ArticleProceedings of the National Academy of Sciences of the United States of America2019
Failure to eliminate a phosphorylated glucose analog leads to neutropenia in patients with G6PT and G6PC3 deficiency.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 98 papers, 1 of them a synthesis that pooled it.
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Who cites it
98 citing papers in PubMed, 1 synthesis or guideline pooled it, 162 citations in OpenAlex.
- Safety of SGLT-2 inhibitors in patients with glycogen storage disease type Ib and their efficacy in treating disease-associated digestive symptoms and disorders.Acta diabetologica · 2026Pooled it
- Empagliflozin in GSD-Ib: Long-term safety and sustained recovery of neutrophil function including NET formation.Molecular genetics and metabolism reports · 2026Article
- Transcriptomics and 4D-DIA proteomic analysis reveal differences in meat quality between Sichuan white rabbits and New Zealand white rabbits.Food chemistry. Molecular sciences · 2026Article
- Shifting Towards Empagliflozin First-Line Therapy in Glycogen Storage Disease Type Ib: A Nationwide Real-World Study.Journal of inherited metabolic disease · 2026Article
- The return of metabolism: biochemistry and physiology of glycolysis.Biological reviews of the Cambridge Philosophical Society · 2026Review
- 1,5-Anhydroglucitol Aggravates Acute Liver Failure via the PPARα Signaling Pathway.Journal of clinical and translational hepatology · 2026Article
- Clinical Outcomes and Management in Late Diagnosed Siblings Affected With Attenuated GSD Ib.JIMD reports · 2026Article
- Structures of the human glucose-6-phosphate transporter provide insights into its transport cycle and substrate recognition.PLoS biology · 2026Article
- Neutrophil Extracellular Traps in Wound Healing of Diabetes: Mechanisms, Inducers, and Therapeutic Implications.Mediators of inflammation · 2026Review
- The glucose-6-phosphatase system in cancer: from endoplasmic reticulum glucose-6-phosphate flux to stemness, immune escape, and therapeutic vulnerability.Frontiers in oncology · 2026Review
- Insights into Neutrophil Dysfunction in Inherited Metabolic Disorders.Journal of innate immunity · 2026Review
- The unanticipated role of the glial-associated glucose-6-phosphatase system in brain homeostasis.iScience · 2025Review
- Structural basis for transport and inhibition of the human glucose-6-phosphate transporter G6PT.Nature communications · 2025Article
- Pathophysiology of the Neutropenia of GSDIb and G6PC3 Deficiency: Origin, Metabolism and Elimination of 1,5-Anhydroglucitol.Journal of inherited metabolic disease · 2025Review
- Spontaneous restoration of premature ovarian insufficiency and conception in a patient with glycogen storage disease type 1b managed with empagliflozin.Hormones (Athens, Greece) · 2025Article
- Clinical and Genetic Profile of 35 Patients with Glycogen Storage Disease Type 1b: A Comparative Analysis Before and During SGLT2 Inhibitor Therapy.Molecular diagnosis & therapy · 2025Article
- Article
- Empagliflozin as treatment in glycogen storage disease type IB patients.Molecular genetics and metabolism reports · 2025Article
- A budget for brain metabolic water production by glucose catabolism during rest, rises in activity and sleep.Fluids and barriers of the CNS · 2025Review
- Article
38 more citing papers are in PubMed but not listed here.
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Authors and funding
11 authors at 4 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Neutropenia represents an important problem in patients with genetic deficiency in either the glucose-6-phosphate transporter of the endoplasmic reticulum (G6PT/SLC37A4) or G6PC3, an endoplasmic reticulum phosphatase homologous to glucose-6-phosphatase. While affected granulocytes show reduced glucose utilization, the underlying mechanism is unknown and causal therapies are lacking. Using a combination of enzymological, cell-culture, and in vivo approaches, we demonstrate that G6PT and G6PC3 collaborate to destroy 1,5-anhydroglucitol-6-phosphate (1,5AG6P), a close structural analog of glucose-6-phosphate and an inhibitor of low-
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