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Chemical Compound Review

CHEBI:15954     [(2R,3R,4S,5R)-2,3,4,5- tetrahydroxy-6-oxo...

Synonyms: CTK3I9725, AC1L98E0, C03251, G6Q, 29832-EP2270011A1, ...
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Disease relevance of glucose-6-phosphate

  • Pretreatment with either flunarizine or diltiazem reduced the decrease in the energy charge potential and the increase in the [( G6P] + [F6P]/[FDP] ratio during ischemia [1].
  • There was a 53% increase in G6P levels in the peritonitis livers, to 540 +/- 155 nanomole/g liver while in young septic rats the G6P decreased 33 per cent [2].
  • Glycogen storage disease type 1 (GSD1) is an inborn error of metabolism caused by deficiency of glucose-6-phosphatase, the enzyme catalysing the conversion of glucose-6-phosphate (G6P) to glucose [3].
  • In a similar murine peritonitis model, which permitted longer survival times, analysis of liver samples at 12 and 18 hours supported the conclusion that G6P was the metabolite that responded first or most consistently to endotoxin and sepsis [4].

High impact information on glucose-6-phosphate

  • Here we propose that the phosphorylation of GSase, which alters the sensitivity to allosteric activation by glucose 6-phosphate (G6P), is a mechanism for controlling the concentration of G6P instead of controlling the flux [5].
  • This increase in GSase fractional activity helps to maintain G6P homeostasis by reducing the G6P concentration required to activate GSase allosterically to match the flux determined by the proximal reactions [5].
  • Tungstate treatment of these rats induced a 42% decrease in serum levels of triglycerides and normalized hepatic G6P concentrations, GPa activity, and PEPCK levels [6].
  • Studies of HKI indicate that the C-terminal half of the molecule is active and is sensitive to inhibition by glucose 6-phosphate (G6P), whereas the N-terminal half binds G6P but is devoid of catalytic activity [7].
  • In contrast, both the N- and C-terminal halves of HKII (N-HKII and C-HKII, respectively) are catalytically active, and when expressed as discrete proteins both are inhibited by G6P [7].

Chemical compound and disease context of glucose-6-phosphate

  • In the saline-treated heart, ischemia increased the levels of G6P and F6P, whereas it decreased the level of FDP [8].

Biological context of glucose-6-phosphate

  • These findings could be explained by partial channelling of Glc6P between glucokinase and glycolysis in the presence of saturating concentrations of Fru(2,6)P(2) [9].
  • We here report the structure of the gene encoding a protein likely to be responsible for G6P transport, and its mapping to human chromosome 11q23 [10].
  • To illustrate the general features of this expanding class, this article discussed the biochemistry, physiology, and molecular biology of Pi-linked antiporters that accept glucose 6-phosphate (G6P) as their primary substrate [11].
  • Tracer uptake from labeled G6P occurred with T(1/2) values that proved insensitive to unlabeled G6P or 100 microM vanadate, and could not be activated over background levels by intravesicular phosphate in the complete absence of G6P hydrolysis [12].
  • Warm cardioplegic induction resulted in more oxygen consumption than cold induction (16.9 versus 8.1 cc/100 gm), and lower levels of glucose-6-phosphate (G6P), suggesting better aerobic metabolism (0.97 versus 1.87 microM/gm wet weight) [13].

Anatomical context of glucose-6-phosphate

  • Most likely, Glc6P rather than 3-phosphoglycerate or triose phosphates is the main substrate for daytime starch biosynthesis in M. crystallinum plants in which CAM has been induced (CAM-induced), similar to non-green plastids [14].
  • This study aimed at directly assessing glucose 6-phosphate (G6P) transport by intact rat liver microsomes [12].
  • The solubilizing effect of G6P and ATP4-, which are potent inhibitors of the enzyme, can be prevented by incubation of mitochondria with Pi or Mg2+ [15].
  • Results showed that when Mg2+ is freely permeable to the cytosol, the in vivo PFK activity, calculated as FDP/G6P ratio, is not increased as it is in intact cells [16].
  • In the attached gingiva, there was no significant change in the G6P, ATP, or CP content [17].

Associations of glucose-6-phosphate with other chemical compounds

  • However, hexokinase (HK) was found to be the rate-limiting step: the glucose-supported reduction rate was only 50% of that of G6P-supported activity [18].
  • The strong enhancement of FDP/G6P ratio is taken as evidence for in vivo stimulation of phosphofructokinase 1 (PFK) (ATP:D-fructose-6-phosphate 1-phosphotransferase; EC [19].
  • 5. Similarly, cardiac HK-I activity (conversion of glucose to G6P) and glycolysis (conversion of glucose to lactate) were higher on gd 9.5 than on gd 13 [20].
  • Using 31P NMR spectroscopy, the accumulation of 2-deoxy-D-glucose-6-phosphate (DG6P) was monitored over time [21].
  • The approach used was to optimize the generation of non-toxic concentrations of NADPH from NADP glucose-6-phosphate (G6P) and G6P dehydrogenase, then use that system to examine the effects of increasing concentrations of Aroclor-1254-induced Fischer 344 male rat liver post-mitochondrial supernatant fluid (S9) upon the mutagenicity of chemicals [22].

Gene context of glucose-6-phosphate

  • To explain the function of the G6Pase complex, a multicomponent translocase catalytic model has been proposed in which different transporters shuttle glucose-6-phosphate (G6P), inorganic phosphate (Pi) and glucose across the microsomal membrane [23].
  • It was suggested that GSD1b patients suffered from a G6P transporter (G6PT) defect and the first mutation in the G6PT gene subsequently recognised [23].
  • A functional assay for the recombinant G6PT protein has been established, which showed that G6PT functions as a G6P transporter in the absence of G6Pase [24].
  • However, microsomal G6P uptake activity was markedly enhanced in the simultaneous presence of G6PT and G6Pase [24].
  • The increased transport activity of GPT in the light suggests a higher requirement for Glc6P import for starch synthesis rather than starch mobilization [14].

Analytical, diagnostic and therapeutic context of glucose-6-phosphate

  • Molecular methods applied to DNA extracted from skin biopsies of the 50 patients yielded 100%, 82% and 44% positivity by PCR minicircle kDNA, PCR-RFLP ITS1rDNA and PCR-glucose-6-phosphate (G6P), respectively [25].
  • Glycation of alphaA-crystallin with G6P showed several high molecular weight (HMW) protein bands on the SDS-PAGE gel; DMPTB inhibited the formation of these HMW proteins [26].


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