ArticleMolecular genetics and metabolism reports2021
The SGLT2-inhibitor dapagliflozin improves neutropenia and neutrophil dysfunction in a mouse model of the inherited metabolic disorder GSDIb.
Article in Molecular genetics and metabolism reports, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed, 10 citations in OpenAlex.
- 1,5-Anhydroglucitol Aggravates Acute Liver Failure via the PPARα Signaling Pathway.Journal of clinical and translational hepatology · 2026Article
- Biochemical characterization of the human ubiquitous glucose-6-phosphatase in neutrophil granulocytes.FEBS open bio · 2025Article
- Causality of genetically determined blood metabolites on inflammatory bowel disease: a two-sample Mendelian randomization study.Scientific reports · 2024Article
- The paradox of autoimmunity and autoinflammation in inherited neutrophil disorders - in search of common patterns.Frontiers in immunology · 2023Review
- The overall benefits of empagliflozin treatment in adult siblings with glycogen storage disease type Ib: one year experience.Archives of medical science : AMS · 2022Article
- Favorable outcome of empagliflozin treatment in two pediatric glycogen storage disease type 1b patients.Frontiers in pediatrics · 2022Article
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Authors and funding
15 authors at 8 institutions in 2 countries.
Funding
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Abstract
Glycogen Storage Disease type 1b (GSDIb) is a genetic disorder with long term severe complications. Accumulation of the glucose analog 1,5-anhydroglucitol-6-phosphate (1,5AG6P) in neutrophils inhibits the phosphorylation of glucose in these cells, causing neutropenia and neutrophil dysfunctions. This condition leads to serious infections and inflammatory bowel disease (IBD) in GSDIb patients. We show here that dapagliflozin, an inhibitor of the renal sodium-glucose co-transporter-2 (SGLT2), improves neutrophil function in an inducible mouse model of GSDIb by reducing 1,5AG6P accumulation in myeloid cells.
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