What it does, reaction by reaction
Gluconeogenesis Carbohydrate Metabolism · Cytosol + mitochondrion + ER
Glucose-6-phosphate + H2O → glucose + Pi
Converts Glucose-6-phosphate H2O into Glucose Pi
› Notes
The endoplasmic-reticulum glucose-6-phosphatase system hydrolyzes glucose-6-phosphate after transport into the ER lumen by glucose-6-phosphate translocase; the glucose and phosphate are returned to the cytosol through transporters. Hydrolysis requires water and is the final bypass of hexokinase/glucokinase, is irreversible, and permits hepatic or renal release of free glucose.
Glycogenolysis (Glycogen Breakdown) Carbohydrate Metabolism · Cytosol + ER (liver)
Glucose-6-phosphate + H2O → glucose + Pi
Converts Glucose-6-phosphate H2O into Glucose Pi
› Notes
In liver and renal cortex, the endoplasmic-reticulum glucose-6-phosphatase system hydrolyzes glucose-6-phosphate after its transport into the ER lumen. This irreversible step enables release of glucose to blood; it is absent from skeletal muscle, explaining why muscle glycogen cannot directly correct hypoglycemia.
Showing all 2 reactions.
What accelerates and inhibits it
Regulation is pathway-specific, so each context is listed separately
Gluconeogenesis
Listed there as: Glucose-6-phosphatase
Substrate availability
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Induced by glucagon and cortisol during fasting; repressed by insulin in the fed state
Glycogenolysis (Glycogen Breakdown)
Listed there as: Glucose-6-phosphatase (liver/kidney)
Substrate availability
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Expression rises in fasting with glucagon/cortisol and falls with insulin
Pentose Phosphate Pathway (Oxidative and Non-oxidative phases)
Listed there as: Glucose-6-phosphate dehydrogenase
NADP+, glucose-6-phosphate; increased NADP+/NADPH ratio
NADPH
Insulin induces expression in liver and adipose tissue during lipogenesis
Recent literature
Europe PMC · fetched just now · sorted by publication date
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1
Recent Advancements in Known and Emerging Risk Factors of Hepatocellular Carcinoma.
Hussain MM, Feng B, Wang JM, Zhai AQ, Li FY, Li FY, Hu HJ. · 2025-11-01
open access unreviewed -
2
JAK/STAT inhibition protects glucocorticoid receptor knockout mice from lethal malaria-induced hypoglycemia and hyperinflammation.
Prenen F, Vandermosten L, Knoops S, Pollenus E, Possemiers H, Dagneau de Richecour P, Caratti G, Cawthorne C,… · 2025-07-23
cited 1× open access unreviewed - 3
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4
[Clinical analysis and follow-up outcomes of 25 pediatric cases with hepatic glycogen storage disease].
Liu WW, Wang MJ, Jin M, Zhang R, Mi MR, Zhong XM. · 2024-11-06
unreviewed -
5
WES-based screening of 7,000 newborns: A pilot study in Russia.
Shubina J, Tolmacheva E, Maslennikov D, Kochetkova T, Mukosey I, Sadelov I, Goltsov A, Barkov I, Ekimov A, Ro… · 2024-07-19
cited 5× open access unreviewed -
6
Pharmacological Activities, Therapeutic Effects, and Mechanistic Actions of Trigonelline.
Nguyen V, Taine EG, Meng D, Cui T, Tan W. · 2024-03-16
cited 40× open access unreviewed -
7
Biochemical pathways represented by Gene Ontology-Causal Activity Models identify distinct phenotypes resulting from mutations in pathways.
Hill DP, Drabkin HJ, Smith CL, Van Auken KM, D'Eustachio P. · 2023-10-01
cited 1× open access unreviewed -
8
Perspectives of Rare Disease Experts on Newborn Genome Sequencing.
Gold NB, Adelson SM, Shah N, Williams S, Bick SL, Zoltick ES, Gold JI, Strong A, Ganetzky R, Roberts AE, Walk… · 2023-05-01
cited 43× open access unreviewed -
9
Glycogen storage disease type I: Genetic etiology, clinical manifestations, and conventional and gene therapies.
Zhong J, Gou Y, Zhao P, Dong X, Guo M, Li A, Hao A, Luu HH, He TC, Reid RR, Fan J. · 2023-07-24
cited 7× open access unreviewed -
10
A molecular signature for the G6PC3/SLC37A2/SLC37A4 interactors in glioblastoma disease progression and in the acquisition of a brain cancer stem cell phenotype.
Torabidastgerdooei S, Roy ME, Annabi B. · 2023-11-16
cited 6× open access unreviewed
External claims. These come from an index outside this database and are not checked against it. Treat them as leads.