alpha-D-glucose
(Synonyms: a-无水葡萄糖酯) 目录号 : GC38885
Alpha-D-Glucose is a primary source of energy for living organisms. It is naturally occurring and is found in fruits and other parts of plants in its free state. It is an intermediate in glycolysis/gluconeogenesis pathway.
Cas No.:492-62-6
Sample solution is provided at 25 µL, 10mM.
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Quality Control & SDS
- View current batch:
- Purity: >99.00%
- COA (Certificate Of Analysis)
- SDS (Safety Data Sheet)
- Datasheet
Alpha-D-Glucose is a primary source of energy for living organisms. It is naturally occurring and is found in fruits and other parts of plants in its free state. It is an intermediate in glycolysis/gluconeogenesis pathway.
| Cas No. | 492-62-6 | SDF | |
| 别名 | a-无水葡萄糖酯 | ||
| Canonical SMILES | O[C@@H]1[C@@H]([C@H]([C@@H]([C@@H](CO)O1)O)O)O | ||
| 分子式 | C6H12O6 | 分子量 | 180.16 |
| 溶解度 | H2O : ≥ 100 mg/mL (555.06 mM); DMSO : 100 mg/mL (555.06 mM; Need ultrasonic) | 储存条件 | Store at -20°C |
| General tips | 请根据产品在不同溶剂中的溶解度选择合适的溶剂配制储备液；一旦配成溶液，请分装保存，避免反复冻融造成的产品失效。 储备液的保存方式和期限：-80°C 储存时，请在 6 个月内使用，-20°C 储存时，请在 1 个月内使用。 为了提高溶解度，请将管子加热至37℃，然后在超声波浴中震荡一段时间。 |
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| Shipping Condition | 评估样品解决方案：配备蓝冰进行发货。所有其他可用尺寸：配备RT，或根据请求配备蓝冰。 | ||
| 制备储备液 | |||
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1 mg | 5 mg | 10 mg |
| 1 mM | 5.5506 mL | 27.7531 mL | 55.5062 mL |
| 5 mM | 1.1101 mL | 5.5506 mL | 11.1012 mL |
| 10 mM | 0.5551 mL | 2.7753 mL | 5.5506 mL |
| 第一步：请输入基本实验信息（考虑到实验过程中的损耗，建议多配一只动物的药量） | ||||||||||
| 给药剂量 | mg/kg |  |
动物平均体重 | g | |
每只动物给药体积 | ul | |
动物数量 | 只 |
| 第二步：请输入动物体内配方组成（配方适用于不溶于水的药物；不同批次药物配方比例不同，请联系GLPBIO为您提供正确的澄清溶液配方） | ||||||||||
| % DMSO % % Tween 80 % saline | ||||||||||
| 计算重置 | ||||||||||
计算结果:
工作液浓度： mg/ml；
DMSO母液配制方法： mg 药物溶于 μL DMSO溶液（母液浓度 mg/mL，
体内配方配制方法：取 μL DMSO母液，加入 μL PEG300，混匀澄清后加入μL Tween 80，混匀澄清后加入 μL saline，混匀澄清。
1. 首先保证母液是澄清的；
2.
一定要按照顺序依次将溶剂加入，进行下一步操作之前必须保证上一步操作得到的是澄清的溶液，可采用涡旋、超声或水浴加热等物理方法助溶。
3. 以上所有助溶剂都可在 GlpBio 网站选购。
Radiation-induced radicals in alpha-D-glucose: Comparing DFT cluster calculations with magnetic resonance experiments
Spectrochim Acta A Mol Biomol Spectrosc 2006 Mar 13;63(4):795-801.PMID:16488658DOI:10.1016/j.saa.2005.10.027.
Using density functional theory (DFT) calculations, an enhanced theoretical examination was made of the radiation-induced radicals in alpha-D-glucose. For the carbon-centred radicals in this sugar, the effect of the model space on the radical geometry as well as on the calculated radical hyperfine coupling tensors was examined. The findings were compared with previously published tensors, as determined by electron paramagnetic resonance (EPR) experiments and single molecule DFT calculations. A cluster approach was adopted, in which intermolecular interactions (predominantly hydrogen bonds) between the radical species and its environment were explicitly incorporated. This substantially improved the correspondence with experimental findings in comparison with single molecule calculations of an earlier examination. In a direct comparison between both computational methods for the glucose radicals, it was shown that the extent of the model space plays an important part in the determination of the radical geometry. Furthermore, the model space also has an impact on the calculated hyperfine coupling tensors. Full cluster EPR calculations, in which the paramagnetic properties are calculated for the entire model space of the cluster, give an excellent agreement with the experimental EPR measurements.
Insulinotropic action of alpha-D-glucose pentaacetate: metabolic aspects
Mol Genet Metab 1998 Jun;64(2):135-47.PMID:9705238DOI:10.1006/mgme.1998.2701.
The metabolism and metabolic effects of alpha-D-glucose pentaacetate were investigated in isolated rat pancreatic islets. Several findings were compatible with the view that the insulinotropic action of alpha-D-glucose pentaacetate is causally related to its capacity to act as a fuel in the islet B-cell. First, the ester was efficiently taken up and hydrolyzed with resulting accumulation of D-glucose in the islet cells. Second, the conversion of alpha-D-[5-3H]glucose pentaacetate to 3HOH and that of alpha-D-[U-14C]glucose pentaacetate to 14CO2 exceeded those found at an equimolar concentration (1.7 mM) of D-glucose and were both inhibited by 2-deoxy-D-glucose (16.7 mM). Last, the ester inhibited the catabolism of both exogenous D-glucose or endogenous fatty acids. Yet, an apparent dissociation between the metabolic and secretory responses to the ester was suggested by the failure of alpha-D-glucose pentaacetate to increase O2 uptake by the islets. Moreover, there were striking differences between the catabolism of the ester and that of unesterified D-glucose, such as a much higher intracellular D-glucose content and an insensitiveness to the inhibitory action of D-mannoheptulose in islets exposed to alpha-D-glucose pentaacetate. Likewise, the ratio between hexose oxidation and utilization was lower for alpha-D-glucose pentaacetate than for unesterified D-glucose in islets concomitantly exposed to the hexose and its ester. It is proposed, therefore, that the insulinotropic action of alpha-D-glucose pentaacetate, although probably linked to the intracellular generation of D-glucose from the ester, may not involve the same coupling process between metabolic and functional events as that currently implied in the process of glucose-stimulated insulin release.
Insulinotropic action of alpha-D-glucose pentaacetate: functional aspects
Am J Physiol 1997 Dec;273(6):E1090-101.PMID:9435523DOI:10.1152/ajpendo.1997.273.6.E1090.
The functional determinants of the insulinotropic action of alpha-D-glucose pentaacetate were investigated in rat pancreatic islets. The ester mimicked the effect of nutrient secretagogues by recruiting individual B cells into an active secretory state, stimulating proinsulin biosynthesis, inhibiting 86Rb outflow, and augmenting 45Ca efflux from prelabeled islets. The secretory response to the ester was suppressed in the absence of Ca2+ and potentiated by theophylline or cytochalasin B. The generation of acetate from the ester apparently played a small role in its insulinotropic action. Thus acetate, methyl acetate, ethyl acetate, alpha-D-galactose pentaacetate, and beta-D-galactose pentaacetate all failed to stimulate insulin release. The secretory response to alpha-D-glucose pentaacetate was reproduced by beta-D-glucose pentaacetate and, to a lesser extent, by beta-L-glucose pentaacetate. It differed from that evoked by unesterified D-glucose by its resistance to 3-O-methyl-D-glucose, D-mannoheptulose, and 2-deoxy-D-glucose. It is concluded that the insulinotropic action of alpha-D-glucose pentaacetate, although linked to the generation of the hexose from its ester, entails a coupling mechanism that is not identical to that currently implied in the process of glucose-induced insulin release.
Metabolism of alpha-D-[1,2-13C]glucose pentaacetate and alpha-D-glucose penta[2-13C]acetate in rat hepatocytes
Arch Biochem Biophys 2000 Sep 1;381(1):61-6.PMID:11019820DOI:10.1006/abbi.2000.1967.
Hepatocytes from fed rats were incubated for 120 min in the presence of alpha-D-[1,2-13C]glucose pentaacetate (1.7 mM), both D-[1,2-13C]glucose (1.7 mM) and acetate (8.5 mM), alpha-D-glucose penta[2-13C]acetate (1.7 mM), or D-[1,2-13C]glucose (8.3 mM). The amounts of 13C-enriched L-lactate and D-glucose and those of acetate and beta-hydroxybutyrate recovered in the incubation medium were comparable under the first two experimental conditions. The vast majority of D-glucose isotopomers consisted of alpha- and beta-D[1,2-13C]glucose. The less abundant single-labeled isotopomers of D-glucose were equally labeled on each C atom. The output of 13C-labeled L-lactate, mainly L-[2-13C]lactate and L-[3-13C]lactate, was 1 order of magnitude lower than that found in hepatocytes exposed to 8.3 mM D-[1,2-13C]glucose, in which case the total production of the single-labeled species of D-glucose was also increased and that of the C3- or C4-labeled hexose was lower than that of the other 13C-labeled isotopomers. In cells exposed to alpha-D-glucose penta[2-13C]acetate, the large majority of 13C atoms was recovered as [2-13C]acetate and, to a much lesser extent, beta-hydroxybutyrate labeled in position 2 and/or 4. Nevertheless, L-[2-13C]lactate, L-[3-13C]lactate, and single-labeled D-glucose isotopomers were also produced in amounts higher or comparable to those found in cells exposed to alpha-D-[1,2-13C]glucose pentaacetate. However, a modest preferential labelling of the C6-C5-C4 moiety of D-glucose, relative to its C1-C2-C3 moiety, and a lesser isotopic enrichment of the C3 (or C4), relative to that of C1 (or C6) and C2 (or C5), were now observed. These findings indicate that, despite extensive hydrolysis of alpha-D-glucose pentaacetate (1.7 mM) in the hepatocytes, the catabolism of its D-glucose moiety is not more efficient than that of unesterified D-glucose, tested at the same molar concentration (1.7 mM) in the presence of the same molar concentration of unesterified acetate (8.5 mM), and much lower than that found at a physiological concentration of the hexose (8.3 mM). The present results also argue against any significant back-and-forth interconversion of D-glucose 6-phosphate and triose phosphates, under conditions in which sizeable amounts of D-glucose are formed de novo from 13C-enriched Krebs cycle intermediates generated from either D-[1,2-13C]glucose or [2-13C]acetate.
Dissimilar effects of D-mannoheptulose on the phosphorylation of alpha- versus beta-D-glucose by either hexokinase or glucokinase
Int J Mol Med 2004 Jul;14(1):107-12.PMID:15202024doi
D-mannoheptulose inhibits D-glucose phosphorylation by hexokinase isoenzymes. The present study aims at investigating whether the pattern of such an inhibition differs in the case of alpha- versus beta-D-glucose. The phosphorylation of alpha- and beta-D-[U-14C]glucose was measured over 60-min incubation at 4 degrees C in the presence of bovine heart hexokinase and over 10 min at 24 degrees C in the presence of human liver glucokinase. The relative extent of the inhibitory action of D-mannoheptulose (0.02-10.0 mM) was always less marked with alpha- than beta-D-glucose. In the case of hexokinase, the experiments conducted at the high concentration of the D-glucose anomers (1.0 mM) revealed that D-mannoheptulose, at low concentrations (0.2-0.5 mM), may unexpectedly increase the phosphorylation of alpha-D-glucose. These findings thus document anomeric specificity in terms of the inhibitory action of D-mannoheptulose upon alpha- versus beta-D-glucose phosphorylation by either hexokinase or glucokinase.