ReviewJournal of inherited metabolic disease2025
Pathophysiology of the Neutropenia of GSDIb and G6PC3 Deficiency: Origin, Metabolism and Elimination of 1,5-Anhydroglucitol.
Review in Journal of inherited metabolic disease, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed.
- 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
- Insights into Neutrophil Dysfunction in Inherited Metabolic Disorders.Journal of innate immunity · 2026Review
- Pathophysiology of the Neutropenia of GSDIb and G6PC3 Deficiency: Origin, Metabolism and Elimination of 1,5-Anhydroglucitol.Journal of inherited metabolic disease · 2025Review
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Authors and funding
4 authors.
Funding
Abstract
Neutropenia in Glycogen Storage Disease Type Ib (GSDIb) and G6PC3 deficiency results from defects in metabolite repair, leading to the accumulation of 1,5-anhydroglucitol-6-phosphate (1,5-AG6P). Treatment currently relies on inhibitors of SGLT2, the renal sodium-glucose co-transporter, which indirectly enhances urinary excretion of 1,5-anhydroglucitol (1,5-AG), the precursor of the toxic 1,5-AG6P that accumulates in neutrophils and is at the origin of these patients' neutropenia. In this context, a detailed understanding of the formation, intestinal absorption, renal reabsorption, and metabolism of 1,5-AG is essential. Here, we review the current knowledge of these mechanisms, their role in the pathophysiology of 1,5-AG6P-related neutropenia, and explore potential strategies to improve treatment outcomes.
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Registered trials
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