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PubMed1989

Accumulation of some hexoses in adipocytes: properties of the system.

Adipocytes accumulate 2-deoxy-D-glucose (2-DG) against significant chemical gradients (J. Foley and J. Gliemann. Biochim. Biophys. Acta 648: 100-106, 1981). The specificity of this accumulation process was examined. Isolated rat adipocytes incubated at 37 degrees C with 0.1 mM hexoses accumulated free 2-deoxy-D-galactose (2-DGal) or D-galactose (Gal) against steady-state gradients of 5.5 +/- 1.2 and 2.5 +/- 0.7, respectively. Like 2-DG, both 2-DGal and Gal are substrates for phosphorylation. Insulin and insulin-mimetic agents increased steady-state accumulations of Gal, 2-DGal, and free and phosphorylated 2-DG (100 nM insulin increased free 2-DG from 2.1 +/- 0.2 to 6.6 +/- 0.3 mM; external 2-DG = 0.1 mM). Removal of extracellular calcium or sodium or the presence of A23187 or ouabain failed to inhibit 2-DG accumulation. Plasma membrane permeabilization induced by either digitonin or high-voltage discharge produced a loss of cellular 2-DG and 2-DG-phosphate without affecting 3-O-methyl-D-glucose equilibration. The data indicate that neither transmembrane ionic gradients nor intracellular compartmentation suffice as explanations of the mechanism of the accumulation process. The possible role of phosphorylation in the process of hexose accumulation is discussed.

Adipose Tissue↗
PubMed1981

Effect of liposome-adipocyte interaction on hexose uptake and insulin action.

The effect of unilammelar lipid vesicles composed of defined acyl chain phosphatidylcholines or binary vesicles comprised of dioleoyl phosphatidylcholine (DOPC) and a variety of other lipid species on insulin action in isolated rat adipocytes was studied. Cells were treated with vesicles and subsequently analyzed for basal and insulin-stimulated hexose uptake. Of the different vesicles tested, only those containing DOPC and phosphatidylserine (PS) markedly inhibited the effect of insulin. The inhibition was a function of PS concentration in the binary vesicle. Basal uptake, on the other hand, was stimulated by PS-containing vesicles. The changes in insulin-stimulated hexose uptake following interaction of adipocytes with DOPC-PS vesicles were accompanied by alterations in the Vmax of the uptake process and in affinity of insulin binding, although the similar ED50 values of the control and vesicle-treated groups suggest that the observed effects on insulin sensitivity may be mediated by an uncoupling of the insulin receptor from transport activation. Several lines of evidence are consistent with vesicle-cell fusion as the pathway of DOPC-PS uptake under these conditions. Fluorescence microscopic analysis of fat cells following their interaction with vesicles filled with fluorescent dye indicated that the internal contents of the adipocytes became generally labeled. Biochemical studies of cell fractionation after the interaction of adipocytes with radiolabeled vesicles and effects of metabolic inhibitors and cell fixatives on vesicle uptake also support the fusion pathway.

Adipose Tissue↗
PubMed1985

Long-term regulation of hexose uptake by isoproterenol in cultured 3T3 adipocytes.

Catecholamines are known to have short-term regulatory effects on fat cell hexose uptake. We examined the long-term effects of catecholamines on the insulin-sensitive 2-deoxyglucose (dGlc) uptake in cultured 3T3-L1 adipocytes. Prolonged exposure (48 h) to isoproterenol (beta-adrenergic agonist) stimulated the basal dGlc uptake up to 90%. The effect was specific, time, concentration, and protein synthesis dependent and reversible. The effect of insulin was unaltered and superimposed on the increase in basal dGlc uptake. The long-term effect of isoproterenol was mimicked by epinephrine, dibutyryl cAMP (DBcAMP), and 1-methyl-3-isobutylxanthine (IBMX). By contrast, short-term exposure to isoproterenol (and epinephrine) induced a protein synthesis-independent increase in basal dGlc uptake (30%) not accompanied by an increase in insulin responsiveness. Moreover, on short-term basis, DBcAMP and IBMX suppressed both the basal and insulin-stimulated uptake up to 50%. Determination of the intracellular nonphosphorylated dGlc during the uptake and of the hexokinase activity revealed that the long-term effect of isoproterenol was most likely due to alterations low in dGlc transport. In conclusion, long-term regulators of hexose uptake are in cultured 3T3-L1 adipocytes, isoproterenol, and other cAMP stimulators. The long-term effect is independent from the short-term regulatory effect of the agents and from the effect of insulin.

1-Methyl-3-isobutylxanthine↗
PubMed1987

Effects of insulin on hexose transport across blood-brain barrier in normoglycemia.

The effects of insulin on 3-O-[14C]methylglucose transport across the blood-brain barrier (BBB) were studied in conscious rats under steady-state normoglycemic conditions. The [14C]methylglucose was infused intravenously at a constant rate, and animals were killed at various times between 5 and 30 min after the initiation of the infusion. The time course of the arterial plasma concentration of [14C]methylglucose was determined in timed arterial blood samples taken during the infusion. Local cerebral tissue concentrations of [14C]methylglucose at the time of killing were determined by quantitative autoradiography of brain sections. The rate constants for inward and outward transport of [14C]methylglucose across the BBB, K1, and k2, respectively, were estimated by a least-squares, best-fit of a kinetic equation to the measured time courses of plasma and tissue concentrations. K1 and k2 were reduced by an average of 24 and 31%, respectively, in gray matter and 7 and 16% in white matter from values estimated similarly in normal insulinemic control rats. The equilibrium distribution ratio, K1/k2, for [14C]methylglucose in brain increased by approximately 10-11% in the hyperinsulinemic animals. Because 3-O-[14C]methylglucose shares the same carrier that transports glucose and other hexoses across the BBB, these results suggest that hyperinsulinemia decreases the rate constants for transport but increases the distribution space for hexoses in brain. These effects are, however, quite small and are probably minor or negligible when compared with the major effects of insulin in other tissues.

3-O-Methylglucose↗
PubMed1991

In vivo location of the rate-limiting step of hexose uptake in muscle and brain tissue of rats.

The uptake of glucose proceeds via facilitated transport from the plasma followed by phosphorylation of intracellular glucose. We have quantified the relative contribution of transport and phosphorylation to the overall rate of hexose utilization into the quadriceps muscle (red and white) and cerebellum of rats anesthetized with pentobarbital sodium. The method employed simultaneous infusions of radiolabeled 3-O-methyl-D-glucose and 2-deoxy-D-glucose. Results were expressed in terms of a parameter ft*, which has theoretical limits of 0 and 1 corresponding to phosphorylation and transport limitation, respectively. In cerebellum, basal rates of transport and phosphorylation were comparable (ft* = 0.32 +/- 0.02). Under conditions of hyperglycemia plus maximum insulin stimulation, phosphorylation limited glucose utilization to a greater extent (ft* = 0.12 +/- 0.02). No effect of hyperinsulinemia alone was observed. In red muscle, transport determined overall glucose utilization in the basal (ft* = 0.96 +/- 0.05) and euglycemic insulin-stimulated states (ft* = 0.90 +/- 0.02). A shift of the rate-limiting step from transport toward phosphorylation was observed in insulin-stimulated red muscle when blood glucose (ft* = 0.64 +/- 0.05) or epinephrine levels (ft* = 0.66 +/- 0.07) were elevated. Neither effect was seen in white muscle. We conclude that the transport step dominates but is not the only determinant of muscle hexose utilization under all conditions.

3-O-Methylglucose↗
PubMed1999

Effects of hexose sugars: glucose, fructose, galactose and mannose on wound healing in the rat.

The effects of four hexose sugars (D-glucose, D-fructose, D-galactose, D-mannose) on the developing granulation tissue in rats were examined. Cylindrical hollow sponge implants were used as an inductive matrix for the growth of granulation tissue. In the test group, the implants were injected with 0.1 ml of solution containing the different hexoses in 0.01, 0.1 and 1 M concentrations daily for 7 days while the implants of the control groups were injected with 0.1 ml of phosphate-buffered saline solution only. Analyses of granulation tissue and wound fluid in the sponge implants were carried out 7 days after implantation. The results demonstrated that galactose caused a significant increase in the accumulation of granulation tissue as estimated by histological analyses, but no significant differences were observed in various chemical analyses. In striking contrast, statistically significant decreases were observed in the number of leukocytes in wound fluid, in the amount of DNA, RNA, collagen hydroxyproline, nitrogen, hexosamines and uronic acids in sponges treated with 0.1 or 1 M mannose, reflecting decreased granulation tissue formation. This effect was also observed in histological analyses of the specimens. There were no major changes in sponges treated with glucose or fructose. In summary, the findings of the present study demonstrate that galactose may enhance wound healing and mannose treatment inhibits the inflammatory reaction in wound healing and decreases granulation tissue formation in an experimental wound model.

Animals↗
PubMed1986

Dietary fat content influences uptake of hexoses and lipids into rabbit jejunum following ileal resection.

After 6 weeks' feeding on a high-fat or low-fat diet, the in vitro uptake of hexoses and lipids was measured in control rabbits with an intact intestinal tract, and in animals submitted to the surgical removal of the distal half of their small intestine. Jejunal villus height, villus surface area and mucosal surface area were higher in unresected control rabbits fed the low- as compared with the high-fat diet, whereas dietary fat content had no effect on villus morphology in resected animals. Mucosal surface area was similar in control and in resected animals fed the high-fat diet, but was lower in resected than in control animals fed the low-fat diet. The active and passive transport properties of the jejunum were influenced by dietary fat manipulation. These absorption changes were qualitatively and/or quantitatively different in animals with an ileal resection from those in animals with an intact small intestine. Dietary fat manipulation had a different effect on the uptake of each lipid probe. The effective resistance of the intestinal unstirred water layer also adapted to changes in the dietary content of fat, but the changes in uptake of hexoses, fatty acids and cholesterol cannot be simply explained by alterations in this diffusion barrier, or by changes in the villus morphology. These findings indicate the importance of dietary fat on villus structure and transport function and their adaptation to ileal resection.

Adaptation, Physiological↗
PubMed1975

Hexose transport in sarcoma virus transformed cells.

Avian and mammalian fibroblast cultures transformed by type C sarcoma viruses show a dramatic enhancement of the rate of hexose transport at the beginning of transformation which is quantitatively and qualitatively different from that seen by variation in culture conditions of nontransformed control cells. The identification of this change as being a transport alteration independent of total glucose metabolism has been shown by use of nonmetabolizable analogues, 2-deoxyglucose, 3-O-methylglucose, and L-glucose. Increased transport rates were not dependent on levels of hexokinase activity. Transport studies of 3-O-methylglucose confirmed these conclusions and further revealed an additional altered nature of hexose transport after transformation by sarcoma virus. 3-O-methylglucose was not only transported more rapidly in the transformed cells than in the parental nontransformed cells, but the sugar "infiltrated" into the transformed cells despite the inhibitory effect of cytochalasin B. This was not seen with control cells. The sarcoma cells were also able to transport L-glucose in contrast to lack of uptake by nontransformed cells. Under conditions in which cell toxicity was not a factor, 2-deoxyglucose and several other sugars present in culture media inhibited transformation by sarcoma viruses. These same sugars reduced the incidence of sarcomas produced by virus in vivo when administered daily to test animals. The transport changes also correlate well with the transformed state as found by other laboratories using temperature-sensitive mutants and revertant cell lines. Collectively these data suggest that manipulation of transport systems may prove useful for control of certain malignancies.

Animals↗
PubMed1981

In vitro effects of a sulfonylurea on insulin action in adipocytes. Potentiation of insulin-stimulated hexose transport.

The mechanism(s) by which the oral sulfonylurea, tolazamide, exerts its extrapancreatic hypoglycemic effects was studied using rat epididymal adipose tissue maintained 20-44 h in the presence or absence of the drug. Insulin binding, hexose transport and glucose metabolism were compared in adipocytes isolated from the cultured tissue. In contrast to earlier reports that suggested that sulfonylureas alter the binding of insulin, neither receptor number nor affinity were changed by tolazamide treatment. The uptake of the glucose analogs 2-deoxyglucose and 3-0-methylglucose in the absence of insulin (i.e., basal) was also unchanged. However, exposure to tolazamide resulted in a potentiation of the stimulatory effects of insulin by approximately 30% at each hormone concentration assayed (0.4-40 ng/ml). This potentiation was dependent on the tolazamide concentration (0.003-0.30 mg/ml), with a maximal effect observed at therapeutic levels. A tolazamide analog hypoglycemic activity in vivo was found not to enhance either basal or insulin-stimulated uptake in vitro. Conversion of 0.1-5.0 mM glucose to CO2 and total lipids in the presence of insulin was also potentiated by tolazamide treatment. The inability of the drug to directly stimulate basal glucose uptake was paralleled by its lack of effect on glucose metabolism. At 50 mM glucose, where transport is no longer rate-limiting, tolazamide did not potentiate metabolism in the absence or the presence of insulin. These studies demonstrate that tolazamide in vitro alters postreceptor insulin action without influencing the receptor, and suggests insulin-stimulated hexose transport as the cellular process responsible for the hypoglycemic effect of sulfonyureas in adipose tissue.

Adipose Tissue↗
PubMed1979

Modified procedures for the determination of hexuronic acids, hexoses and proteins using the Auto Analyzer II system.

Previous automated procedures for the determination of hexuronic acids, hexoses and proteins have been modified to suit the Technicon Auto Analyzer II system. The present methods were highly reproducable and the detection limits showed to be in the order of 10 micrograms/l (hexuronic acids and hexoses) and 60 micrograms/l (protein) when 0.13--0.34 ml of the sample was used.

Autoanalysis↗
PubMed1982

Glycosylation of human glomerular basement membrane collagen: increased content of hexose in ketoamine linkage and unaltered hydroxylysine-O-glycosides in patients with diabetes.

To study the glycosylation of glomerular basement membrane collagen (GBMC) in diabetes, kidneys were obtained at autopsy from 5 patients with insulin-requiring diabetes of long duration and diabetic complications, and from 5 control subjects. Glomeruli were prepared by sieving and collagen was isolated by limited pepsin proteolysis followed by salt precipitations. Amino acid analyses of the collagen preparations, after acid hydrolysis, indicated a composition consistent with that of type IV collagen. No differences in the relative contents of various amino acids, and in particular, 3-hydroxyproline, 4-hydroxyproline and hydroxylysine, were noted between diabetic and control samples. Non-enzymatic glucosylation was assessed by measuring hexose in ketoamine linkage with thiobarbituric acid after conversion to 5-hydroxymethylfurfural. In 4 of the 5 patients studied, glucosylation values exceeded the mean +2 S.D. of the controls; in the fifth subject glucosylation was in the high normal range. No correlation between the severity of diabetes and hexose content of GBMC was noted, however. In further studies, enzymatic glycosylation of GBMC was assayed after alkaline hydrolysis by separation of glucosylgalactosyl-O-hydroxylysine, galactosyl-O-hydroxylysine, and unsubstituted hydroxylysine in an amino acid analyzer. No differences in the relative contents of hydroxylysine-O-glycosides were evident between diabetic and control GBMC. The results suggest that non-enzymatic glucosylation, but not glycosylation catalyzed by collagen glucosyl and galactosyl transferases, is increased in diabetes. The increased carbohydrate content of collagen may lead to decreased turnover and/or excessive accumulations of basement membrane collagen thus contributing to the vascular complications of diabetes.

Adult↗
PubMed1991

Assay of keratan sulfate as anion-exchanger bound hexose.

An assay for keratan sulfate in papain digests of human intervertebral disc and other tissues has been developed. The digest is applied to the acetate form of a tertiary amine acrylic anion-exchange resin, the oligosaccharide hexose is removed by washing the resin with 0.2 M sodium acetate buffer pH 5.0, then the keratan sulfate is eluted quantitatively with 1.0 M pyridinium sulfate pH 2.5 and assayed for hexose by the anthrone reaction. The keratan sulfate content of human intervertebral disc tissues ranged from 7 to 78 mumole galactose equivalents/g fresh weight; the root mean square error was 2 mumole/g; 10-25 mg of tissue were required. The separation of oligosaccharides from keratan sulfate was confirmed by gel permeation chromatography, sugar composition, ester sulfate analysis, and nuclear magnetic resonance.

Acetates↗
PubMed2001

Subcellular distribution and kinetic properties of cytosolic and non-cytosolic hexokinases in maize seedling roots: implications for hexose phosphorylation.

Hexose phosphorylation by hexokinases plays an important role in glycolysis, biosynthesis and control of sugar-modulated genes. Several cytosolic hexokinase and fructokinase isoforms have been characterized and organelle-bound hexokinases have also been detected in higher plants. In this study a hexokinase activity is described that is inhibited by ADP (K(i)=30 microM) and mannoheptulose (K(i) congruent with 300 microM) in non-cytosolic fractions (mitochondria, Golgi apparatus and microsomes) obtained from preparations of seedling roots of maize (Zea mays L.). The catalytic efficiency (Vmax/Km) for both ATP and glucose in all non-cytosolic hexokinase fractions is more than one order of magnitude higher than that of cytosolic hexokinase and fructokinases. Low (30%) or no ADP and mannoheptulose inhibition is observed with hexokinase and fructokinase activities derived from the cytosolic compartment obtained after ion exchange and affinity chromatography. The soluble fructokinase (FK) shows fructose cooperativity (Hill n>2). The Vmax/Km ratio is about 3-fold higher for ATP than for other NTPs and no difference for hexose phosphorylation efficiencies is found between cytosolic hexokinase and fructokinase isoforms (FK1, FK2) with ATP as substrate. The K(i) for fructose inhibition is 2 mM for FK1 and 25 mM for FK2. The data indicate that low energy-charge and glucose analogues preferentially inhibit the membrane-bound hexokinases possibly involved in sugar-sensing, but not the cytosolic hexokinases and fructokinases.

Adenosine Diphosphate↗
PubMed1975

Carbohydrate transport in Moniliformis dubius (Acanthocephala). I. The kinetics and specificity of hexose absorption.

The uptakes of 14C-glucose, -2-deoxyglucose, -mannose, -N-acetylglucosamine, -3-0-methylglucose, -fructose, and -galactose by female Moniliformis dubius were nonlinear, saturable functions of hexose concentration. Kinetic and inhibition studies indicated that glucose and 2-deoxyglucose were absorbed via a single common transport locus. Mannose, N-acetylglucosamine, 3-0-methylglucose, fructose, and galactose (in decreasing order of effectiveness) inhibited the uptake of glucose in a completely competitive manner; their absorptions appeared to be mediated by the glucose transport locus and, to some degree, by one or more additional transport systems. Kinetic studies suggested that the apparent inhibitions of 14C-glucose uptake by maltose and glucose-6-phosphate were due to free glucose liberated through the action of surface hydrolases. The uptake of 14C-glucose was also inhibited by salicin, alpha-methylglucoside, and beta-methylglucoside, but not by pentoses, L-hexoses, sugar alcohols, disaccharides (except maltose), gluconic acid, glucuronic acid, phlorizin, or ouabain. Glucose uptake was not Na+-dependent.

Acanthocephala↗
PubMed1990

Regulation of hexose transport in aortic endothelial cells by vascular permeability factor and tumor necrosis factor-alpha, but not by insulin.

Vascular permeability factor (VPF) is mitogenic for bovine aortic endothelial (BAE) cells, whereas tumor necrosis factor (TNF) is cytostatic and was found to completely block the mitogenic response to VPF. In contrast to the apparently antagonistic mitogenic effects that these two factors elicit, chronic exposure of BAE cells to either VPF of TNF resulted in significant (about 3-fold) increases in the rates of hexose transport. The concentrations required for half-maximal stimulation were 2 ng/ml (40 pM) for TNF and 4 ng/ml (100 pM) for VPF. Exposure to both factors simultaneously resulted in a greater stimulation of transport (about 7-fold) than exposure to either factor alone. Northern blot analysis indicated that the amount of message for the GLUT-1/erythrocyte form of the glucose transporter was specifically increased by treatment with VPF (5-fold), TNF (25-fold), or to both cytokines together (35-fold). Expression of mRNAs for the insulin-sensitive muscle/adipose transporter (GLUT-4), brain/fetal skeletal muscle transporter (GLUT-3), or the hepatic transporter (GLUT-2) were not detected in either control or treated cells. Acute or chronic exposure to insulin (10(-9) to 10(-6) M) did not activate hexose transport in BAE cells. Thus, glucose transport in aortic endothelial cells can be up-regulated by either VPF, a growth stimulator, or by TNF, a growth inhibitor, but not by insulin. The additive effect of the two cytokines together may be important in the control of increased glucose metabolism at sites of inflammation.

Animals↗
PubMed1986

Hexose-independent activation of glycogen synthase and pyruvate dehydrogenase by insulin is dissociated in the mouse BC3H-1 cell line.

We have studied the effects of insulin on several aspects of cell metabolism in the insulin-sensitive, nonfusing muscle cell line BC3H-1. In the absence of exogenous hexose, insulin did not alter basal glycogen synthase percentage I activity, or attenuate the increase in intracellular cAMP content, the activation of glycogen phosphorylase a, or the decrease in glycogen synthase I brought about by beta-adrenergic receptor activation with epinephrine. In contrast, both insulin and the tumor-promoting phorbol ester, tetradecanoylyl phorbol acetate markedly increased mitochondrial pyruvate dehydrogenase activity in the absence of hexose. Both glycogen synthase phosphatase and glycogen synthase kinase activities were present in BC3H-1 cell extracts and were regulated in the expected manner by glucose 6-phosphate and cAMP, respectively. Since the pattern of partial insulin resistance seen in BC3H-1 myocytes would require that several potentially insulin-sensitive enzymes be insensitive to insulin-generated signals, the most likely explanation for these data is that the myocytes are defective in some mechanism of insulin signaling which is independent of the mechanism for pyruvate dehydrogenase activation.

1-Methyl-3-isobutylxanthine↗
PubMed1988

The coupling of metabolic to secretory events in pancreatic islets: does hexose transport affect cationic fluxes?

Poorly metabolized hexoses, such as 3-O-methyl-D-glucose, 2-deoxy-D-glucose and D-galactose failed to reproduce the inhibition of 86Rb outflow, the early inhibition and secondary rise in 45Ca efflux and the stimulation of insulin release evoked by D-glucose in perifused rat islets. Insulin release induced by either D-glucose or 2-ketoisocaproate was also unaffected by 3-O-methyl-D-glucose. It is concluded that hexose transport in islet cells does not represent in itself a significant determinant of the cationic and secretory response to D-glucose.

3-O-Methylglucose↗
PubMed1984

Hexose uptake regulation mediated through aerobic pathways: schism in a fibroblast mutant.

A protracted type of down-regulation of the hexose transport system in cultured fibroblasts that depends on one main factor in their nutritional state, the presence or absence of metabolizable D- aldohexoses in the culture fluid, is discussed. Fructose feeding is unable to elicit a down-regulation, whereas mannose and D-glucosamine, regulation of the transport system. This down-regulation or transport curb depends on oxidative energy metabolism, because inhibitors of this type of metabolism bring about a striking release of the transport curb. Studies with a fibroblast mutant that lacks the enzyme glucosephosphate isomerase (D-glucose-6-phosphate ketol-isomerase, EC 5.3.1.9, abbreviated phosphoglucose isomerase) (pgi-) have indicated that two types of metabolism are needed: 1) oxidative energy metabolism, which in the pgi- mutant can still be generated effectively from L-glutamine or, in its absence, from mannose or D-glucosamine; 2) glucose-6-phosphate metabolism, either its catabolism through the pentose shunt or through the anabolic pathway to UDP glucose and UDP galactose. The schism in carbohydrate metabolism in the pgi- fibroblasts is clearly reflected through the development of the metabolically mediated curb of the hexose transport or uptake system.

3-O-Methylglucose↗