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PubMed1996

Characterisation of the Aspergillus nidulans frA1 mutant: hexose phosphorylation and apparent lack of involvement of hexokinase in glucose repression.

Hexose phosphorylation was studied in Aspergillus nidulans wild-type and in a fructose non-utilising mutant (frA). The data indicate the presence of at least one hexokinase and one glucokinase in wild-type A. nidulans, while the frA1 mutant lacks hexokinase activity. The A. nidulans gene encoding hexokinase was isolated by complementation of the frA1 mutation. The absence of hexokinase activity in the frA1 mutant did not interfere with glucose repression of the enzymes involved in alcohol and L-arabinose catabolism. This suggest that, unlike the situation in yeast where mutation of hexokinase PII abolishes glucose repression, the A. nidulans hexokinase might not be involved in glucose repression.

Amino Acid Sequence↗
PubMed1966

The effect of uranyl nitrate on intestinal transfer of hexoses.

1. Uranyl nitrate in a concentration of 3 x 10(-4)M caused reduction in mucosal transfer of glucose but not of galactose nor 3-O-methyl-glucose by sacs of rat everted intestine. At this concentration uranyl nitrate had little effect on glucose metabolism (measured by glucose disappearance).2. Uranyl nitrate in a concentration of 3 x 10(-3)M caused reduction in transfer of glucose, galactose, 3-O-methyl-glucose and fluid, and inhibited glucose metabolism.3. Uranyl nitrate did not inhibit entry of glucose into the intestine under anaerobic conditions.4. Glucose was found to inhibit or stimulate galactose transfer depending on the conditions. The inhibitory action is presumably by competition for a common carrier, whereas stimulation indicates that glucose metabolism can supply energy for galactose transfer.5. It is suggested that there are two different routes for glucose in the cell, one of which is uranyl sensitive and not used by galactose, and the other is uranyl insensitive and shared by both hexoses. The implications of this are discussed in relation to transport and metabolism.

Animals↗
PubMed1992

A submucosal mechanism of action for prostaglandin E2 on hexose absorption and metabolism in mouse intestine.

1. The involvement of prostaglandin E2 (PGE2) in hexose absorption and metabolism was studied in mouse small intestinal villus cells. 2. Phlorizin-sensitive, Na(+)-dependent alpha-methyl-D-glucoside (alpha-MG) uptake (0.8 mM) during 2 min cell incubations (37 degrees C) was 74 +/- 4 nmol (mg protein)-1. Maximal uptake was 110 +/- 8 nmol (mg protein)-1, representing an accumulation of 50-fold. Metabolism of D-glucose (5 mM) to L-lactate was 38 nmol min-1 (mg protein)-1. 3. Incubation of isolated cells with indomethacin or PGE2 did not affect alpha-MG uptake or D-glucose metabolism. By including indomethacin during cell isolation from whole intestine, alpha-MG uptake was inhibited dose dependently (50-250 microM) by up to 70% (P < 0.001). PGE2 present during both isolation and incubation inhibited by 85% (P < 0.001) at 1 microM and by 27% (P < 0.05) at 0.1 microM, with no effect at lower concentrations. alpha-MG uptake was reduced to 38% (P < 0.01) when 1 microM-PGE2 and 250 microM-indomethacin were presented in combination. When present during cell isolation and incubation, 1 microM-PGE2 inhibited lactate production by 24% (P < 0.05), except when present in combination with 250 microM-indomethacin. Indomethacin, itself, had no effect on lactate production. 4. A submucosal mechanism is proposed to account for the observed inhibitory effects of PGE2 on brush-border uptake of alpha-MG and cellular lactate production. Indomethacin appears to exert not only an effect of its own, possibly via PG-independent actions within the submucosa, but at high concentrations also disrupts the effects of exogenously applied PGE2.

Animals↗
PubMed2004

Role of hexose transport in control of glycolytic flux in Saccharomyces cerevisiae.

The yeast Saccharomyces cerevisiae predominantly ferments glucose to ethanol at high external glucose concentrations, irrespective of the presence of oxygen. In contrast, at low external glucose concentrations and in the presence of oxygen, as in a glucose-limited chemostat, no ethanol is produced. The importance of the external glucose concentration suggests a central role for the affinity and maximal transport rates of yeast's glucose transporters in the control of ethanol production. Here we present a series of strains producing functional chimeras between the hexose transporters Hxt1 and Hxt7, each of which has distinct glucose transport characteristics. The strains display a range of decreasing glycolytic rates resulting in a proportional decrease in ethanol production. Using these strains, we show for the first time that at high glucose levels, the glucose uptake capacity of wild-type S. cerevisiae does not control glycolytic flux during exponential batch growth. In contrast, our chimeric Hxt transporters control the rate of glycolysis to a high degree. Strains whose glucose uptake is mediated by these chimeric transporters will undoubtedly provide a powerful tool with which to examine in detail the mechanism underlying the switch between fermentation and respiration in S. cerevisiae and will provide new tools for the control of industrial fermentations.

Biological Transport↗
PubMed1973

Abnormal cell envelope ultrastructure of a Saccharomyces mutant with invertase formation resistant to hexoses.

The most obvious morphological characteristic of Saccharomyces mutant FH4C cells is the tendency to form clumps (production of invertase and alpha-glucosidase by this mutant is highly resistant to repression by hexoses). This peculiar feature arises from the abnormal cell envelope ultrastructure of the mutant. Clumps are formed as a result of the failure of the cell wall of the bud to separate from that of the mother cell. The cell wall also shows irregular thickening. There are many cells with a doughnut shape and with small budlike protrusions. Abnormal septation and wall invagination into vacuoles give rise to cells of differing sizes and irregular profiles. Many vesicles, tubules, and coiled membranous bodies originate from invaginations of the plasmalemma. These structures are frequently observed in the cell wall or the periplasmic space. The cells of mutant FH4C growing in 0.2 M glucose, unlike parent strain 303-67, contain many mitochondria. Large numbers of glycogen deposits are also found in many cells of FH4C.

Cell Membrane↗
PubMed1977

Pyruvate formation during the catabolism of simple hexose sugars by Escherichia coli: studies with pyruvate kinase-negative mutants.

Escherichia coli K-12 mutants lacking the adenosine 5'-monophosphate-activated pyruvate kinase have been isolated accidentally and used to prepare further mutants additionally devoid of the fructose bisphosphate-activated pyruvate kinase. Such double mutants totally devoid of pyruvate kinase activity still grow well under aerobic conditions on sugars that are catabolized by the phosphoenolpyruvate (PEP):sugar phosphotransferase system, but they grow poorly on non-phosphotransferase system sugars. This suggests that although pyruvate kinase plays a major role in the formation of pyruvate from PEP during growth on non-phosphotransferase system sugars, the operation of the PEP:sugar phosphotransferase system can contribute significantly to pyruvate production from PEP. In the absence of pyruvate kinase and an active PEP:sugar phosphotransferase system the methylglyoxal glycolytic bypass may also function to some extent for the formation of pyruvate during the catabolism of simple hexose sugars. No unique physiological role can yet be ascribed to the adenosine 5'-monophosphate-activated pyruvate kinase as a result of these studies.

Escherichia coli↗
PubMed1992

Cloning, sequencing, and expression of the Zymomonas mobilis fructokinase gene and structural comparison of the enzyme with other hexose kinases.

The frk gene encoding the enzyme fructokinase (fructose 6-phosphotransferase [EC 2.7.1.4]) from Zymomonas mobilis has been isolated on a partial TaqI digest fragment of the genome and sequenced. An open reading frame of 906 bp corresponding to 302 amino acids was identified on a 3-kbp TaqI fragment. The deduced amino acid sequence corresponds to the first 20 amino acids (including an N-terminal methionine) determined by amino acid sequencing of the purified protein. The 118 bp preceding the methionine codon on this fragment does not appear to contain a promoter sequence. There was weak expression of the active enzyme in the recombinant Escherichia coli clone under control of the lac promoter on the pUC plasmid. Comparison of the amino acid sequence with that of the glucokinase enzyme (EC 2.7.1.2) from Z. mobilis reveals relatively little homology, despite the fact that fructokinase also binds glucose and has kinetic and structural properties similar to those of glucokinase. Also, there is little homology with hexose kinases that have been sequenced from other organisms. Northern (RNA) blot analysis showed that the frk transcript is 1.2 kb long. Fructokinase activity is elevated up to twofold when Z. mobilis was grown on fructose instead of glucose, and there was a parallel increase in frk mRNA levels. Differential mRNA stability was not a factor, since the half-lives of the frk transcript were 6.2 min for glucose-grown cells and 6.6 min for fructose-grown cells.

Amino Acid Sequence↗
PubMed1996

Galactose induces in Saccharomyces cerevisiae sensitivity of the utilization of hexoses to inhibition by D-glucosamine.

Inhibition by glucosamine of the utilization of hexoses by Saccharomyces cerevisiae is induced by growing the cells in media with galactose as carbon source. The intensity of inhibition parallels the induction of the galactose pathway. These findings contrast with the fact that glucosamine is a substrate of the constitutive glucose but not of the inducible. galactose transport and phosphorylation systems. The inhibition by glucosamine is pH dependent; the extent seems to be related with phosphorylation of the hexosamine, as shown by its greater effect with substrates or with conditions that less interfere with the phosphorylation of the inhibitor. Inhibition is not a consequence of ATP depletion of the cell. Intracellular accumulated glucosamine derivatives impair the transport of glucose and mannose in yeast cells grown in galactose-supplemented media but not those grown with glucose or ethanol supplements (i.e., under conditions in which the utilization of these sugars is inhibited). However, impairment of the transport is not enough to explain the characteristics of the observed inhibition. The changes induced by growing the yeast in galactose that render the cells sensitive to glucosamine are under the control of the gal80 and gal4 genes.

Culture Media↗
PubMed1982

Na+-dependent hexose transport in vesicles from cultured renal epithelial cell line.

Apical membrane vesicles were prepared from cultured epithelia formed by LLC-PK1 cells using a calcium precipitation technique. alpha-Methylglucoside uptake into this vesicle preparation was markedly stimulated by sodium and inhibited by phlorizin. In addition, a transient "overshoot" of intravesicular alpha-methylglucoside concentration above its equilibrium value was observed under initial sodium gradient conditions. The specificity of this sodium-dependent hexose transporter closely resembled that found in the mammalian kidney brush border membrane, e.g., alpha-methylglucoside, D-glucose, and D-galactose apparently share the transporter while 2-deoxy-D-glucose, mannose, and fructose do not. Kinetic analysis of the sodium-dependent component of alpha-methylglucoside flux into LLC-PK1 apical membrane vesicles indicates the existence of single transporter with Km congruent to 2 mM and Vmax congruent to 3 nmol.min-1.mg protein-1. Measurement of alpha-methylglucoside uptake as a function of sodium concentration is consistent with a sodium:sugar stoichiometry of approximately 2:1.l There is a good correlation over time between the development of the concentrating capacity of the intact epithelium for alpha-methylglucoside and the transport properties of the vesicle preparation.

Animals↗
PubMed1986

Role of cell replication in regulation of Na-coupled hexose transport in LLC-PK1 epithelial cells.

The glucose concentration in growth medium has been shown to regulate the number of sodium-coupled glucose transporters in LLC-PK1 epithelial cells. Epithelia grown in high concentrations of glucose express fewer transporters than epithelia grown in low concentrations of glucose. In the present work, the effect of a dose of ionizing radiation sufficient to block the incorporation of thymidine was examined in order to gauge the importance of cell replication in the hexose transport regulatory process. The low rate of thymidine incorporation in the plateau phase was completely eliminated by ionizing radiation. Under conditions of irradiation that completely blocked thymidine incorporation, down-regulation, namely the loss of alpha-methylglucoside-concentrating capacity, brought about by switching the epithelium from low to high glucose-containing medium, is independent of the irradiation and therefore most likely is also independent of cell replication. In contrast, the up-regulatory phenomenon is strongly impaired by radiation. This impairment may be due to specific radiation impairment of gene expression necessary for the up-regulatory process. It is apparent from the dose-response data that up-regulation is not inhibited by irradiation in a simple manner and is not inhibited at the same radiation dose as cell replication.

Animals↗
PubMed1985

Inhibition of hexose transport in adipocytes by dexamethasone: role of protein synthesis.

The ability of the synthetic glucocorticoid, dexamethasone, to alter 3-O-methylglucose transport was investigated using isolated rat adipocytes. A maximally effective dose of dexamethasone (10(-7) M) inhibited transport up to 80% within 60-90 min. Inhibition of transport was evident as early as 15-30 min after addition of steroid, and was prevented by both actinomycin D and cycloheximide. When added within 45 or 60 min after dexamethasone, actinomycin D interfered with the cells' ability to respond to the steroid but had no effect when added between 60 and 90 min or longer after the steroid. Cycloheximide interfered with steroid-induced inhibition of transport when added at any time before the 15- to 30-min period immediately preceding the transport assay. This interference with hormone action appeared to be independent of the length of time cells were exposed to dexamethasone before addition of cycloheximide. Thus cells that were maximally inhibited by dexamethasone by 90 min became only partially inhibited when cycloheximide was added at 90 or 120 min, and cells were incubated for an additional 60 or 30 min, respectively. These findings are consistent with the following: dexamethasone inhibits glucose oxidation as a result of inhibiting hexose transport; inhibition of transport by dexamethasone requires the synthesis of RNA during the first 45-60 min after steroid addition and requires protein synthesis during the entire incubation period with dexamethasone; and transport is inhibited within minutes after protein synthesis is initiated.

3-O-Methylglucose↗
PubMed1995

SAM prevents impairment of glucose-stimulated insulin secretion caused by hexose deprivation or starvation.

Succinic acid monomethyl ester (SAM) was recently proposed as an insulinotropic tool in non-insulin-dependent diabetes mellitus. Three models were now used to investigate whether SAM protects the B-cell against the impairment of glucose-stimulated insulin release caused by either glucose deprivation or starvation. In the first model, preincubation of the islets for 180 min at low glucose concentration in the presence of SAM prevented the decrease in the secretory response to D-glucose otherwise observed during a subsequent incubation. In the second model, an impaired secretory response to D-glucose was observed after 3-day culture at low (2.8 or 5.6 mM) as distinct from high (11.1 mM) hexose concentration and the presence of SAM in the culture medium again protected against this anomaly. In the third model, the infusion of SAM for 3 days to starved rats restored the secretory potential of isolated islets to a level comparable to that otherwise found in fed rats. Thus, during glucose deprivation or starvation, SAM is indeed able to maintain B-cell responsiveness to D-glucose.

Animals↗
PubMed1996

The effect of GIP and glucagon-like peptides on intestinal basolateral membrane hexose transport.

The effect of gastric inhibitory polypeptide (GIP) and the related glucagon-like peptides-1 and -2 (GLP-1 and GLP-2) on jejunal basolateral membrane glucose transport was investigated to determine if the upregulation produced by luminal hexoses could be explained by the release of one or more of these peptides. Luminal perfusion of the rat jejunum for 4 h, under pentobarbital sodium anesthesia, with 100 mM D-glucose produced a significant increase in plasma GIP levels. Vascular infusion of saline containing 100-800 pM GIP also increased the maximal transport rate for carrier-mediated glucose uptake in jejunal basolateral membrane vesicles. The effect of vascular 400 pM GIP was maximal after 1 h and maintained out to 4 h. The effect of luminal glucose could be blocked by preinjection with anti-GIP antibodies, whereas an antineurotensin antibody had no effect. Vascular infusion with 800 pM GLP-1-(7-36) amide had no effect, but GLP-2 (400 and 800 pM) increased the D-glucose maximal transport rate. An anti-GLP antibody was able to block the response to luminal glucose.

Animals↗
PubMed2003

Active hexose correlated compound enhances resistance to Klebsiella pneumoniae infection in mice in the hindlimb-unloading model of spaceflight conditions.

Previous studies have demonstrated that resistance to infection is decreased in Swiss Webster female mice maintained in the hindlimb-unloading model (Aviles H, Belay T, Fountain K, Vance M, and Sonnenfeld G. J Appl Physiol 95: 73-80, 2003; Belay T, Aviles H, Vance M, Fountain K, and Sonnenfeld G. J Allergy Clin Immunol 110: 262-268, 2002). This is a model of some of the aspects of spaceflight conditions, including lack of load bearing on hindlimbs and a fluid shift to the head. Active hexose correlated compound (AHCC), extracted from Basidiomycete mushrooms, has been shown to induce enhancement of immune responses, including enhanced natural killer activity. In the present study, AHCC was orally administered to mice to determine whether the treatment could decrease immunosuppression and mortality of mice maintained in the hindlimb-unloaded model and infected with Klebsiella pneumoniae. The results of the present study showed that administration of AHCC by gavage for 1 wk (1 g/kg body wt) before suspension and throughout the 10-day suspension period yielded significant beneficial effects for the hindlimb-unloaded group, including 1). decreased mortality, 2). increased time to death, and 3). increased ability to clear bacteria. The results suggest that AHCC can decrease the deleterious effects of the hindlimb-unloading model on immunity and resistance to infection.

Administration, Oral↗
PubMed1985

Adaptation of hexose uptake by the rat jejunum induced by the perfusion of sugars into the distal ileum.

The effects of perfusing solutions of different composition into the distal ileum of the rat, on glucose or galactose absorption from the jejunum has been determined in vivo. The rate of glucose absorption via the active, phlorhizin-sensitive pathway was increased significantly when either glucose or maltose were present in the lower ileum. In contrast, the presence of galactose, lactose and fructose produced only minimal effects on active glucose absorption. The phlorhizin-insensitive component of glucose absorption was unaffected by the presence of sugar in the distal region. Perfusion of glucose into the ileum enhanced the active uptake of the poorly metabolized hexose, galactose, from the jejunum. The administration of cycloheximide abolished the increase in active glucose absorption induced by distal maltose perfusion. The response to distal glucose (a) required the sugar to be perfused for a minimum of 3 h before increases in absorption became significant, and (b) was not dependent on distal glucose absorption by the phlorhizin-sensitive pathway. The possible mechanisms involved in this adaptive response are discussed. The enhancement of jejunal absorption may be important in man in conditions where glucose is present at abnormally high levels in the distal ileum.

Animals↗
PubMed1986

Adaptation of colonic uptake of hexoses and lipids following ileal resection: effect of variations in the fat content of the diet.

This study was undertaken to determine the effect of varying the dietary composition of fat (corn oil and lard) on the colonic uptake of lipids (medium-chain-length fatty acids, cholesterol and decanol) and hexoses (D-glucose, galactose and 3-O-methyl glucose) in control rabbits with an intact intestinal tract, and in animals submitted 6 weeks previously to the surgical removal of the distal half of their small intestine. Food intake was similar in the control and resected animals fed the high-fat (HF) or the low-fat (LF) diet. Body weight gain was lower in control animals fed LF than HF, but was lower in resected animals fed HF than LF. Colonic adherent mucosal fluid volume was unaffected by diet or by ileal resection, but colonic weight was lower in resected than control animals fed LF. Colonic uptake of glucose and 3-O-methyl glucose but not galactose was changed by ileal resection and by dietary fat changes. Colonic uptake of fatty acids and cholesterol was also different in HF than LF, and in resected as compared with control animals, but these changes were not explained by variations in the effective resistance of the colonic unstirred water layer. Thus colonic transport function is altered by the manipulation of the dietary content of fat and by resection of the ileum.

Adaptation, Physiological↗
PubMed1969

Familial renal glycosuria: a genetic reappraisal of hexose transport by kidney and intestine.

Renal glucose titration studies were carried out in 10 members of two pedigrees with familial renal glycosuria to test the accepted hypothesis of autosomal dominant inheritance and to investigate the genetic significance of "type A" and "type B" renal glycosuria. In one family, a brother and sister each had a moderately reduced threshold and tubular maximum for glucose (type A), but both of their parents reabsorbed glucose normally. In the second family, two brothers had severe type A renal glycosuria, their mother and one brother had a mild type A defect, and another brother demonstrated a reduced threshold, an exaggerated splay, and a normal tubular maximum, indicative of type B glycosuria.Hexose transport by intestinal mucosa was also investigated in controls and in the three brothers with the most severe renal glycosuria. D-glucose-(14)C and 3-O-methylglucose-(14)C were accumulated by jejunal mucosa from controls by processes which were saturable and concentrative. No differences in hexose transport were observed in the patients with renal glycosuria. We conclude that familial renal glycosuria can be inherited as an autosomal recessive trait; that mild and severe type A renal glycosuria and type B renal glycosuria can occur in the same pedigree; and that defective reabsorption of glucose by the kidney need not be accompanied by abnormalities in intestinal glucose transport. These findings indicate that glucose transport in the gut and kidney are not mediated by identical mechanisms, and that several different mutations are responsible for the phenotypic variability in familial renal glycosuria.

Adult↗
PubMed1976

Pancreatic beta cell replication: effects of hexose sugars.

Neonatal rat pancreatic monolayer cultures were utilized to investigate the effects of various hexose sugars on insulin release and beta cell replication. Sugars tested were D-glucose, L-glucose, 3-O-methyl-D-glucose, D-mannose and D-fructose. These agents were added at varying concentrations to a control medium containing a baseline level of 5.5 mM D-glucose. Replication was estimated by incubating cultures with [3H]thymidine and determining the frequency of beta cell labelling in aldehyde-thionin stained radioautographs. Although the addition of D-glucose to the control medium resulted in a concentration-dependent increase in both insulin release and beta cell replication, the sensitivity of these two processes to glucose differed. Insulin release was stimulated by a 2.75 mM elevation in the D-glucose concentration of the control medium, while an elevation of 11 mM D-glucose was required to increase the frequency of beta cell replication. Moreover, while insulin release was maximally stimulated by an 11 mM elevation in the concentration of D-glucose, the frequency of replication continued to rise as the concentration of D-glucose was further increased. The specificity of these responses to D-glucose was demonstrated by the inability of 11 mM L-glucose or 11 mM 3-O-methyl-D-glucose to stimulate beta cell replication. D-mannose and D-fructose were less potent insulin secretagogues than D-glucose on an equimolar basis and neither compound enhanced beta cell replication at a concentration of 11 mM. However, higher concentrations of D-mannose (16.5 and 22 mM) enhanced beta cell replication, while comparable concentrations of D-fructose did not. These results indicate that the sensitivity of insulin release and beta cell replication to D-glucose differ, and that in addition to D-glucose, D-mannose is also capable of stimulating beta cell replication.

Animals↗