Disease relevance of D-glucose

• Aldohexose dehydrogenase from Gluconobacter cerinus-1 [1].
• Sugar-casein GPs from aldohexose, ketohexose, and aldopentose sugar sources were recovered on day 18 of heating and compared for bioactive properties using human embryonic intestinal cell (Int-407) and adenocarcinoma cell (Caco-2) lines [2].

High impact information on D-glucose

• METHODS AND RESULTS: Chronic high-glucose-medium (22. 2 mmol/L) treatment increased platelet-derived growth factor (PDGF)-BB-mediated VSMC migration, [3H]thymidine incorporation, and cell number compared with VSMCs treated with normal-glucose medium (5.6 mmol/L+16.6 mmol/L mannose) [3].
• The latter, derived from 023 and deficient in phosphoglucose isomerase, has been used to map the metabolic requirements for aldohexose-mediated down-regulation or "curbing" of hexose transport [4].
• The PAI-1 could not be removed by incubating ECM in high salt (2 mol/L NaCl), sugars (1 mol/L galactose, 1 mol/L mannose), glycosaminoglycans (10 mmol/L heparin, 10 mmol/L dermatan sulfate), or epsilon-aminocaproic acid (0.1 mol/L) [5].
• Such an anomeric preference diminished at high concentrations of the D-glucose anomers, i.e. when the effect of the aldohexose upon d-fructose phosphorylation became progressively less marked [6].
• Sera from 11 healthy human volunteers contained an average of 54.1 +/- 11.9 mumol/L mannose (range 36-81 mumol/L) [7].

Biological context of D-glucose

• 2. L-Rhamnose, L-mannose and L-lyxose were inducers of the sugar-H+ symport and of L-[14C]rhamnose transport activity [8].
• Despite these analogies between both the respective fate of D-glucose and D-fructose and the reciprocal metabolic effects of the two hexoses in islets from control and STZ rats, the secretory response to the ketohexose in islets from STZ rats was preferentially suppressed, relative to that evoked by the aldohexose [9].
• The precursor was prepared by selective acetylation and triflation of L-mannose [10].
• D-glucose, although slightly decreasing D-[5-(3)H]fructose utilization, augmented the oxidation of the ketohexose, indicating that the aldohexose stimulates preferentially the oxidative, as distinct from anaerobic, modality of glycolysis [11].

Anatomical context of D-glucose

• The enzymatic activities involved in glucose 1,6-bisphosphate metabolism also decrease, but the levels of aldohexose 1,6-bisphosphates remain essentially constant during differentiation of erythroid cells [12].
• L-Fucose and L-rhamnose significantly inhibited T-cell FN-mediated monocyte agglutination at concentrations as low as 0.01 mM; D-glucose, D- or L-galactose, D- or L-mannose and D-fucose were not inhibitory at 10-100 mM [13].
• The concentrations of fructose 2,6-bisphosphate and aldohexose 1,6-bisphosphates also decrease during sheep reticulocyte maturation in parallel to the 6-phosphofructo 2-kinase and the glucose 1,6-bisphosphate synthase activities [14].
• Partial purification and characterization of an aldohexose 1-P phosphatase from pig skeletal muscle [15].
• Alcohol also impaired the capacity of Day 9 mouse embryos to metabolize [14C]glucose under culture conditions in vitro and significantly increased the amount of the aldohexose accumulating in the fetal membrane fluid when administered on Day 14 of pregnancy [16].

Associations of D-glucose with other chemical compounds

• Hydrate/aldehyde ratios vary with aldohexose configuration, ranging from 1.5 to 13, with gluco exhibiting the smallest ratio and gulo the largest [17].
• Response of rat small intestinal active aldohexose transport to elevation of mucosal cyclic AMP by forskolin and 3-isobutyl-1-methylxanthine in vitro [18].
• Mannose is an aldohexose component of a number of glycoproteins in cellular membranes and blood plasma [19].
• The 2 components which reacted with the lectins were: 1. the apical surface of the olfactory epithelium, which was rich in L-mannose, N-acetyl-glucosamine, or sialic acid residues, and 2. the goblet cells which presented N-acetyl-glucosamine or sialic acid and N-acetyl-galactosamine [20].
• The aldohexose dehydrogenase from the thermoacidophilic archaeon Thermoplasma acidophilum (AldT) is a 28 kDa molecular-weight enzyme that catalyzes the oxidation of various aldohexoses, with a preference for NAD+ rather than NADP+ as a cofactor [21].

Gene context of D-glucose

• The Ta0754 gene product exhibited aldohexose dehydrogenase activity, and the Ta0191 gene product exhibited weak 2-deoxyglucose dehydrogenase activity [22].
• (2)H Equilibrium isotope effects (EIEs) on aldohexose anomerization were measured in D-galactose 3 and D-talose 8 selectively (13)C- and (2)H-labeled at C1 and H1 [17].
• Analysis of bacterial glucose dehydrogenase homologs from thermoacidophilic archaeon Thermoplasma acidophilum: finding and characterization of aldohexose dehydrogenase [22].
• As confirmed by transepithelial potential difference (PD) measurements, there is a distinct fructose transporter that does not evoke a PD, along with one or more aldohexose transporters that do evoke a PD [23].

Analytical, diagnostic and therapeutic context of D-glucose

• Crystallization and preliminary crystallographic analysis of NAD+-preferring aldohexose dehydrogenase from the thermoacidophilic archaeon Thermoplasma acidophilum [21].

References