The SGLT2-inhibitor dapagliflozin improves neutropenia and neutrophil dysfunction in a mouse model of the inherited metabolic disorder GSDIb

Roberta Resaz, Federica Raggi, Daniela Segalerba, Chiara Lavarello, Alessandra Gamberucci, Maria Carla Bosco, Simonetta Astigiano, Antonia Assunto, Daniela Melis, Mariavittoria D'Acierno, Maria Veiga-da-Cunha, Andrea Petretto, Paola Marcolongo, Francesco Trepiccione, Alessandra Eva

Research output: Contribution to journalArticlepeer-review

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.

Original languageEnglish
Article number100813
JournalMolecular Genetics and Metabolism Reports
Volume29
DOIs
Publication statusPublished - Dec 2021

Keywords

  • 1,5-anhydroglucitol-6-phosphate
  • Dapagliflozin
  • Glycogen storage disease type 1b
  • Mouse model
  • Neutrophils
  • Renal sodium-glucose co-transporter-2

ASJC Scopus subject areas

  • Molecular Biology
  • Genetics
  • Endocrinology

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