Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “HEXOSES”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 235 records · Page 13Linked to original sources
PubMed2005

Glucagon-like peptide-2 protects against TPN-induced intestinal hexose malabsorption in enterally refed piglets.

Premature infants receiving chronic total parenteral nutrition (TPN) due to feeding intolerance develop intestinal atrophy and reduced nutrient absorption. Although providing the intestinal trophic hormone glucagon-like peptide-2 (GLP-2) during chronic TPN improves intestinal growth and morphology, it is uncertain whether GLP-2 enhances absorptive function. We placed catheters in the carotid artery, jugular and portal veins, duodenum, and a portal vein flow probe in piglets before providing either enteral formula (ENT), TPN or a coinfusion of TPN plus GLP-2 for 6 days. On postoperative day 7, all piglets were fed enterally and digestive functions were evaluated in vivo using dual infusion of enteral ((13)C) and intravenous ((2)H) glucose, in vitro by measuring mucosal lactase activity and rates of apical glucose transport, and by assessing the abundances of sodium glucose transporter-1 (SGLT-1) and glucose transporter-2 (GLUT2). Both ENT and GLP-2 pigs had larger intestine weights, longer villi, and higher lactose digestive capacity and in vivo net glucose and galactose absorption compared with TPN alone. These endpoints were similar in ENT and GLP-2 pigs except for a lower intestinal weight and net glucose absorption in GLP-2 compared with ENT pigs. The enhanced hexose absorption in GLP-2 compared with TPN pigs corresponded with higher lactose digestive and apical glucose transport capacities, increased abundance of SGLT-1, but not GLUT-2, and lower intestinal metabolism of [(13)C]glucose to [(13)C]lactate. Our findings indicate that GLP-2 treatment during chronic TPN maintains intestinal structure and lactose digestive and hexose absorptive capacities, reduces intestinal hexose metabolism, and may facilitate the transition to enteral feeding in TPN-fed infants.

Algorithms↗
PubMed1996

Kinetics of hexose uptake by the small and large intestine of the chicken.

The kinetic parameters of hexose uptake by the small and large intestine of the chicken have been determined in vitro. Rates of initial influx of alpha-methyl-D-glucoside and L-glucose were measured in everted sleeves of the duodenum, jejunum, ileum, proximal cecum, and rectum. Results show the following. 1) Maximal transport capacity values for alpha-methyl-D-glucoside show that the jejunum is the segment that is best suited for Na(+)-mediated uptake. 2) The calculated apparent Michaelis constant values were (in mmol/l) 11.6 for duodenum, 7.8 for jejunum, 3.5 for ileum, 2.4 for proximal cecum, and 7.1 for rectum. This suggests that, with the exception of the rectum, the affinity of the carrier for alpha-methyl-D-glucoside progressively increases in the distal direction. 3) Diffusion constant values indicate that influx of hexoses by a passive mechanism in the duodenum and proximal cecum is significantly higher than in the other segments. 4) The sum of passive and mediated mechanisms confers to the duodenum and jejunum a high capacity to absorb hexoses. The ileum, proximal cecum, and rectum have a quantitatively minor role, albeit significant, in completing the absorptive function.

Animals↗
PubMed1990

Hexose uptake and transport in polymorphonuclear leukocytes from patients with glycogen storage disease Ib.

Neutrophil functions and glucose metabolism are known to be impaired in glycogen storage disease (GSD) Ib patients. The uptake of nonmetabolizing glucose analogues into polymorphonuclear leukocytes (PMN) of GSD Ib patients was studied. 2-Deoxyglucose (2-DOG) and 3-O-methylglucose are transported across the cell membrane by facilitated diffusion mediated by the glucose transporter. Because 2-DOG is phosphorylated within the cell, its uptake rate reflects hexose transport as long as phosphorylation is not rate-limiting. These conditions prevail only at low 2-DOG concentrations. Transport of 5 microM DOG into GSD Ib patient PMN was found to be similar to controls (4.3 +/- 0.5 and 4.65 +/- 1.77 pmol/min X 10(6), respectively). In contrast, 2-DOG uptake at high concentrations (2 mM) decreased by 70% in patient PMN compared with control cells (0.17 +/- 0.06 and 0.51 +/- 0.11 nmol/min X 10(6), for patients and controls, respectively). Transport of 3-O-methylglucose (a glucose analogue that does not undergo intracellular phosphorylation) was not different in patient PMN compared with controls (1.86 +/- 0.53 and 2.19 +/- 0.30 nmol/min X 10(6), respectively). Hexose monophosphate shunt activity in PMN of GSD Ib patients at a glucose concentration of 2 mM was 43% of control values, whereas at 10 microM it was similar to controls. Taken together, these results suggest that the defect in glucose uptake and metabolism found in GSD Ib patient PMN is due to an impairment in hexose phosphorylation rather than in a reduction in the transmembrane glucose transport activity.

3-O-Methylglucose↗
PubMed1978

On the biochemical nature of triose- and hexose-stimulated insulin secretion.

The differential effects of several specific inhibitors of intermediary metabolism, mannoheptulose, 2-deoxylucose, and iodoacetate, were studied with isolated perifused pancreatic islets stimulated with glucose, mannose, glyceraldehyde, dihydroxyacetone, or alpha-ketoisocaproate. Insulin release rates and/or capacities to metabolize these caloric stimuli served as indicators of the inhibitors' actions. Mannoheptulose and 2-deoxyglucose blocked hexose-stimulated hormone release and hexose metabolism concomitantly, but left the functional and metabolic actions of trioses unaltered. Iodoacetate blocked hexose- and triose-stimulated hormone release as well as their metabolism in a parallel fashion. The action of alpha-ketoisocaproate was not affected by any of these three inhibitory agents. The data are most easily explained by a theory that incorporates metabolic signals, arising during the degradation of insulin-releasing fuel molecules, as an integral component in the process of beta-cell stimulation.

Animals↗
PubMed1986

The inhibitory effect of phlorhizin and phloretin on hexose transport in the liver.

The inhibitory effect of phlorhzin on renal tubular glucose absorption has been known for a long time now. But its aglycone, phloretin is almost completely devoid of such an action in the kidney although it is more active than phlorhzin on sugar transport mechanism in human erythrocytes. The present investigation was designed to find out the effects of these two chemically related substances on hexose transport in the liver. The effect of 1mM phlorhzin or ImM phloretin on the transport of D-stereoisomers of glucose, galactose and fructose using the first pass extraction technique. It was found that phloretin was a better inhibitor of hexose transport in the liver. The difference between the effect of phlorhizin, and the phloretin was highly significant. The inhibitory pattern of the two chemical substances on the three hexoses indicate a discrimination between galactose transport and glucose or fructose transport in the liver.

Animals↗
PubMedDate not supplied

[Content of hexuronic acids, hexoses and tyrosine in the lung tissue in experimental pneumoconiosis].

Content of hydroxyproline, thyrosine, hexuronic acids, hexoses and dry weight of lungs were studied in animals with pneumoconiosis, caused by various agents: two types of silicosis, induced by crystalline and condensed modifications of silica, and anthracosis, caused by anthracite. The data obtained showed that in all the types of pneumoconiosis dry weight of defatted lungs was increased with simultaneous increase of hydroxyproline content in the tissue. The more pronounced alterations were observed in silicosis. In all the types of pneumoconiosis within the experimental period content of hexuronic acids was higher in impaired animals as compared with control ones; the increase in content of hexuronic acids preceded the accumulation of hydroxyproline. Content of hexoses and thyrosine was distinctly increased within 2 days, which apparently correlated with the processes of exudation. Then it was decreased and at the later steps of the impairment amount of hexoses and thyrosine was shown to increase with simultaneous accumulation of hydroxyproline. Dynamics of accumulation of non-collagen components of connective tissue in lungs depended upon the type of a dust to which the animals were exposed.

Animals↗
PubMed1989

Enzymes of carbohydrate metabolism in fast-growing Rhizobium grown on hexoses or succinate.

Enzymatic evidence supports that succinate mediates repression of hexose-catabolising enzymes in fast-growing Rhizobium sp. (Cicer arietinum). Enzymes of the Embden-Myerhof-Parnas, Entner-Doudoroff and pentose phosphate pathways were found present in hexose-grown cells but not in succinate-grown cells. These however could be induced by the presence of hexoses.

Carbohydrate Metabolism↗
PubMed1987

Hexose transport regulation in cultured fibroblasts derived from normal and type II diabetic patients.

The kinetics of saturable and nonsaturable sugar transport were studied in normal and Type II diabetic cultured skin fibroblasts under fast or slowly growing conditions. The Km of hexose transport for fast and slow-growing normal fibroblasts was 1.38 +/- 0.3 and 0.88 +/- 0.12 mM, respectively, while those of the diabetic fibroblasts were 1.57 +/- 0.29 and 0.8 +/- 0.19 mM, respectively. The respective transport Vmax for normal and diabetic fast-growing cells was 13.9 +/- 0.8 and 12.95 +/- 2.4 nmoles 2-DG/mg protein/min. For slowly growing cells of both groups, a transport Vmax of 11.5 +/- 2.4 and 11.3 +/- 1.7 nmoles 2-DG/mg protein/min was obtained. No significant differences were observed in the Km or Vmax of hexose transport under these various growth conditions between normal and diabetic cell cultures. Nonsaturable sugar uptake as determined by L-glucose or cytochalasin B inhibited 2-DG uptake was variable, but no significant differences were observed between the normal and Type II diabetic cells. The activation energies for saturable and nonsaturable sugar uptake were not different among the two donor groups. Insulin stimulation of hexose transport was studied in the presence and absence of dexamethasone (5 X 10(-6) M) at varying insulin concentrations. No difference was observed in the amount of insulin necessary to obtain a maximum stimulatory response (approximately 33 nM insulin in both groups). Also, the insulin concentration required to achieve a one-half maximal response was not significantly different in the donor groups (i.e., 3.53 +/- 0.6 nM for normals and 3.98 +/- 1.1 nM for diabetics.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1986

The effects of hexose 6-O-sulfate esters on human natural killer cell lytic function.

Natural cell-mediated cytotoxicity (NCMC) is inhibited by some neutral hexoses and hexose phosphates at 25 to 100 mM concentrations. In this study we describe the effects of hexose 6-O-sulfate esters on NCMC against K-562 target cells. Mannose 6-sulfate, galactose 6-sulfate, N-acetylglucosamine 6-sulfate, and N-acetylgalactosamine 6-sulfate inhibit NCMC in a dose-dependent manner at concentrations of 10 mM and below. Inhibitory effects of mannose 6-sulfate and galactose 6-sulfate were evident at concentrations as low as 1.25 mM. The neutral forms of these sugars, glucose and glucose 6-sulfate, did not inhibit NCMC over this range of concentrations. Comparison of the inhibitory effects of sulfated and phosphorylated forms of mannose and galactose indicated that the sulfated forms are much more potent inhibitors. Formation of effector cell:target cell conjugates was unaffected by the presence of sugar sulfates. Calcium pulse experiments demonstrated that inhibitory effects of sugar sulfates were exerted after the Ca++-dependent triggering step in the NK lytic process. Kinetic studies showed that addition of sugars as long as 60 min after initiation of cultures yielded potent inhibitory effects. Sugar sulfates were not toxic for effector cell populations and effectors were not refractory for lytic function after removal of sugars. Sugar sulfates were inhibitory against multiple tumor types in both human and murine NK lytic assays. These results suggest that the sugar sulfates inhibit NK cells at a postconjugation, posttriggering step involving lectin-like receptors or lectin-like molecules.

Acetylglucosamine↗
PubMed1981

[Evaluation of the severity and degree of myocardial infarct by indicators of fractional determination of protein-bound hexoses in the blood serum].

The time course of the content of hexose fractions was compared with the size of the myocardial infarction appraised from the ECG and with the clinical course of the acute period of myocardial infarction in 100 patients. The degree and duration of the increase in the blood glucosaminoglycane content were determined by the size of the focus of myocardial damage and the severity of its clinical course. The extent of the damage to the myocardium was found to be in accord with the increase in the content of the fraction of glucosaminoglycane hexoses. The results of the study suggest that determination of the content of glucosaminoglycane hexoses in blood may serve as an index of the severity of the myomalacia processes in the myocardium. A decrease in the level of the fraction coincides in time with the average terms of the onset of reparative processes in the myocardium which are determined from the findings of pathology.

Adult↗
PubMed1981

Hexose transport in normal and SV40-transformed human endothelial cells in culture.

The mechanism of glucose entry into human vascular endothelial cells was studied in monolayer cultures of normal (primary) and virally (SV40) transformed umbilical vein endothelium. Radioisotopic uptake studies with the glucose analogues 2-deoxy-D-glucose, and 3-O-methyl-D-glucose, and the nonmetabolizable stereoisomer L-glucose, indicated the presence of a saturable, stereospecific hexose carrier mechanism in both cell types. In other experiments with D-glucose and 3-O-methyl-D-glucose, the phenomenon of countertransport was demonstrable. Hexose transport was not affected by KCN, dinitrophenol, or ouabain, but was inhibited by phloretin and phlorizin in a pattern consistent with facilitated diffusion. Kinetic constants were obtained for both 2-deoxy-D-glucose and 3-O-methyl-D-glucose uptake. Similar Km values (range, 3.3-4.7 mM) were noted with normal and transformed cells, whereas the apparent Vmax was 0.56 nmol/microliter cytosol/minute for primary cells and 1.7-2.5 nmol/mu cytosol/minute for transformed cells. Under standard culture conditions, as well as following 18 hours of serum deprivation, insulin at concentrations up to 10(-5) M did not appear to influence hexose uptake in either cell type. Metabolism of 14C(U)-D-glucose to 14CO2 also was not stimulated by insulin. The presence of an insulin-insensitive, facilitated transport system for glucose in vascular endothelium has relevance for glucose metabolism in this tissue, and potentially for the association of certain vascular diseases (e.g., diabetic microangiopathy, atherosclerosis) with altered glucose homeostasis.

Biological Transport↗
PubMed1982

Regulation of hexose transport in BALB/c 3T3 preadipose cells: effects of glucose concentration and 12-O-tetradecanoylphorbol-13-acetate.

Like many cell types in culture, both undifferentiated and differentiated BALB/c 3T3 preadipose cells respond to glucose deprivation with an increased uptake of 2-deoxy-D-glucose (deoxyglucose) and 3-O-methyl-D-glucose (methylglucose). Glucose readdition to glucose-deprived cultures resulted in a prompt fall in uptake activity; in undifferentiated cells, a half-maximally effective concentration of glucose was approximately 0.5 mM, while 0.1 mM was ineffective. Several hexoses differed in their efficacy of "deactivating" methylglucose transport in glucose-deprived cells; it appeared that a particular hexose must be metabolized beyond the 6-phosphate form to deactivate the transport system. Previous studies have shown that the phorbol ester 12-O-tetradecanoylphorbol-13-acetate (TPA) stimulates hexose transport in undifferentiated and differentiated BALB/c 3T3 cells. In this study, it was found that TPA (and insulin in differentiated cells) prevented the glucose-induced deactivation of transport activity. Glucose-induced deactivation of transport activity was also prevented by cycloheximide or actinomycin D addition concomitantly with glucose. In glucose-starved cells, agents such as TPA and insulin appear to override a cellular control mechanism sensitive to the external concentration of glucose, so that elevated levels of transport activity are maintained under environmental conditions (i.e., a return to physiological glucose concentrations) that normally induce a fall in transport activity.

3-O-Methylglucose↗
PubMed1984

Effects of valinomycin on hexose transport and cellular ATP pools in mouse fibroblasts.

The K+ ionophore valinomycin at concentrations of 1 X 10(-8) M and over, stimulated 2-deoxy-D-glucose (2DG) and 3-O-methylglucose (3OMG) uptake in Swiss 3T3 fibroblasts. The rate-limiting step of 2DG uptake was transport rather than phosphorylation, in the control or valinomycin-treated cells. Kinetic analysis showed that valinomycin increased the Vmax for 2DG uptake without change of the Km. The valinomycin-stimulated 2DG uptake was insensitive to 10 micrograms/ml cycloheximide, and extracellular K+ concentrations between 0.1 and 50 mM. On the other hand, valinomycin at the concentration of 1 X 10(-8) M and over, induced a rapid decrease in cellular ATP content, followed by stimulation of 2DG uptake and recovery of the ATP content. A similar relationship between the reduction of cellular ATP content and the subsequent stimulation of 2DG uptake was observed when the cells were treated not only with 2,4-dinitrophenol and iodoacetic acid, but also with other monovalent cation ionophores or inhibitors of oxidative phosphorylation. These results suggest that valinomycin may posttranslationally stimulate hexose transport by increasing the number of functional carriers of hexose or changing their mobility, and the rapid decrease in cellular ATP pools by valinomycin may be a trigger of the stimulation of the hexose transport in Swiss 3T3 fibroblasts.

2,4-Dinitrophenol↗
PubMed1990

Involvement of hexose transport in myogenic differentiation.

A high (HAHT) and a low (LAHT) affinity hexose transport system are present in undifferentiated rat L6 myoblasts; however, only the latter can be detected in multinucleated myotubes. This suggests that HAHT is either down-regulated or modified as a result of myogenesis. The present investigation examined the relationship between HAHT and myogenic differentiation. While myogenesis could be inhibited by the potent hexose transport inhibitor phloretin, it was not affected by phlorizin which had no effect on hexose transport. This relationship was further explored using six different HAHT-defective mutants. All six mutants, altered in either the HAHT transport affinity (Type I mutants) or capacity (Type II mutants), were impaired in myogenesis. Since these mutants were selected from both mutagenized and non-mutagenized cells with different reagents, or with different concentrations of the same reagent, the deficiency in myogenesis was likely due to changes in HAHT properties. This notion was confirmed by the observation that growth of Type I mutants in high D-glucose concentrations could rectify the defect in myogenesis. D-glucose was unlikely to rectify the defect in myogenesis, if this defect was due to a second unrelated mutation that may have arisen during isolation of the mutants. Since both types of mutants were not altered in LAHT, D-glucose should still be taken up into the cells. The fact that the glucose-mediated increase in fusion could not be observed in Type II mutants (deficient in the HAHT transporter) suggested that myogenesis was dependent on the presence of D-glucose or its metabolites in specific HAHT-accessible compartments. It is tempting to speculate that trans-acting regulators involved in myogenesis may be synthesized from the glucose metabolites in these specialized HAHT-accessible compartments.

Animals↗
PubMed1987

Metabolic characterization of mouse bone marrow cells responsive to estrogenic inhibition: hexose monophosphate shunt enzyme activity in enriched populations of mature cells and progenitor cells.

Compounds with estrogenic activity cause initial toxic responses in the bone marrow characterized by hypocellularity and stem cell myelotoxicity. To elucidate the biochemical nature of these toxic responses, bone marrow cells were collected from mice treated with pharmacological doses of estrogenic chemicals, separated into enriched cell populations, and the enzymatic responses of the individual cell types characterized. Female B6C3F1 mice were injected s.c. with five daily doses of 0.07-5.6 mu moles diethylstilbestrol (DES) or 17-beta estradiol. At 4 days posttreatment body and organ weights were recorded and bone marrow was collected for enumeration and assay of stem cell proliferative responses and enzyme analyses. Treatment with higher dose levels of either estrogenic chemical caused equivalent thymic atrophy, but DES resulted in greater liver and spleen hypertrophy than estradiol. Hexose monophosphate shunt dehydrogenase enzymes in unfractionated bone marrow cells were more sensitive to inhibition by lower estrogen doses than representative enzymes from glycolysis of the Kreb's Cycle, and on an equimolar basis were inhibited to a greater extent by DES than by estradiol. Enzyme analyses after density gradient cell separation indicated that 70-80% of the hexose monophosphate shunt enzyme activity in bone marrow from untreated mice occurred in the enriched band of cells containing predominantly granulocyte-macrophages. The majority of the enzyme inhibition induced by DES treatment could also be ascribed to this cellular population. Furthermore, it was shown that DES had a greater inhibitory effect on the proliferative capacity of the committed stem cells than on the multipotential stem cell population, and the main response was again expressed in the enriched band of cells containing predominantly granulocyte-macrophage precursors. Preliminary endocrine ablation experiments indicated estrogen inhibition of hexose monophosphate shunt enzyme activity was independent of the adrenal and the ovary, but was mediated through the thymus at lower estrogen concentrations.

Adrenalectomy↗
PubMed1977

Cell shape and hexose transport in normal and virus-transformed cells in culture.

The rate of hexose transport was compared in normal and virus-transformed cells on a monolayer and in suspension. It was shown that: 1) Both trypsin-removed cells and those suspended for an additional day in methyl cellulose had decreased rates of transport and lower available water space when compared with cells on a monolayer. Thus, cell shape affects the overall rate of hexose transport, especially at higher sugar concentrations. 2) Even in suspension, the initial transport rates remained higher in transformed cells with reference to normal cells. Scanning electron micrographs of normal and transformed chick cells revealed morphological differences only in the flat state. This indicates that the increased rate of hexose transport after transformation is not due to a difference in the shape of these cells on a monolayer.

Animals↗
PubMed2001

Functional analysis of the hexose transporter homologue HXT5 in Saccharomyces cerevisiae.

The HXT5 gene encodes a functional hexose transporter that has moderate affinity for glucose (K(m)=10 mM), moderate to low affinity for fructose (K(m)=40 mM) and low affinity for mannose (K(m)>100 mM). The sole presence of Hxt5p in an otherwise hexose transport null mutant is sufficient to sustain a flux through glycolysis from glucose to fermentative products. However, the presence of HXT5 as the sole hexose transporter gene results in extremely poor growth on glucose, which suggests the involvement of glucose repression in the transcriptional regulation of HXT5. From Northern blot analysis on the members of the HXT family and studies with HXT5 tagged with the green fluorescent protein (GFP), it is evident that HXT5 is transcribed and translated during conditions of relatively slow growth, during growth on non-fermentable carbon sources and in particular during sporulation. In wild-type batch cultivations on fermentable carbon sources, Hxt5p is abundant in stationary phase or after depletion of the fermentable carbon source, which seems independent of the carbon source. The deletion of HXT5 does not result in a clear phenotype. A shift of stationary phase cells to fresh glucose medium resulted in somewhat slower resumption of growth in the hxt5 deletion strain compared to the wild-type strain. The abundance of Hxt5p during stationary phase, sporulation and low glucose conditions suggests that HXT5 is a 'reserve' transporter, which might be involved in the initial uptake of glucose after the appearance of glucose. Other possible functions of the protein encoded by HXT5 will be discussed in the context of the results.

Blotting, Northern↗
PubMed2001

Optimization of the production of Chondrus crispus hexose oxidase in Pichia pastoris.

Hexose oxidase (D-hexose:O(2)-oxidoreductase, EC 1.1.3.5, HOX) normally found in the red alga Chondrus crispus was produced heterologously in different host systems. Full-length HOX polypeptide was produced in Escherichia coli, but no HOX activity could be detected. In contrast, active HOX could be produced in the methylotrophic yeast Pichia pastoris. Several growth physiological and genetic approaches for optimization of hexose oxidase production in P. pastoris were investigated. Our results indicate that specific growth conditions are essential in order to produce active HOX with the correct conformation. Furthermore, HOX seems to be activated by proteolytic cleavage of the full-length polypeptide chain into two fragments, which remain physically associated. Attempts to direct HOX to the extracellular compartment using the widely used secretion signals from Saccharomyces cerevisiae invertase or alpha-mating factor failed. However, we show in this study that HOX is transported out of P. pastoris via a hitherto unknown mechanism and that it is possible to enhance this secretion by mutagenesis from below the detection limit to at least 250 mg extracellular enzyme per liter.

Alcohol Oxidoreductases↗