Disease relevance of 3-O-Methyl-d-glucose

• After 12 days of hypoglycemia, the Km for 3-O-methyl-D-glucose transport in isolated rat islets, normally 18-20 mM, was 2.5 mM [1].
• Nonglycolytic acidification of murine radiation-induced fibrosarcoma 1 tumor via 3-O-methyl-D-glucose monitored by 1H, 2H, 13C, and 31P nuclear magnetic resonance spectroscopy [2].
• Affected family members manifested mild to severe seizures, developmental delay, ataxia, hypoglycorrhachia, and decreased erythrocyte 3-O-methyl-D-glucose uptake [3].
• By contrast, calculated transport rate constants for 3-O-methyl-D-glucose, when adjusted for the hyperglycemia and the increased passive glucose movement, are not altered in the diabetic animal [4].
• Uptake of D-glucose and 3-O-methyl-D-glucose by insulinoma cells was rapid so that the intracellular concentration of D-hexoses approximated the concentration in the incubation medium by 15-30 s [5].

High impact information on 3-O-Methyl-d-glucose

• D-Glucose, but not L-glucose or 3-O-methyl-D-glucose, stimulates 45Ca2+ uptake by both lanthanum-displaceable and lanthanum-nondisplaceable pools in pancreatic islets [6].
• Furosemide inhibits 3-O-methyl-D-glucose equilibrium flux in isolated adipocytes [7].
• Glucose-stimulated Na+ absorption was decreased in ileal epithelium, and absorption of 3-O-methyl-D-glucose was decreased in both jejunum and ileum [8].
• It was first shown that the presence of 2.0 mg per ml of endotoxin in the mucosal bath did not significantly alter the tissue's histology or permeability to 3-O-methyl-D-glucose [9].
• The addition of D-glucose resulted in a dose- and time-dependent stimulation of (+)-[3H]amphetamine binding, whereas incubation with L-glucose, 2-deoxy-D-glucose, or 3-O-methyl-D-glucose failed to increase the number of (+)-[3H]amphetamine binding sites [10].

Chemical compound and disease context of 3-O-Methyl-d-glucose

• Malabsorption of 3-O-methyl-D-glucose and D-xylose was prevalent in all groups of patients with AIDS but not in asymptomatic, well patients with HIV [11].
• METHODS: Jejunal to caecal transit times were assessed in 20 seronegative controls and 60 HIV seropositive subjects from serum analysis of 3-O-methyl-D-glucose and sulphapyridine after ingestion of the monosaccharide and sulphasalazine in aqueous solution [12].
• Septic patients had decreased L-rhamnose/3-O-methyl-D-glucose urine excretion ratios (0.14 +/- 0.07) compared with normal controls (0.28 +/- 0.08, p < .001), consistent with decreased gastrointestinal functional absorptive capacity in sepsis [13].
• Phlorizin (0.05 mmol/l), which completely inhibited net 3-O-methyl-D-glucose absorption in control tissue, had no significant effect on transmissible gastroenteritis jejunum [14].

Biological context of 3-O-Methyl-d-glucose

• The increased generation of ROIs, activation of apoptosis, and induction of apoptosis were also observed in cells incubated with 3-O-methyl-D-glucose, a glucose derivative that is taken up by the cells but not metabolized [15].
• Phosphorylation of 3-O-methyl-D-glucose does not occur in these cells [16].
• Kinetics of 3-O-methyl-D-glucose transport in isolated rat hepatocytes [17].
• The same stimuli were tested for their effect on the cell volume by the 3-O-methyl-D-glucose (OMG) uptake method of Kletzien et al [18].
• The cell line (ts-H6-15) is a derivative of SV-3T3 cells, exhibiting a transformed phenotype at 32 degrees C and a normal phenotype at 39 degrees C. For cells actively growing at either temperature, a marked decrease in the rate of 3-O-methyl-D-glucose (3-O-MeG) transport is observed as cell population density increases [19].

Anatomical context of 3-O-Methyl-d-glucose

• GLUT1 immunoreactivity was normal, but 3-O-methyl-D-glucose uptake into erythrocytes was significantly reduced, suggesting a quantitatively normal, but functionally impaired, GLUT1 protein at the cell membrane [20].
• The impairment of the plasma membrane is expressed 30 sec after exposure to the drug, as measured by the 86Rb uptake, and lasts for at least 12 hr according to the reduced 3-O-methyl-D-glucose uptake [21].
• We have measured in vivo WBGU, FGU, and K(in) and K(out) of 3-O-methyl-D-glucose in forearm skeletal muscle by combining the euglycemic clamp technique, the forearm-balance technique, and a novel dual-tracer (1-[3H]-L-glucose and 3-O-[14C]-methyl-D-glucose) technique for measuring in vivo transmembrane transport [22].
• Exposure of insulin-responsive, differentiated 3T3-L1 cells (adipocytes) to 0.1 to 1.0 microgram/ml of insulin for 3 to 48 h resulted in a persistent state of enhanced 2-deoxy-D-glucose and 3-O-methyl-D-glucose uptake [23].
• Rapid kinetic techniques were employed to measure the transport of the nonmetabolizable hexose, 3-O-methyl-D-glucose, in suspensions of human HeLa cells, mouse L- and P388 leukemia cells, and Chinese hamster ovary cells in zero-trans entry and exit and equilibrium exchange procedures [24].

Associations of 3-O-Methyl-d-glucose with other chemical compounds

• Human spermatozoa rapidly incorporated D-glucose and 3-O-methyl-D-glucose but excluded the glucose-analogue alloxan, which may explain their resistance against the toxic effects of this diabetogenic drug, in spite of their intrinsic sensitivity to organic peroxides such as tert-butyl hydroperoxide [25].
• Estrogen stimulation of 3-o-methyl-D-glucose uptake in isolated rat hepatocytes [26].
• The effect of hyperglycaemia on sugar transport was studied by comparing transepithelial permeation and tissue content of 3-O-methyl-D-glucose (3-O-MG), beta-methyl-D-glucoside (beta-MDG) and D-glucose in isolated mucosae of guinea-pig jejunum mounted in a flux chamber [27].
• Active uptake of 3-O-methyl-D-glucose also increased, permeability to glucose remained unchanged, and proline uptake reversibly decreased (probably due to the lower protein content of the carbohydrate-containing diets) [28].
• The transport rates of radiolabeled ascorbic acid and dehydroascorbic acid, as well as, labeled 3-O-methyl-D-glucose and L-glucose from a central plasma compartment into aqueous and vitreous humors and cerebrospinal fluid were studied in vivo [29].

Gene context of 3-O-Methyl-d-glucose

• These cell lines express in vivo influx and efflux transporters, such as P-glycoprotein (P-gp) and GLUT1, which is capable of 3-O-methyl-D-glucose transport [30].
• At saturating 3OMG and at low external [H+] (pH 7.5), the transient STP1 currents were eliminated [31].
• The inhibitory effect of hyperosmolality on NHE3 activity and the uptake of 3-O-methyl-D-glucose was the same in all three cell lines [32].
• Effects of insulin-like growth factor-I and its analogue, long-R3-IGF-I, on intestinal absorption of 3-O-methyl-D-glucose are less pronounced than gut mucosal growth responses [33].
• Furthermore, the incorporation of C109 into rat adipocytes greatly reduced the plasma membrane GLUT4 level and the 3-O-methyl D glucose flux in host cells without affecting total cellular GLUT4 content [34].

Analytical, diagnostic and therapeutic context of 3-O-Methyl-d-glucose

• Effects of vascular perfusion on the accumulation, distribution and transfer of 3-O-methyl-D-glucose within and across the small intestine [35].
• Six healthy lean male subjects (age 33 +/- 3 yr, body mass index 22.7 +/- 0.6 kg/m(2)) underwent a 4-h IVGTT (0.3 g/kg glucose enriched with 3-6% D-[U-(13)C]glucose and 5-10% 3-O-methyl-D-glucose) preceded by a 2-h investigation under basal conditions (5 mg/kg of D-[U-(13)C]glucose and 8 mg/kg of 3-O-methyl-D-glucose) [36].
• 3-O-methyl-D-glucose improves desiccation tolerance of keratinocytes [37].
• The in vivo absorption of 3-O-methyl-D-glucose (3MG) as a marker of intestinal function has not been studied in an animal model [38].
• Gel chromatography of solubilized Ehrlich cell plasma membranes and preformed asolectin vesicles coupled to a freeze-thaw cycle results in the reconstitution of 3-O-methyl-D-glucose transport [39].

References