action of isoferulic acid at concentration sufficient to inhibit the activity of protein kinase C (PKC). The obtained data suggest that an activation of alpha1A-AR by isoferulic acid may increase the glucose uptake via PLC-PKC pathway in C2C12 cells.

Adrenergic alpha-Antagonists↗